NATIONAL INSTITUTE OF SIDDHA

Chennai – 47

THE TAMIL NADU DR. M.G.R. MEDICAL

UNIVERSITY, CHENNAI – 32

A STUDY ON

MADHU MEGAM
(DISSERTATION SUBJECT)

For The Partial Fullfillment Of The

Requirements To The Degree Of

DOCTOR OF MEDICINE (SIDDHA)

BRANCH I– MARUTHUVAM DEPARTMENT

APRIL – 2012
 CERTIFICATE

Certified that I have gone through the dissertation submitted by

Dr.P.VIJAYAKUMAR, a student of final M.D(S), Branch-I, Department of
Maruthuvam, National Institute of Siddha, Tambaram Sanatorium,
Chennai-47, and the dissertation work has been carried out by the
individual only. This dissertation does not represent or reproduce the
dissertation submitted and approved earlier.

Place: Chennai-47 Prof. Dr.K.Manickavasakam MD(S),

Date: Director I/C & Head of the Department
Dept. of Maruthuvam
National Institute of siddha
Chennai - 600 047.

CERTIFICATE

Certified that I have gone through the dissertation submitted by

Dr.P.VIJAYAKUMAR, a student of final M.D(S), Branch-I, Department of
Maruthuvam, National Institute of Siddha, Tambaram Sanatorium,
Chennai-47, and the dissertation work has been carried out by the
individual only. This dissertation does not represent or reproduce the
dissertation submitted and approved earlier.

Place: Chennai-47 Prof. Dr.K.Manickavasakam MD(S),

Date: Director I/C & Head of the Department
Dept. of Maruthuvam
National Institute of siddha
Chennai - 600 047.
 ACKNOWLEDGEMENT

I feel immense awe and huge gratitude in my kindness of thanks to God almightly for making this
dissertation have its present form.

In all humility,I salute with great thanks to the Tamil nadu Dr.M.G.R Medical University and
Dept of AYUSH, Ministry of health and family welfare, Govt of India for granting permission
to take this study.

Its with enormous pleasure that I expressed my heartful gratitude to Prof.

Dr.K.Manickavasakam MD(S),Director i/c and Head of the department of Maruthuvam,
National Institute of Siddha, Chennai-47.

I express my sincere thanks to Prof.Dr.M.Murugesan MD(S),Dean,HOD dept of nanju

maruthuvam NIS,Chennai-47.

I express my sincere thanks to Prof.Dr.R.S.Ramasamy MD(S),Head Of the Department of

Sirappu Maruthuvam and Hospital Superintendent,NIS,Chennai-47.

I express my deep sense of gratitude to Associate prof.Dr.J.Indhira Devi MD(S),for her valuable
guidance and support.

I express my deep sense of gratitude to Dr.T.Lakshmikantham MD(S),for her valuable guidance

and support.

I express my sincere thanks to Dr.H.Vetha Merlin Kumari MD(S) for her valuable guidance and
support.

I express my heartful thanks to Dr.H.Nalini Sofia MD(S) for her memorable support and
encouragement.

I express my sincere gratitude to Mr.M.Subramanian Msc,SRO,NIS,Chennai-47.for his guidance

in statistical analysis.

I acknowledge my thanks to Prof.dr Rajavel indira MD (patho).for his support and guidance in
histopathological studies.

I extend my thanks to Dr. R murugesan, IIT guindy.

I extend my sincere thanks to Dr. D.Aravind Asst.professor,in Medicinal botany NIS .

I Convey My Thanks To Dr.V.Suba, M.Pharm.,Ph.D, Associate professor, Dept. of

Pharmacology ,NIS,chennai .

I extend my sincere thanks to each and every faculties of NIS especially faculties of Library and
Laboratory for their support thought this dissertation work.

Finally, I Would like to convey my regards to Dr.R.selva ganesa pandian MD(s),my very
supportive batchmates and friends for their valuable support and contribution on my study.they
will remain in my heart for their kindness.
 CONTENTS

S.No Title Page No

1 Introduction 1

2 Aim And Objective 3

3 Review of literature

a.Siddha Aspects 4

b.Modern Aspects 40

4 Materials and methods 78

5 Observations and results 86

6 Discussion 122

7 Summary 127

8 Conclusion 128

9 Annexure-I (Proforma)

10 Annexure –II (Trial drug peparation )

11 Annexure –III (Raw drugs review)

12 Annexure –IV (Preclinical study)

13 Annexure-V (Certificates)

14 Bibliography
 INTRODUCTION

Siddha system is considered to be one of the ancient system of medicine in

the world. Siddha is a complete holistic medical system that has been practiced in India
for two thousands of years above.

The siddha system of medicine has derived its name from the word
"Siddhi" which means "Perfection" or "Eternal bliss". Siddhi refers to the eight
supernatural powers that are attainable by man. Those who attained these supernatural or
perfection or siddhi were called "Siddhars". They realised that if the body could be made
strong and perfect, they could get rid of death and diseases.

They have fully investigated and studied the cause and the effects of
the diseases and all kinds of drugs, minerals and poisons. They imparted
their knowledge for the upliftment of the human life style.

Panchapootha theory has also been described by Siddhars. The

panchapoothas are Akasa (ether), Kaattru (vayu or air), Thee (agni or fire) Neer (appu or
water) Nilam (earth or piruthuvi).

Every form of matter has to be considered as panchapoothas in its orgin

Vali( ) Azal ( ) Iyam ( ) are the three main Physiological regulators of

the body and mind. They are called "Muththathukkal". They remains always in a state of
equipoise in healthy individuals. Increase or decrease of one or more will cause disease.

Generally when a medicine is administrated Siddha Physician prescribes

diet regimen according to the nature of the medicine and severity of the disease. As over
intake or consuming unbalanced and incompatible diet is considered to the prime
causative factor for upsetting the tridhosa balance leading to manifestations of various
ailments.

Madhumegam is also called as "Neerizhivu" characterised by increased

and frequent passing of urine, which is sweet in odour, resulting in gradual diminition of
udalthathus.

Siddhars also described that 20 types of pramegam according to

tridhoshas and are described on the basis of colour, consistency, taste, smell, weight,
sedimentation etc.

The evidence or proof for this disease has been described by "Yugi
Munivar" in his text "Vaidhya Chinthamani 800". Four varieties under vatham, Six due to
pitham, and ten due to kabam. One among in Pitha is called Madhu megam.

The signs and symptoms of "madhumegam" in siddha text may be

correlated with that of "Diabetes mellitus" in modern science.

Accorging to Yugimuni & Agasthiar this disease is due to Kanma or Karmam that
is hereditary, also due to dietetic variations. According to "Nadi Nool" it is said to be due
to over indulgence in sex. Pittha thadhu is highly accountable for the maintenance of life
process, with proper treatment the severity of the disease can be controlled by potent
drugs with diet regimen and yoga.

The modern clinical entity "Diabetes Mellitus" resembles one of the

variety of pittha prameham ie. "Madhumegam" very closely. The former being a
metabolic disorder caused by insufficient insulin action or its deficiency characterised by
raised blood sugar level, the chief clinical features are polyuria, polyphagia, polydipsia,
ketonuria, hypokalemia, cellular dehydration etc. The author is very obliged to do this
work and to prepare some facts in this disease and principles involved in the care of this
disease.
 AIM AND OBJECTIVE

AIM

The Purpose of this study is to Evaluate the safer and efficacy of the Siddha Herbal
formulation THETRAN VIDHAI KUDINEER in the management of Madhumegam
(Type II Diabetes Mellitus) as an open clinical trial.

OBJECTIVES

1.To prepare the trial drug THETRAN VIDHAI KUDINEER as per Siddha literature
(Gunapadam Mooligai ) and analysis of qualitative and quantitative constituents present
in the trial drug.

2.To establish the toxicological profile by performing acute oral toxicity studies and sub
chronic toxicity studies on mice and rats following WHO guidelines.

3.To analyze the prevalence of Madhumegam among the society through Age, Sex,
Occupation, Distribution etc…

4.To Study the Safety and efficacy of the test drug through an open clinical trial.
 REVIEW OF LITERATURES

SIDDHA ASPECT

MADHUMEGAM

According to siddhars the imbalance of Tridosha causes totally 4448

diseases to human being.Among them megarogam is considered to be the emperor of
diseases.

Madhumegam has been described by many siddhars in their texts. The

aetiology, pathogenesis, classification,clinical features, diagnosis and prognosis have
been dealt in detail in these texts.

Synonyms of Madhumegam:

Neerizhivu, vegumoothiram, madhu prameham, inippuneer, meganeer,

Thithippuneer.

Definition (Iyal):

It is a clinical condition characterized by frequent passage of urine more

than the normal resulting in deterioration and diminution of seven thathus.

“ ஈ

The above description quotes that ant and flies are attracted to the site of
voided urine and when the urine is heated it gives honey odour .
 “

This poem comprises the clinical features of Madhumegam

Noi Varum Vali (Etiology):

a.The authentic etiological factors described by various siddhars are as follows.

‘Nfhijau; fytp Nghij

nfhOj;j kPd; ,iwr;rp Nghij

ghJtha; nea;Ak;ghYk;

gupTld; cz;guP hfpy;

Nrhj ghz;LUt kpf;f

Rf;fpy gpuNkfe;jhd;
XJ ePupopT Nru

Tz;nld mwpe;J nfhs;Ns”

- mfj;jpau; 1200
The above poem quotes that excessive intake of rich food like ghee, fish,
milk, toddy and excessive indulgence in sex leads to madhu megam. The same also
discussed in "Yugi sinthamani"

‘cw;gtpf;Fk; ghy; nea;ahy; ,iwr;rp nfhs;sy;

Tupiraha kPdj
; d;dhy; mUtpUj;j

kw;gtpf;Fk; gjhu;j;jj;jhy; kJu t];jhy;

ke;jq;fs; jidGrpj;jy; Ntfhg; gz;lq;

Fw;gtpf;Fq; FSj;j td;d kq;if Nfh\;b

Fwpj;j epj;jpiu jtpu;jy; mf;fpdp ke;jk;

jw;gtpf;Fe; ruPue;jhd; kpfg; gUj;jw;

rQ;rye;jhd; kpfg;gaj;jhy; jupf;Fk; NehNa”

- a+fpitj;jpa rpe;jhkzp

‘,ak;gNt MW Fsk; gpd;dQ; nra;jy;

Vw;wkha; khw;whd; ngz; rq;fk; nra;jy;

gak;gNt ghyfu;fSf; nfhspj;J jpd;dy;

eiu g+j;jnfhq;ifahs; ehafd; Nkhfj;jhy;

kiw Nghw;Wq; fUg;gj;jpy; tsu;e;jJ NkfNk”

- jpU%yu;

‘];jpupNghfk; nra;jjpdhy; NtTnfhz;L

rpuR kl;Lk; nte;JUfpf;fdNy kPwpf;

FwpAlNd Nkfe;jhd; nfhLik nra;J

Fiwe;J tUk; jhJnty;yhk; Fd;wpg; NghFk”;

- FUehb

‘fd;dp kaf;fj;jhy; fz;bL NkfNk”

- ehbE}y;
 ‘epiw g+j;j nfhq;ifahs; ehafd; Nkhfj;jhy;

kiw Nghw;Wk; fUg;gj;jpy; tsu;e;jJ NkfNk”

- jpU%yu;

‘fpue;jp Gz;;zpuz Nkff;fPrfndDe; Jd;khu;f;fd;

mUe;jjp vd;Dk; ghQ;rhyp ad;idiaf; fz;Zw;whNd”

- Njud; kUj;Jt ghujk;

The conclusion from the above said, all Siddhars attribute Diabetes mainly
due to excessive indulgence in sex which results in depletion of total strength of body as a
whole, making the individual susceptible to this disease.

d. Psychosomatic Factors

Yugimunivar and other Siddhars stress a great importance to

Psychosomatic factor. All antisocial activities ultimately result in subjective guiltiness
and psychosomatic stress resulting in disease like diabetes, peptic ulcer and hypertension.

‘kjq;nfhz;L ngupNahiu itifahYk;

khju; fw;Gepiyik jd;id mopf;ifahYk;

gjq;nfhz;l rptNahfp rhgj;jhYk;

gj;Jtif rpNyw;gdq;fs; NkfePuhk; “

- a+fpKdp itj;jpa rpe;jhkzp

E) Kanma Noi

In the views of Theraiyar, Agasthiar and Thirumoolar, Madhu megam also

occurs as a result of bad deeds commited in his or her past or previous births.
 ‘Mkg;gh kdpju; nra;j fu;kj;jhNy

mufuh Nkfnkd;w uhrhthNy

fhkg;gh yjpdhy; grpAg;g ehYq;

iff;flq;fh Neha;fs; tUk; fu;kj;jhNy “

- mfj;jpaKdptu; fu;kfhz;lk;

Noi Enn (Classification)

Twenty varieties of meha disorders have been discussed by Yugimuni and Agasthiar,

‘nrhy;Ynkd;W Nfl;lTld; rptD kg;Ngh

Njtpiaj;jhd; Kfk;ghHj;J thuha; Njtp

my;Ynkd;Nw NkfkJ ,uz;L gj;J

kfpo;e;J eP NfSnkd;W trdpj;jhNu”

‘trdpj;j NkfkJ ,uz;Lgj;J

thjj;jpw; gpwe;j ryk; ehNyahFk;
gprdpj;j gpj;jj;jp Yw;gtpj;j

Nguhd rye;jhD khWkhFk;

Njrdpj;j Nrl;L kj;jpy; cw;gtpj;j

rPuhd rye;jhDk; gj;NjahFk;

,rdpe;j ,jDila FzhFzq;fs; “;

- A+fp itj;jpa rpe;jhkzp

The saint Yugi classified megam into 20 types.
ie., this Vatha 4, Pitha 6 and Kabha 10 types.
 ‘jf;f jhuzp khdplj;Njhu;fs; Nfs;

gf;f khryk; tifAkhNk

ef;f ehafd; ehafpf;Nf nrhy;

kpf;f ee;jp tpsk;gp tpjpj;jNj”

‘RopAk; thjk; ehd;fhYk; fak; gpj;jkhwhYk;

fopAk; Nrj;Jkk; gj;jhYk;> nrhy;Yk; ehyQ;rha; Njhd;Wk;

topAk; thjk; ehd;fhNk khU jtpo;je; jd;dhNy”

- Njiuau; thflk;

As per Thirumoolar Vaidyam 600, Prameham is also called as Premeham

Neerizhivu. In Agasthiyar texts and "Yugi muni Vaidhya Chinthamani 800"
Madhumegam is one among the 20 varieties of Prameham. Each author who have dealt
mega disorders have differently classified them under three doshas and have given names
according to their concept. But the number, signs and symptoms of the classified
disorders are almost identical in the description of the disease. Different types of clinical
disorders have been described on the basis of colour, consistency, taste and smell etc.

Classification:

Classification of Prameham as in various texts of siddha system of

medicine are as follows,

(i) Yugimuni Vaidhya Chinthamani 800 as follows,

Varieties of pramegam under Vatham:

1. nea; kz ePu;

2. gR kz ePu;

3. Cd; kz ePu;

4. rPo; ePu;
 Varieties of pramegam under Pitham:

1. ahidf;nfhOg;G kz ePu;

2. fw;whio kz ePu;

3. Rz;z kz ePu;

4. ,dpg;G Nkfk;

5. gspq;F ePu;

6. Kaw;FUjp ePu;

Varieties of pramegam under Kabham:

1. trh ePu;

2. njsp ePu;

3. %is cUf;FePu;

4. ,sePu; ePu;

5. fs; ePu;

6. Rf;fpy ePu;

7. Njd; ePu;

8. cg;G ePu;

9. fO ePu;

10. ,iwr;rp ePu;

(iii) Thirumoolar 600

In Thirumoolar 600 text meham is classified into 21 varieties, they are as

follows,

1.Muyarchiyal Vanthamegam (Self acquired-6 )

 2.Karuppathal Vanthamegam (Hereditary (or) Constitutional-5 )

3.Palakkaarana Megam (Miscellaneous-7 )

b) Signs and Symptoms of Madhumegam

Yugimuni has described the signs and Symptoms of Madhumegam as follows

‘$whd NkfkJ ,UgJf;Fk;

Fze;jid rptd; nrhy;y Njtp Nfl;f

jhwhd jhfnkhL Nrhf Nkfe;

jupahky; ePupopj ypUky;%r;R

Mwhd mUrprj;jp rpj;j gpuik

mbf;fbf;Fj; jz;zuP j
; h dd;dq; Nfl;ly;

<whd ,Lg;Gf;Fs; fLg;G fhzy;

vYk;G ow;wNyh nlupTlz;lhNk”

‘vupNthL ruPunky;yh kiwgl;lhw; Nghy;

vopYlk;G Nehjy; epj;jpiu apy;yhik

tupNthL kha;Tnkj;j Tk;gwpj;jy;

kdJ rQ;ryg;gLjy; fhw;W Ntz;ly;

nkupNthL Nky;%r;R kpfTz;lhjy;

tpf;fNyhL kaf;fe;jhd; nkj;jf; fhzy;

njupNthL Njfnkq;Fk; ntSUz;lhjy;

Njfnkj;j thNyhgg;gLjy; fhNz”

 ‘jd;ikaha;r; rye;jhDk; gRg;G kQ;rs;

jhdpwq;Fk; gPrKq; NfhrKq; fLf;Fk;

mz;ikahabf;fbf;F ePuwq;F

kbf;fbf;F miuehop jdpNy jhDk;

ntz;ikaha bajdpw;whd; gpbf;Fk;

kpf;fhd; rlk; ntSj;J Nkdp fd;Wk;

gz;ikaha;g; gQ;rthz;ljdpw; nfhy;Yk;

gfu;fpd;w kJ Nkfj;jpd; ghq;FjhNd”

- a+fpitj;jpa rpe;jhkzp

Passing of urine in large quantity at frequent intervals, while passing

urine the patient experience burning and spasmodic pain in the urethra and dull pain in
the testis.

The urine thus passed is cold, slimy to touch, has brownish yellow colour,
produces white sediments which adhere to the bottom of the vessel in which it is
collected. The skin is pale and there is generalised tenderness. If it is not diagnosed in
time and not instituted proper treatment with diet restriction, the disease will run a
fulminating course resulting in death within five years of period.

c. Avathaigal (Complications of Madhumegam)

Yugimuni has described the complications of madhumegam as

"Avathaigal". There are ten avathaigal described one by one as follows.

‘fhzNt Kjytj;ij ruPue;jhDq;

fdkhfg; gUj;jpWfp ePuj

; ;Jthuk;

NtzNt tz;lhf;fp afyk; gz;Z

kpf;f tpuz;lhktj;ij tpsk;gf; Nfsha;

%zNt %j;jpug; gPilAkhr;Rf;fpy

KfKOj; Nj[Rjhd; kpfNt Fd;Wk;

ehzNt%d;whF ktj;ijf;Fj; jhd;

ehtwSk; thAtJ kPWe;jhNd”.

‘jhwhd ehyhktj;ij aq;f jhfQ;

rd;dpaJ ghjKz;lhike;jtj;ijj;

Njwhd ePu; ngUFe;jhJ el;lk;

epiyahSktj;ijAlw; fpilnfhs;shJ

%dhd %u;r;ir tUNkotj;ij

kpf;ftNuhrfQ; Rthre; Njf rhl;bak;

Vdhd vl;lhjtj;ij jhNd

vOfpue;jp gpsitAe;jhd; kpfTz;lhNk

cz;lhF nkhd;gjhktj;ij Nfsha;

xOf;fhd thrhuq; fpUkpAz;lhk;

gz;khd gj;jhe;jhdtj;ij Nfsha;

ghukha; raq;nfhz;L guj;Jf;NfFk;”

‘ntz;lhF Nkfe;jh dpUgJf;Fk;

tpsq;fpaNjhu; jrtjj;ij tptuq; nrhd;Ndhk;

mz;lhFQ; rhj;jpat rhj;jpakpuz;L

kwpe;J nfhz;L tlthf ttpo;jQ; nra;Na”

- a+fpitj;jpa rpe;jhkzp
1) First symptoms for meha disease is obesity and dilation of urethral canal.

2) Body becomes dry and loses its lusture due to excessive secretion
and flow of urine mixed with vital fluid (semen)

3) Dryness of the tongue and distension of abdomen due to formation and

accumulation of excessisve gas.

4) Delerium (Toxic condition) supervenes following dehydration due to

excessive ellimination of tissue fluid.

5) Restlessness due to loss of vital fluid in urine.

6) Breathlessness and restlessness

7) Nausea, tastelessness, laboured breathing, exhaustion.

8) Carbuncle and multiple abscess formation.

9) Maggot formation and generalised emaciation.

10) Intractable troublesome, Emaciation(shayam ) with profuse expectoration leading

to death.

The above complications occur in undiagnosed and improperly treated cases.

The complications of madhumegam described in siddha text is really correlated with

Diabetes mellitus in modern science.

Mukkutra Verupaadugal (Pathology of Madhu Megam)

‘FwpAlNd Nkfe;jhd; nfhLik nra;J

Fiwe;J te;J tUe;jhJ nty;yhq; Fd;wpg; NghFk;".

-gjpndd; rpj;jh; ehb Ehy;

The whole ancient medicine is based upon the 'Thridoshic theory'.
Due to intrinsic and extrinsic factors, the Iyam thathu in the body gets altered.
This is followed by the derangement of vatham(abanan) which affects udal thathukal one
by one . Finally the function of vatham and pitham also altered resulting in derangement
of normal structure and functions of the seven thathus.

Basic Concepts of Mukkutram

The Mukkuttram are

1. Vatham

2. Pitham

3. Kabam

I. Vatham

Vatham is one of the vital humour responsible for all motions of on body.
It is classified into 10 types based on the functions.

Location of Vatham in our body

Vatham is located in abanan, Faeces, Idakalai, Spermatic cord, Nerve

plexus, Joints, Hair follicles and Muscles, Bones and Thigh.Increase (or) decrease of
Vatham can cause some standing symptoms which are below,

Increase

Pain in the body, twitching & piercing pain, inflammation, reddish

complexion, roughness of skin, hardness of limbs, astringent sense of taste in the mouth,
taste not palatable, sweating during sleep, traumatic pain, constipation, oliguria, blackish
discolouration of skin,stool, urine and muddy conjuctiva, tremors, abdomen distention,
insomnia, and breathlessness.

Decrease

Body pain, feeble voice, diminished competence of intellectual functions

and syncope etc.
Types of Vatham:

1. Piranan (Uyir Kaal)

It is mainly responsible for respiration and it is necessary for proper

digestion and control knowledge.

2. Abanan (Keezhnokku Kaal)

It is responsible for voiding of urine, stools, semen and menstrual flow.

3. Viyanan (Paruvkaal)

It is used to feel all types of Sensations. It carries nutrients to all over

the body flexes and extends the movable joints.

4. Uthanan (Maelnokku kaal)

Responsible for all kinds of upward motion such as nausea, vomiting

and eruption.

5. Samanan (Nadukkaal)

Considered essential for proper digestion assimilation and carries the

digested nutrients to each and every organ.

6. Nagan

Helps in opening and closing of the eyes.

7. Koorman

Responsible for yawning, vision and lacrimation.

8. Kirugaran

Responsible for salivation, nasal secretion and appetite.

9. Dhevathathan

Induces and stimulates a person to become alert, get anger, to quarrel,

to sleep, to become lazy etc.
10. Dhananjeyan

Resides in the cranial cavity and produces bloating of the body after death.
This leaves from the body after 3 days forming a way through the skull bone.

In case of Madhumegam:

1.Abanan - Affected ( increased urine volume and frequency of

micturation).

2.Viyanan - Affected (altered sensation).

3.Udhanan - Affected (nausea, vomiting).

4.Koorman - Affected (Blurring of vision)

5.Kirugaran - Affected (Polydipsia).

6.Samanan - Affected ( Indigestion )

II. Pitham

It is the thermal life force of the body. Pitha in the body is followed by
the derangement of metabolic energy caused by the involvement of Vatha.

Location of Pitham in our body

Pingalai, Piranan, Urinary bladder, Heart, Moolakkini, Head, Abdomen,

Sweat, Blood, Saliva and Digested material etc.Increase or decrease of Pitham can cause
some standing symptoms which are below.

Increase :

Yellowish discolouration of eyes, skin, urine and motion. Polyphagia, polydipsia, burning
sensation all over the body, sleeplessness, acidity, profuse sweating and dizziness etc.,

Decrease :

Loss of appetite, cold, pallor, symptoms associated with defective

growth of Kapham.
Types of Pitham

1. Anar Pitham : It peps up the appetite aids in digestion.

2. Ranjaga Pitham : It is responsible for the colour and contents of the blood.

3. Pirasaga Pitham : Complextion of the skin.

4. Sathaga Pitham : Necessary to carry out regular works properly.

5. Aalosaga Pitham : It is responsible for the perception of Vision.

In case of Madhumegam

1. Anar Pitham

Affected – Polyphagia

2. Alosaga Pitham :

Affected - Blurring of Vision.

III. Kabam

It is responsible for the stream lined functions of the body and body
defence mechanism to be intact.

Location of Kabam in our body

Samanan, Suzhumunai, Vinthu, Head, Fat, Marrow, Nose, Colon,Joints

etc.Increase or decrease of Kabam can cause some standing symptoms which are below,

Increase

Loss of appetite, excessive salivation, heaviness, excessive musculature,

dyspnoea, excessive sleep, fair complexion, itching, dullness, cold, loss of sensation,
sweetness in mouth and indigestion etc.,

Decrease

Prominence of bony edges, dry cough, lightness, profuse sweating and

palpitation.
Types of Kabam

1. Avalambagam

Lies in the respiratory organs, exercises authority over other Kabams

and controls heart and circulatory system.

2. Kilethagam

It is found in stomach as its seat moistens the food, softens and helps it
for digestion.

3. Pothagam

Tongue is the centre for pothagam, it is responsible for the sense of taste.

4. Tharpagam

Head is the centre for tharpagam, it gives cooling to the eyes.

5. Santhigam

It lies in the joints and is responsible for the lubrication and true
movements of joints.

Udal Kattugal:

These are seven basic principles which constitute the entire body. There
are 7 Udal Kattugal described in Siddha text.

1. Saram

It strengthens the body and mind.

2. Senneer

It is responsible for the nourishment, Strength, Vigour and healthy

complexion.

3. Oon

It gives structure and shape of the body and is responsible for the
movement of the body.
4. Kozhuppu

It helps for lubrication of joints and other parts of the body to facilitate their
functions.

5. Enbu

It supports the body structure and protects the organs. It is responsible

for the posture and movement of the body.

6. Moozhai - It nourishes the bone marrow.

7.Sukkilam/ Suronitham - Responsible for sexual urge and reproduction.

Udal Kattugal Increased features Decreased features

Dryness of the skin

Leads to a disease identical to the
diminished activity of the
increase in kabam like loss of
1) Saaram sense organs, lassitude,
appetite ,profuse salivation,
Loss of weight, Intolerance
depression etc.
to sounds.
Increased blood pressure, boils in
Eagerness to sour foods.
eye brow, scalp neck, lips and
2) Senneer Tiredness, lassitude, cold
legs, skin jaundice, hemaeturia,
anaemia.
Colic pain.
Deposition of fat around the neck,
3) Oon face, abdomen, thigh, genitalia, Muscle wasting, tiredness.
etc.,
Identical feature of increased oon
Loin pain, emaciation
4) Kozhuppu associated with dyspnoea on
splenomegaly.
exertion
Pain in joints, loss of hair,
Excessive ossification and
extraction of foot, weak
5) Enbu dentition
bone and nail.
6) Moozhai Weariness of the body and Osteporosis and sunken
 eye,swollen interphalangeal joints, eyes.
oliguria and non healing ulcer.
7) Sukkilam (or) Increased sexual activity urinary Pain in the genitalia, failure
Suronitham calculi etc. to Reproduction.
In Madhumegam all seven thathus are affected.

1. Saram - Tiredness

2. Senneer - Reduced Strength

3. Oon - Weight loss

4. Kozhuppu - Weight loss (or) obese

5. Enbu - Joint pain

6. Moolai - affected

7. Sukkilam - Body becomes dry and loses its lusture due

to excessive flow of urine mixed with vital fluid.

In the case of Madhumegam frequent passage of increased amount of

urine results in gradual diminution of seven thathus.

‘rupahf Nkfj;jhy; mghd thA

jhd; Giff;F NkNywpf; fghyr; #lhk;

ngupjhd Nkfj;jhy; mj;jpnte;J

Nghkg;gh jitnte;J uj;jk; tw;wpg;

Gupthfpj; jrthAthy; ke;jq; nfhz;L

ngUe;jPdp kyge;jk; cjhdthA

tpupthfp Njfnky;yhk; tplePuhNy

nka;aope;j Nkfnkd;w jpUgjhr;Nr”

- rpj;j kUj;Jtk;

In this poem Oon and Senneer were affected.

Udal Vanmai:

Udal Vanmai means the body gets resistant to a disease because of

the formation of humoral antibodies, that is called immunity.

(a) Iyarkai Vanmai

Three uyir thathus plays a vital role in the formation of Natural immunity
of the body right from birth onwards.

(b)Seyarkai Vanmai.

Improving the health through nutritious food, medicines, karpams,

vaccines all fall into this category i.e acquiring the immunity by human measures.
Kayakarpam both specific and nonspecific special karpams gives immunity to our body
both as prevention and treatment to the diseases.

(c) Kala Vanmai

Developing the immunity according to age season and environment.

Piniyari Muraimai(method of diagnosis)

Pini means the disease which affect the body. Any interruption of the normal
functions of any body part, organ or system.

Ari means identify. Muraimai means rules.

Piniyari murimai is the method of diagnosing the disease affecting the people. It is
based upon the following aspects.

1) Poriayalarithal

2) Pulanalarithal

3) Vinnathal

4) Envagai thervugal

5) Naadi Paritchai
 The above principles corresponds to the methodology of inspection, palpation and
interrogation of modern science.

Poriyalarithal and Pulanalarithal:

Gnanendriyam

Organ Sense
Mei (Skin) Touch
Vaai (Mouth-tongue) Taste
Kan (Eye) Vision
Mookku (Nose) Smell
Kaadhu (Ear) Hearing

Kanmendhriyam

Organ Function

Kai (Upper limb) Movements of upper limbs

Kal (Lower limbs) Movements of lower limbs

Vai (Mouth) Speaking

Eruvai (Anal orifice) Defaecation

Karuvai(Reproductive orifice) Reproduction

Pori is considered as the five sense of perception namely Nose, Tongue,

Eye, Skin and Ear. While Pulan are five object of senses. They are Smell, Taste, Vision,
Sensation and Sound. Physician's pori and pulan are used as the
tools for examing the pori, pulan of the patient.Vinathal is obtaining
the informations regarding the history of the disease, its clinical features etc., from the
patient or his immediate relatives who are taking care of him, when
the patient is not in a position to speak or if the patient is a child.
Vinathal:

It has a procedure for gathering information about the patients name, age,
occupation, nativity, socio-economic status, family history, dietary habits, allergic factors,
period of suffering from the complaints, history of previous episodes, relevant history of
habits and treatment etc from the patient or from his immediate relatives, if the patient is
not in person to speak or if the patient is child.

In madhumegam vinathal is very much useful for piniyarimuraimai,

occupation, family history, dietary habits, proper treatment and socio economic status are
very important for madhumegam.

Envagai thervugal:

Eight different kinds of tests to be applied or attended by a physician

before arriving a correct diagnosis. These are also called Attavitha Paritchai or
Attasthanna Parikshai.

Envagai thervukal is considered as Physician's Instruments.

‘ehb guprk; eh epwk; nkhop tpop

kyk; %j;jpuk; ,it kUj;JtuhAjk;”

nka;Fwp epwe;njhdp tpop ehtpU kyk; iff;Fwp

- Njiuau;

In Agasthiyar Vallathi 600, Envagai thervugal has been mentioned as

Atta Vitha Paritchai.

‘njhYf;fYw;W ml;ltpj guPl;ir jd;id

Jyf;fKWk; gz;bjNu njspthfg;

gFj;jwpa ehbia eP gpbj;J ghU

gfu;fpd;w thu;j;ijiag; ghu; ehit ghU

tFf;fupa Njfkiu njhl;Lg;ghU

 tskhd ruPuj;jpd; epwj;ijg; ghU

rfpf;fupa kyj;ijg;ghu; ryj;ijg; ghU

rhu;e;j tpop jidg;ghu;j;J njsptha;f; fhNz”.

- mfj;jpau; ty;yhjp 600

1. Naadi (Pulse)

2. Sparisam (Palpation)

3. Naa (Tongue examination)

4. Niram (colour of the body)

5. Mozhi (Speech)

6. Vizhi (Eye Examination)

7. Malam (Motion examination)

8. Moothiram (Urine examination)

Therefore to arrive at the diagnosis for any disease, it is imperative

to apply the Envagai thervugal.

Naadi (Pulse)

Naadi is the vital force. Any change in the three dhoshas are best
diagnosed by feeling the nadi. Naadi is an important observation for diagnosis and
prognosis. Naadi is responsible for the existence of life and can be felt one inch away
from the wrist on the radial side by means of palpation with the tips of index, middle and
ringfinger corresponding to Vatham, Pitham and Kabam.

Site and procedure to feel Naadi according to Agasthiyar

‘fupKf dbia tho;j;jpf;

ifjdpy; ehb ghu;f;fpy;

ngUtpuyq;Fyj;jpy;
 gpbj;jb eLNt njhl;lhy;

xUtpu Nyhby; thjk;

cau; eL tpuypw; gpj;jk;

jpUtpuy; %d;wp Nyhby;

rpNyj;Jk ehbjhNd”

-mfj;jpau; ehb

Normally the three humors Vatham, Pitham and Kabam exist in the ratio
1: ½ : ¼ The derangement in these ratio leads to various disease entities and is best
diagnosed by feeling the Naadi.

Naadi in Madhumegam,

‘,UkpNa gpj;jKk; thjKk; $by;

kUTy Nkfk; thUjp NghyhFk;

cUtk; NtwhF Kz;lTlw; fha;e;jpLk;

cUfNt T+NdhL cwpQ;rp ,dpf;FNk”

- jpU%yu; ehb

The above stanza describes that excessive elimination of urine containing

sugar are always primarily due to combined vitiation of Vatha, and Pitha
functional factors in the body. The pitha and vatha vitiation is indicated
clinically by excessive hunger, thirst, over-eating, emaciation and passing of
large quantities of urine.

‘ghu;j;jpL %d;Wk; gjpe;J nkype;J epw;fpy;

Nju;e;jpL Nkfk; ce;Njhd;wpNa nghUj;jp nka;apy;”

- jpU%yu; ehb

The above lines indicate that when there is any functional alteration of
the vatha, pitha and kaba all the full clinical pictures of meganeer appears.
 ‘,dpf;fpd;w thjj;jpil Nrupy; Iae;jhd;

gdpf;fpd;w fs;Sg; gjdpNghy; ePNuhLk;

fdpf;fpd;w Nkdpfiue;J ntSg;NgWk;

fdpf;FkJ Nkfe; jg;ghijahNk”

- jpU%yu; ehb

The above poem indicates that initially vatha and kabam get deranged
leading to vitiation of pitha thathu also finally. When the aggravated vatha naadi
combines with aggravated kaba naadi, there is genesis of meha disease in the body.
The meganeer thus formed and eliminated has the consistency and appearance of toddy.
The affected individual's body is emaciated thin and pale. This is
the typical clinical picture of madhumegam.

‘Juzkld; ePu;g;ghL nfu;gg

; g; ghlhdhw;

nrhy;YfpNwd; ehbnay;yhe; fod;W fhZk;”

- gupg+uz ehb

In the above lines, it is said that all the three naadis are feeble and weak
in madhumegam.

‘gw;gpbf;f Nkfk; vd;why; gpj;j kPWk;

ghyfNd fhq;if nfhz;L ePuhk; ghNu”

- gupg+uz ehb

By the above lines it is clearly stated that aggravation of pitha naadi results in increased

udal kaangai. Eventually this leads to emaciation of seven udalthathus resulting in

meganeer.
 ‘ ePu; Nkfkhdtu;f;F ehb fhZk;

epu;zakha; ehbnay;yhk; ngyNk nfl;Lf;

fhu;Nkfk; Nghy te;j vupapd; NkNy

fz;L tpOk; GOg;NghyNt Guz;L fhZk;”

- gupg+uz ehb

All three naadies are felt feeble in those suffering from Neerizhivu Noi.
The character of the pulse is compared to that of a wriggling movements of
a worm that has fallen into the fire.

Sparisam (Palpation)

The following points are elicited by Sparisam, the temparatue of skin (heat
or cold), smoothness, roughness, softness, sweat, dryness, sensation, dryness,

Malam (Faeces)

In the examination of Malam, Niram (Colour), Nurai (Froth), Erugal

(Solid), Elagal (Semisolid or liquid), quantity (increased or decreased) smell can be noted
other examination like presence of blood, mucus, undigested matter
in the stools and odour can also be studied.

Moothiram (Urine)

In the examination of urine, colour, odour, quantity of urine, the presence

of froth, deposits, blood, pus, inorganic sediments, abnormal constituents such as sugar,
protein etc, and the frequency of micturitions are to be noted.

The diagnosis is usually arrived at by methods of urine examinations called.

i) Neerkuri

ii) Neikuri
Collection of Urine:

‘mUe;Jkh wpujKk; mtpNuh jkjha;

m‡fy ;myh;jy; mfhyt+z; jtpu;e;jow;

Fw;ws tUe;jp cwq;fp itfiw

Mbf; fyrj; jhtpNa fhJ nga;

njhU K$u;j; jf;fiyf; Fl;gL ePupd;

epwf;Fwp nea;f;Fwp epUkpj;jy; flNd”.

- Njuu; ePuf
; ;Fwp nea;Fwp

Prior to the day of urine examination, the patient should be advised to take a
balanced diet and should have good rest. The first voided urine of the patient is collected
in a glass container. A drop of gingely oil is added into the container without any
disturbances and the air spreading kept under sun light and the tendency of the oil drop is
examined with in 1½ hours.

i)Neerkuri

‘te;j ePu; fup vil kzk; Eiu vQ;rnyd;

iwe;jpa Ystif aiwFJ KiwNa”

-Njuh; ePh;f;Fwp nea;f;Fwp Ehy;

In Neerkuri Niram, Edai, Manam, Nurai and Enjal of the urine voided is
noted.This has been already mentioned in Envagai thervugal.

‘mUg;g Kw;whu;f; ft;tpjp tpyf;Nf”

-Njuh; ePh;f;Fwp nea;f;Fwp Ehy;

The urine should be examined only according to the rules

and regulations but at time of emergency they can be relaxed.
 Niram : It indicates the colour of urine voided.

Edai : It indicates the quantity of urine

(increased or decreased quantity)

Manam : In indicates the smell of urine voided.

Nurai : It indicates the frothy nature of urine voided.

Enjal : It indicates the deposit of urine

Neerkkuri of Madhumegam is studied as follows :

Niram : Clear and white. This is due to Kaba vitiation and it is

not amenable to treatment.

Edai : Urine is thick and its consistency is like honey.

Manam : Smells like honey. Ants and flies are attracted towards
the voided urine. It indicates that it contains some sweet
substances which attracts the ants and flies.

Nurai : It is frothy at the time of urination.

Enjal : Large quantity of urine is passed. This will result in

the loss of large volume of water and life sustaining
minerals resulting in fatigue, exhaustion and weakness.

If the urine is lightly transparent, it indicates the vitiation of kaba in which the
prognosis is said to be very bad. Efficient and adequate timely treatment does not give
relief to the patient.

The above findings of Neerkuri in Madhumegam is described in

Siddha texts are as follows.

‘Gz;zuP ; Nkfg;Gz; fz; khg;gpzp

ez;zpy; epj;jpa ehjpak; MnkDk;”

- epj;jpa eh jPgk;
The physical features of urine in madhumegam

‘md;dNk Nfzp khe;ju;

mUe;JePu; kpfTk; nghq;fpj;

jd;DNs jtU tz;zk;

jq;fpNa kpFjpahfp

,e;epw kpy;yhehS

kpiltplh jpwq;Fkhapd;

tpd;dKk; nra;Ak; nta;a

ntF%j;jpuj;jpd; thNw”

‘cz;ikahe; Rj;j rPjsj; Jjkhu;

,e;ePu;g; grg;glhjpj;tDa;Ae;juk;

Ke;ePu; ngUf;fopo;thd; ca;j;nyhf;Fnk”

- Njud;
The description of some characters of the urine in siddha system agree
with the description of the physical feature of diabetic urine by modern science. The
name of the disease itself indicates that the urine passed contains a substance which is not
only sweet but also emanates the odour of honey.

Neikuri

A drop of gingely oil is dropped into a wide vessel containing the urine to
be tested and kept it under the sunlight in a air tight place. The variations of the three
thathus in disease can be diagnosed by the behaviour of gingely oil
in the surface of urine .

‘muntd ePzb
; d‡Nj thjk;”

The drop of oil lengthening like a snake indicates Vatham.

‘MopNghw; gutpd; m‡Nj gpj;jk;”

The drop of oil spreading like a ring it indicates Pitham.

‘Kj;njhj;J epw;fpd; nkhoptjd; fgNk”

If the oil drops assumes a pearl shape it is persumed to be kabha.

By the careful examination of the urine with gingely oil, the physicians can know
whether the disease is curable or not. For this purpose Siddhars have explained various
spreading tendencies of oil on urine surface to define the prognosis of disease.

Noi kanippu vivaadham : (Differential diagnosis of glycosuria )

(1) Thelineer

The signs and symptoms of the thelineer were polyuria (voided urine is
clear and snow like appearence), polydipsia, loss of appetite, loss of body weight,
dryrness of skin, constipation or diarrhoea, muscle cramps.

Due to the presence of loss of appetite and absence of excessive sugar in

blood and urine sample, this disease can be differentiated from Madhumegam.

(2) Due to prolonged intake of diuretics

Due to the history of prolonged intake of diuretics the patient may have
symptoms of polyuria. But due to the absence of excesssive sugar in blood and urine
sample the sympotms can be differentiated from madhumegam.

Noi Nidhanam (Prognosis):

As per Siddha system four types of Megam formed as a result of

Vathaneer can be curable.The six types arising due to the vitiation of pitham can be
cured with proper treatment.

But then ten types of pramegam arising due to Iyyam are incurable by
proper treatment.

‘nra;aNt tr;rpukhe;jjz;lkhd
nrakhd KJF jz;ikg;gw;wpepw;Fk;

nga;aNt ngUeuk;gpy; Nkfe;jhDk;

 gpwf;Fnkd;Nw jhdwpe;J thjj;jd;dhy;

gpa;aNt gpwe;j ryk; ehy rhj;ak;

gpj;jj;jpw; gpwe;jj rykhWk; rhj;ak;

igaNt Nrl;Lkj;jpw; gpwe;j gj;Jk;

gukDiuj;jhu; rhj;jpak; guhgupf;Nf”

- a+fpitj;jpa rpe;jhkzp

Maruthuvam (Treatment)

‘itj;jpar; nray; itj;jpakhNk

gythW khWjile;J nfLf;fpd;w cliy epiyf;Fk;gb

khWjy; mZfhkYk; xNu jd;ikahf

nra;Jk; mjdhyhQ; nrapyf; Fiwapd;wp

elf;fr; nra;tJ njJNth mJNt itj;jpak;”;

- jpU%yu; 800
So, in Siddha treatment is not only for removal of disease, but for the
prevention and improving the body condition. This is said as follows :

Kaappu (Prevention)

Neekkam (Treatment)

Niraivu (Restoration)

Siddha system has unequivocally stated that even during the time of
conception, some defects creep into the fertilised embryo.

The defects form the basis for the manifestation of certain constiutional
diseases later on during the existence of the individual.

The disease for which no known cause is given are designated as diseases
of idiopathic origin or heriditary disorders. In Siddha system such diseases are described
as karma noikal.
a. Kaappu (prevention)

To prevent karma (idiopathic or hereditary diseases) the Siddha science

has advocated preventive measures to be taken into consideration even while arranging
for marital alliances the object of which is to be get healthy pregnancy to build a robust
and healthy nation. The rules affecting healthy alliances have been eloborately described
in the science of Astrology. They married on the basis of physical, emotional, intellectual
and social compatibility.

b. Neekkam (Treatment)

The three Uyir thathus which are responsible for organisation,

regularisation and integration of the bodily structures and their physiological functions
are always kept in a state of equilibrium by word, thought, deed and food of the
individual. The general aetiological factors for constitutional discomfort is said to be
incompatible diet, mental and physical activites.

When treating for removal of the diseases the following principles must
be noted.

‘Neha;ehb Neha;Kjy; ehb mJ jzpf;Fk;

tha;ehb tha;gg
; r; nray;”

‘cw;whdsTk; gpzpasTq; fhyKq;

fw;whd; fUjpr; nray;”.

So, it is essential to know the disease and the cause for the onset of
disease, before treating the patient so also to the nature of the patient, the severity
of illness, the season and time of the occurrence of the diseases must be observed.

c. Niraivu (Restoration)

Patient needs good discussion and motivation and persuasion to accept the
eventuality of diabetes and prepare for a lifestyle that provides optimisation of metabolic
status.Megam, suitable effective medicinal preparations have to be administered in the
beginning itself to neutralise and eliminate the megam from the body tissues.
 Siddhars aimed at bringing the three doshas in equilibrium in the treatment
of disease. Towards this end we treat with herbs and mineral preparations are used, while
treating Madhumegam.

‘Ntu;ghU jioghU kpQ;rpdf;fhy; nky;y nky;y

gw;g nre;J}uk; ghNu”

There are thousand preparations for Madhumegam and for its

complications found in various Siddha text books Kudineer, Chooranams, Ilahams,
Paspam and Chendooram.

Line of treatment according to Theraiyar Maruthuva Bharatham :

In Maruthuva Bharatham, it is said that the disease has been caused

by excessive sexual indulgence, leads to the formation of Megam which gradually affect
all the seven thathus and finally sets in the Genitourinary system resulting in excessive
secretion and elimination of urine, tasting sweet as honey.

‘fd;dp kaf;fj;jhy; fz;bL; NkfNk

fpue;jp Gz;zpuz; Nkf fPrfnkd;Dk; Jd;khuf;fd;

mUe;jjpnad;Dk; ghQ;rhypad;idiaf; fz;Zw;whNd”

- Njiuau; kUj;Jt ghujk;

In theraiyar Maruthuva bharatham, Megam is alluded to Keesagan and

Madhumegam is alluded to Sainthavan, are also alluded to certain metals
namely Bheeman for Rasam (Mercury), Dharmar for Ayam (Iron) and other brothers for
Steel, Silver, Gold, Lead and Copper.

‘nfhd;iw khiyiag; Nghl;L rape;jtidf;

nfhy;nydf; nfhy;ykd;d ky;y jg;gbNa

MFnjd;rpe; JgjpagPkid abj;jy;

Kbj;jy; gbf;fNs tpONt”

 Arjuna was wearing the Kontraimalai at the time of killing Sainthavan by
his weapon pasupathasthram which is compared to Passupathasthra Mathirai. Paasu
pathasthra mathirai is administered along with Kontrai flower juice as appropriate
anupanam for Madhumegam and its complications.

Diet in Siddha system :

Siddha system lays a great importance on the observation of rules

regarding diet in everyday life because the Siddha system has rightly realised, that
the basic factor of the body is food. That is Annamaya Kosam is the first among the five
Kosams constituting our physical and mental existence. To prevent
the occurrence of the disease, eloborate inference regarding food item in our daily diet is
given in the textbook of Siddha.

‘czNt kUe;J kUe;Nj czT”

‘kUe;njd Ntz;lhthk; ahf;iff;

fUe;jpajw;wJ Nghw;wp Az;zpd;

jPasT md;wp njupahd; ngupJz;zpd;

NehasT ,d;wpg; gLk;

khWghby;yhj Tz;b kWj;Jz;bd;

CWghb y;iyA apu;f;F”

- jpUf;Fws;
Generally when a medicine is administrated Siddha Physician prescribes
diet regimen according to the nature of the medicine and severity of the disease. As over
intake or consuming unbalanced and incompatible diet is considered to the prime
causative factor for upsetting the tridhosa balance leading to manifestations of various
ailments, Regarding diet regimen in Madhumega there is special instructions found in
Agasthiyar Karma Kandam and Agasthiayar Ayulvetham - 1200.

‘g+nkha;jpUf;F KUq;ifapiyg; g+Tk; gpQ;Rk; Glyq;fha;

jPikay;y KRl;ltpiy rpwe;j fhzpj; J}Jtisj;

 jhNkapjidj;jhd; $l;L jg;gh njhopAk; gpuNkfk;

ehkhk; tpahjp mlq;fSf;F etpd;wfwpfspJthNk”

- mfj;jpau; MAs; Ntjk;

List of food items recommended for Madhumegam patients:

 Kelvaragu(Ragi) Thuthuvalai(Climbing Brinjal)

 Sirukeerai(Amaranthus) Peerkku(Ridged gourad)

 Murungai Poo Eraal

 Gothumai(Wheat) Athipinchu(Cluster fig)

 Ponnanganni(sessile plant) Venthayam(Greek hayes)

 Pagal(Bitter gourad) Murungai(House radish)

 Pudal(Snake gourad) Ellu(Gingelly)

 Avarai(The tanners cassia) Sirupayaru(Green gram)

DIET -SHEET

1400 Calories Diabetic Low Chloesterol Diet -Vegeterian

MORNING

6.00-7.00 AM : Coffee/Tea/ (Without Sugar)

BREAKFAST

8.00-9.00 AM: Idlies-3 /Chappathi -3 / Dosai -2 , Pongal ¾ cup Dhal vada

1,Chutney,Sambar-1/2 cup.

MID MORNING

10.30-11.00 AM: Vegetable halfboiled-1cup/Vegetable saled/Vegetable

Soup./Butter milk 1 cup/Lime /Tomoto juice /Tea/Coffee 1
cup(Without suger)
LUNCH

1.00-2.00 PM : Rice-1 cup (or)Cooked Wheat-1 cup/ Chappathi -1Sambar

¼ cup Green leafy ¼ cup,Rasam-2cup,Vegetable
porial,Skimmed Curd -1 Cup /Butter milk-2 cupWhole
Grams -1kgs/day (Bengal Gram,Green Gram, Cow
Pea/Rajmah).

TEA TIME

3.00-4.00 PM : Whole Wheat Bread -1 Slice With Gram/Dhal/ Vegetable

Filling (or) Wheat Rava kitchadi -1/2 kgs (or) Rice Flakes uppuma-
1/2kgs Coffee/ Tea / -1 Cup (Without Sugar).

DINNER

8.00-9.00 PM: Same as Lunch (or)Chappathi -3,Dhal,Vegetables

(Saled/kootu/ Poriyal)

BED TIME : 1 Cup of Skimmed Milk (Without Sugar)

OIL FOR COOKING

Ground oil/ Gingelly oil/ Sun flower oil-10gms/day

Skimmed Milk Allowance-500ml/day

AVOID FOODS:

Crab,Ghee,friedfoods,suger,honey,glucose,jam,jaggeryswee
ts,cakes,pastries,tendercoconutwater,softdrinks,alcoholic
beverage horlicks,boost,bournvita,complan,dryfruits like
dates,figs, raisins, banana,mango,jackfruit,sapota,custard
apple and grapes.

Yogasana treatment for Madhumegam :

Yoga according to Thirumanthiram is the attainment of spritual,

psychological and physical perfection. As the body is said to be the abode of divinity, the
Siddha saint Thirumoolar has advised each and every individual aspiring for self
realisation should practice Yogasanam.
The following Aasanas are advised for controlling Madhumegam :

1. Chakkaraasanam

2. Villaasanam

3. Mayuraasanam

4. Mathsyaasanam

6. Pachimothaasanam

7. Pujangaasanam

8. Padmaasanam

9. Sarvaangaasanam
 MODERN ASPECT

DIABETES MELLITUS

Definition:

Diabetes mellitus is a clinical syndrome characterized by hyperglycaemia

due to absolute or relative deficiency of insulin. Lack of insulin affects the metabolism of
carbohydrate , protein and fat and causes a singnificant disturbance of water and
electrolyte homeostasis.

Epidemiology

Diabetes is world wide in distribution and the incidence of both type 1 and
type 2 diabetes is rising. It is associated with several contributory factors including
increased longevity, obesity, unsatisfactory diet, sedentary lifestyle and increasing
urbanization. Diabetes is the single most important metabolic diseases of humans. It can
affect nearly every organ system in the body, and is recognized as one of the leading
causes of death and disability worldwide.

India is “The diabetic capital of the world “as it is presently estimated to

have over 40 million individuals affected by this deadly disease.It is expected to rise
more rapidly in the future because of increasing obesity and reduced activity levels.

However, the prevalence of both types of diabetes varies considerably

around the world , and is related to differences in genetic and environmental factors. A
pronounced rise in prevalence occurs in migrant populations to industrialized countries,
e.g. Asian and Afro-Carribbean immigrants to the United Kingdom. The prevalence of
known diabetes in Britain is around 2-3%. Many more cases of type 2 diabetes remain
undetected.
Classification:

Etiologic Classification of Diabetes Mellitus

I. Type 1 diabetes (-cell destruction, usually leading to absolute insulin deficiency)

A. Immune-mediated

B. Idiopathic.

II. Type 2 diabetes (may range from predominantly insulin resistance with relative insulin
deficiency to a predominantly insulin secretory defect with insulin resistance)

III. Other specific types of diabetes

A. Genetic defects of -cell function characterized by mutations in:

1. Hepatocyte nuclear transcription factor (HNF) 4 (MODY 1)

2. Glucokinase (MODY 2)

3. HNF-1 (MODY 3)

4. Insulin promoter factor (IPF) 1 (MODY 4)

5. HNF-1 (MODY 5)

6. Mitochondrial DNA

7. Proinsulin or insulin conversion

B. Genetic defects in insulin action

1. Type A insulin resistance

2. Leprechaunism

3. Rabson-Mendenhall syndrome

4. Lipoatrophic diabetes

C. Diseases of the exocrine pancreas-pancreatitis, pancreatectomy, neoplasia,

cysticfibrosis, hemochromatosis, fibrocalculous pancreatopathy
D. Endocrinopathies acromegaly, Cushing‟s syndrome, glucagonoma,
pheochromocytoma, hyperthyroidism, somatostatinoma, aldosteronoma

E. Drug- or chemical-induced Vacor, pentamidine, nicotinic acid, glucocorticoids, thyroid

hormone, diazoxide, -adrenergic agonists, thiazides, phenytoin, interferon, protease
inhibitors, clozapine, beta blockers

F. Infections: congenital rubella, cytomegalovirus, coxsackie

G. Uncommon forms of immune-mediated diabetes: “stiff-man” syndrome, anti-insulin

receptor antibodies

H. Other genetic syndromes sometimes associated with diabetes:

Down‟s syndrome, Klinefelter‟s syndrome, Turner‟s syndrome, Wolfram‟s syndrome,

Friedreich‟s ataxia, Huntington‟s chorea, Laurence-Moon-Biedl syndrome,myotonic
ystrophy, porphyria, Prader-Willi syndrome.

IV. Gestational diabetes mellitus (GDM)

MODY : Maturity onset of diabetes of the young.

Anatomy of the pancreas:

Pancreas is a retro-peritoneal, fleshy organ, has both endo and exocrine

function. It is supra-umbilical, intrahepatic, posterio-abdominal, retroperitoneal organ,
crossing the mid-line from right to the left. As it‟s retroperitoneal, the organ does not
move with respiration.

Generally, it has head, neck, body and tail. The head of the pancreas is
within the concavity of the deodenum. The neck crosses the portal vein. The body
crosses the great vessels of the abdomen like, inferior vena cava, aorta, and left renal
blood vessels. The tail of the pancreas is in the left hypochondrium and, it contacts the
hilum of the spleen. The superior border is related to spleenic artery.

The anterior border gives attachment of transverse mesocolon.

Histophysiologically, this is a compound tubular gland showing endo and exocrine
functions of which are correlated with pituitary gland.
Microscopic anatomy of islets of – langerhands

They are found more in the tail of the pancreas than in the other parts.
They form about 1 – 2% of pancreatic weight. There are about 2 millions of islets in
human pancreas. Each islet has an epithelial mass, tunneled by labyrinthine capillaries.
The position of the islets is mostly within the lobules, rather than between them. Each
spheroid islet is surrounded by reticular membrane. Islet tissue is arranged in irregular
anastomosing cellular plates. Their epithelial cords are separated by blood vessels. A
sphincter controls the blood supply. The histological structure of the islets shows Alpha,
Beta and Delta cells, of which,

Alpha cells form 20% and glucagon secreting

Beta cells form about 75% and insulin secreting

Delta cells form about 5% and gastrin secreting.

Beta cells are the source of insulin hormone. The cells are polyhedral, the
nuclei are centrally or eccentrically placed, the cytoplasm is grannular, filled with
prominent secretary vacuoles containing few ribosomes. The secretory granules show
species variations. In man they are spherical or elongated crystalline body.

INSULIN BIOSYNTHESIS, SECRETION, AND ACTION:

Biosynthesis

Insulin is produced in the beta cells of the pancreatic islets. It is initially

synthesized as a single-chain 86-amino-acid precursor polypeptide, preproinsulin.
Subsequent proteolytic processing removes the aminoterminal signal peptide, giving rise
to proinsulin. Proinsulin is structurally related to insulin-like growth factors I and II,
which bind weakly to the insulin receptor. Cleavage of an internal 31-residue fragment
from proinsulin generates the C peptide and the A (21 amino acids) and B (30 amino
acids) chains of insulin, which are connected by disulphide bonds.

The mature insulin molecule and C peptide are stored together and
cosecreted from secretory granules in the beta cells. Because the C peptide is less
susceptible than insulin to hepatic degradation, it is a useful marker of insulin secretion
and allows discrimination of endogenous and exogenous sources of insulin in the
evaluation of hypoglycemia. Human insulin is now produced by recombinant DNA
technology; structural alterations at one or more residues are useful for modifying its
physical and pharmacologic characteristics.

Secretion

Glucose is the key regulator of insulin secretion by the pancreatic beta cell,
although amino acids, ketones, various nutrients, gastrointestinal peptides, and
neurotransmitters also influence insulin secretion. Glucose levels >3.9 mmol/L (70
mg/dL) stimulate insulin synthesis, primarily by enhancing protein translation and
processing, as well as inducing insulin secretion. Glucose stimulates insulin secretion
through a series of regulatory steps that begin with transport into the beta cell by the
GLUT2 glucose transporter.

Glucose phosphorylation by glucokinase is the rate-limiting step that

controls glucose-regulated insulin secretion.

Metabolic Actions of Insulin

Anabolic actions:

a. Carbohydrate metabolism:

Insulin increases the glucose transport (muscle, adipose tissue),

phosphorylation, glycogenesis, glycolysis, pyruvate dehydrogenase activity and pentose
phosphate shunt.

b.Lipid metabolism:

Insulin increases the triglyceride synthesis , fatty acid synthesis(liver) and

lipoprotein lipase activity(adipose tissue).

c. Protein metabolism:

Insulin increases the amino acid transport and protein synthesis.

Anticatabolic actions

a. Carbohydrate metabolism:

Insulin decreases the gluconeogenesis and glycogenolysis.

b. Lipid metabolism:

Insulin decreases the lipolysis, lipoprotein lipase(muscle), ketogenesis and

fatty acid oxidation(liver)

c. Protein metabolism:

Insulin decreases protein degradation.

Normal Blood Sugar Level

In normal persons, blood glucose level is controlled within a narrow range.

After the overnight fasting, in early morning, the blood glucose level ranges between 80
and 90 mg/dl of blood. Between first and second hour after meals (post prandial), the
blood glucose level raises to 120-140 mg/dl. The glucose level in the blood is brought
back to normal at the end of second hour after the meals

Necessity Of Regulation Of Blood Glucose Level

Regulation of blood glucose level is very essential because, glucose is the

only nutrient that can be utilized by tissues of brain, retina and germinal epithelium of the
gonads.

Role of Liver in the Maintenance of Blood Sugar Level

Liver acts as an important glucose buffer system. When blood glucose

level increases after a meal, the excess glucose is converted into glycogen and stored in
liver. Afterwards, when blood glucose level falls, the glycogen in liver is converted into
glucose and released into the blood from the liver cells.

ROLE OF INSULIN IN THE MAINTENANCE OF BLOOD SUGAR LEVEL:

Insulin is the antidiabetic hormone, as it reduces blood sugar level. It

reduces the blood sugar level by the following actions.

1.Transport and uptake of Glucose

When a food with excess amount of carbohydrate is taken, the blood sugar
level is increased. Immediately, pancreas secretes insulin. The insulin facilitates the
transport of glucose from the blood into the cells by increasing the permeability of cell
membrane to glucose.

Insulin enhances the uptake of glucose by all the tissues particularly by

liver, muscle and adipose tissues. However, insulin is not required for glucose uptake in
some tissues like brain (except hypothalamus), renal tubules, mucus membrane of
intestine and red blood cells.

2.Peripheral utilization of Glucose

The glucose entering the cells is oxidized by most of the cells

immediately. The rate of utilization depends upon intake of glucose, and the glucose
utilization is enhanced by insulin.

3.Storage of Glucose

Insulin promotes the rapid conversion of glucose into glycogen

(glycogenesis) in muscle and liver. Thus, glucose is stored in these two organs in the
form of glycogen. The insulin causes conversion of glucose into fatty acids.

4.Inhibition of Glycogenolysis

Insulin prevents the breakdown of glycogen into glucose in muscles and

liver.

5.Inhibition of Gluconeogenesis

Insulin prevents gluconeogenesis i.e., it prevents the formation of glucose

from proteins by following ways:

a.Inhibiting the release of amino acids from muscle and

b. Inhibiting the activities of enzymes involved in gluconeogenesis.

Thus insulin decreases the blood sugar level in following manner;

1. Facilitating the transport and uptake of glucose by the cells.

2. Increasing the peripheral utilization of glucose.

3. Conversion of glucose into glycogen in liver and muscle.

 4. Prevention of glycogenolysis.

5. Inhibition of gluconeogenesis.

Role Of Glucagon In The Maintenance Of Blood Sugar Level

1.Glucagon increases glycogenolysis (breakdown of glycogen into

glucose) in liver. And, the glucose thus formed is released from the liver cells into the
blood. Glucagon does not induce glycogenolysis in muscle

2.Glucagon increases gluconeogenesis (formation of glucose from

proteins) in liver. It promotes gluconeogenesis by:

a.Activating the enzymes which convert pyruvate into phosphoenol

phruvate and

b.Increasing the transport of amino acids into the liver cells. These amino
acids are utilized for glucose formation.

Role Of Other Hormones In The Maintenance Of Blood Sugar Level

I.Growth Hormone

Growth hormone increases the blood sugar level by the following ways:

1.Decrease in the peripheral utilization of glucose for the production of

energy

2.Increase in the deposition of glycogen in the cells

3.Decrease in the uptake of glucose by the cells

4.Diabetogenic effect of growth hormone

II.Cortisol

Cortisol increases the blood glucose level by acting on liver cells and the
peripheral tissues. Following are the actions of cortisol on glucose metabolism.
 a.It increases the gluconeogenesis in liver from amino acids. When the
amino acids enter the liver, gluconeogenesis is accelerated.

b.It decreases the glucose (anti-insulin action) uptake by peripheral cells

and the utilization of glucose.

III. Adrenaline

Adrenaline increases the blood glucose level. Blood glucose level is

increased by the glycogenolysis in liver and muscle. So, a large quantity of glucose
enters the blood.

IV. Thyroxine

Thyroxine increases the blood sugar level by the following ways;

a. It increases the absorption of glucose from gastrointestinal tract.

b. It increases the breakdown of glycogen into glucose.

c. It accelerates the process of gluconeogenesis.

TYPE 1 DIABETES

(INSULIN DEPENDENT DIABETES MELLITUS)

Pathogenesis

Genetic Considerations

The genetic contributions to type 1 DM involve multiple genes. The

development of the disease appears to require inheritance of a sufficient complement of
genes to confer susceptibility to the disorder. The concordance of type 1 DM in identical
twins ranges between 30 and 70%, indicating that additional modifying factors must be
involved in determining whether diabetes develops.

The major susceptibility gene for type 1 DM is located in the HLA region
on chromosome 6. Polymorphisms in the HLA complex appear to account for 40 to 50%
of the genetic risk of developing type 1 DM.
Environmental Factors

It has been proposed that lack of exposure to pathogenic organisms in

early childhood limits maturation of the immune system and increases susceptibility to
autoimmune disease („the hygiene hypothesis‟).

1 Viruses

2.Diet

3.Stress

4.Immunological factors

Viruses

The evidence that viral infection might cause some forms of type 1
diabetes is derived from studies where virus particles known to cause cytopathic or
autoimmune damage to beta cells. The viruses have been isolated from the pancreas.

Virusus that causes type 1 diabetes include

Mumps,Coxsackie B4, retroviruses, rubella (in utero), cytomegalovirus

and Epstein-Barr virus.

Diet:

Dietary factors may influence the development of type 1 diabetes. Bovine

serum albumin (BSA), a major constituent of cow‟s milk, has been implicated in
triggering type 1 diabetes. It has been shown that children who are given cow‟s milk early
in infancy are more likely to develop type 1 diabetes than those who are breastfed. BSA
may cross the neonatal gut and raise antibodies which, because of the close homology
between BSA, the Beta chain of HLA class II antigens and a heat-shock protein expressed
by beta cells, could cross-react with and cause damage to beta cell components.Various
nitrosamines and coffee have been proposed as potentially diabetogenic factors.

Stress:

Stress may progress the development of type 1 diabetes by stimulating the

secretion of counter-regulatory hormones and possibly by modulating immune activity.
Immunological Factors

Type 1 diabetes is a slow T cell-mediated autoimmune disease. Family

studies have produced evidence that destruction of the insulin-secreting cells in the
pancreatic islets takes place over many years. Hyperglycaemia accompanied by the
classical symptoms of diabetes occurs only when 70-90% of beta cells have been
destroyed.

TYPE 2 DM

( NON INSULIN DEPENDENT DIABETES MELLITUS)

Type 2 DM is a heterogeneous disorder with a complex etiology that

develops in response to genetic and environmental influences. Central to the development
of type 2 DM are insulin resistance and abnormal insulin secretion. Although controversy
remains regarding the primary defect, most studies support the view that insulin
resistance precedes insulin secretory defects.

Risk factors for Type 2 Diabetes Mellitus

1. Family history of diabetes (i.e., parent or sibling with type 2 diabetes)

2. Obesity (i.e., „>20% desired body weight or BMI> 27 kg/m2)

3. Age > 45 years.

4. Race/ethnicity(e.g. African American, Hispanic American, Native

American, Asian American, Pacific Islander)

5. Previously identified IFG or IGT.

6. History of GDM or delivery of baby over 9 Ibs.

7. Hypertension (blood pressure> 140/90 mmHg)

8. HDL cholesterol level<0.90 mmol/L (35 mg/dL) and/ or a triglyceride

level>2.82 mmol/L(250 mg/dL)

9. Polycystic ovary syndrome.

Genetic Considerations

Type 2 DM has a strong genetic component. Although the major genes

that predispose to this disorder have yet to be identified, it is clear that the disease is
polygenic and multifactorial.

Various genetic loci contribute to susceptibility, and environmental factors

(such as nutrition and physical activity) further modulate phenotypic expression of the
disease. The concordance of type 2 DM in identical twins is between 70 and 90%.
Individuals with a parent with type 2 DM have an increased risk of diabetes; if both
parents have type 2 DM, the risk in offspring may reach 40%. Insulin resistance, as
demonstrated by reduced glucose utilization in skeletal muscle, is present in many
nondiabetic, first-degree relatives of individuals with type 2 DM. However, definition of
the genetic abnormalities of type 2 DM remains a challenge because the genetic defect in
insulin secretion or action may not manifest itself unless an environmental event or
another genetic defect, such as obesity, is superimposed.

Environmental Factors

1.Lifestyle

2.Malnutrition in utero

3.Age

4.Pregnancy

1. Life Style

Epidemiological studies of type 2 diabetes provide evidence that

overeating, especially when combined with obesity, middle-aged people with diabetes eat
significantly more and are fatter and less active than their non-diabetic siblings. Obesity
probably acts as a diabetogenic factor (through increasing resistance to the action of
insulin) in those genetically predisposed to develop type 2 diabetes.

2. Malnutrition In Utero

Retrospective analysis of the birth weight of males born an inverse

relationship between weight at birth and at 1 year, and the development of type 2 diabetes
in late adulthood.
 It is proposed (but not yet proven) that malnutrition in utero may
programme beta cell development and metabolic functions at a critical period, so
predisposing to type 2 diabetes later in life. Smoking during pregnancy has also been
implicated.

3. Age

Age is an important risk factor for type 2 diabetes. Over 70% of all cases
of diabetes occur after the age of 50 years. Type 2 diabetes is principally a disease of the
middle aged and elderly, affecting 10% of the population over the age of 65.

4. Pregnancy

During normal pregnancy, insulin sensitivity is reduced through the action

of placental hormones and this affects glucose tolerance. The term „gestational diabetes‟
refers to hyperglycaemia occuring for the first time during pregnancy. Repeated
pregnancy may increase the likelihood of developing irreversible diabetes, particularly in
obese women; 80% of women with gestational diabetes ultimately develop permanent
clinical diabetes requiring treatment.

Pathogenesis of type 2 diabetes

Insulin resistance

Increased hepatic production of glucose and resistance to the action of

insulin in muscle are invariable in both obese and non-obese patients with type2 diabetes.
Insulin resistance may be due to any one of three general causes: an abnormal insulin
molecule, an excessive amount of circulating antagonists, or target tissue defects. The last
is the most common cause of insulin resistance in type 2 diabetes and seems to be the
predominant abnormality in those with more severe hyperglycaemia.

A characteristic feature of type 2 diabetes is that it is often associated with

other medical disorders including obesity, hypertension and hyperlipidaemia. It has been
suggested that this cluster of conditions, all of which predispose to cardiovascular disease,
is a specific entity ( the „insulin resistance syndrome‟ or „metabolic syndrome‟ ), with
insulin resistance being the primary defect.

The features of insulin resistance syndrome are Hyperinsulinaemia, type 2

DM or impaired glucose tolerance, hypertension, low HDL cholesterol;elevated
triglycerides, central(visceral)obesity, microalbuminuria, increased fibrinogen, increased
plasminogen activator inhibitor-1and elevated plasma uric acid.

Pancreatic beta cell failure

In type 2 diabetes there is only moderate reduction in the total mass of

pancreatic islet tissue which is consistent with a measurable fall in plasma insulin
concentration when related to the blood glucose level. However, some pathological
changes are typical of type 2 diabetes, the most consistent of which is deposition of
amyloid. This is accompanied by atrophy of the normal tissue, particularly islet epithelial
cells. Islet amyloid is composed of insoluble fibrils formed from islet amyloid
polypeptide (also known as amylin). Small quantities of islet amyloid are very common
in elderly non-diabetic patients, and the role of islet amyloid in the pathogenesis of type 2
diabetes is uncertain. Deposition of amyloid is probably not a cause of diabetes but rather
reflects a pathological process which is increased in type 2 diabetes.

MODY GENETICALLY DEFINED, MONOGENIC FORMS OF DIABETES

MELLITUS

MODY comprises a phenotypically and genetically heterogeneous subtype

of DM. Onset of the disease typically occurs between the ages of 10 and 25. Five
different varities of MODY,

MODY1, MODY2, MODY3, MODY4, MODY5.

MODY2 the most common variant, is caused by mutations in the

glucokinase gene. As a result of glucokinase mutations, higher glucose levels are required
to elicit insulin secretory responses, thus altering the set point for insulin secretion.

GESTATIONAL DIABETES:

Gestational diabetes, defined as hyperglycaemia diagnosed for the first

time in pregnancy, is a common problem. It occurs in individuals who have an inherited
predisposition to develop diabetes and may take the form of either type I or type II
diabetes. The hyperglycaemia may not disappear after delivery. It is associated not only
with increased rates of perinatal mortality and neonatal morbidity but also with a high
incidence (possibly as great as 80% at 25 years postpartum) of subsequent clinical
diabetes (both type I and type II) in the mother. Normalisation of metabolism, whether by
treatment with dietary measures alone or, more commonly, with additional treatment in
the form of insulin, undoubtedly reduces the fetal risk; its effect on diminishing the
maternal risk of subsequent diabetes is less certain.

CLINICAL FEATURES OF DIABETES

The clinical features of the two main types of diabetes are compared below.

Comparative Clinical Features Of Type 1 And Type 2 Diabetes

TYPE 1 TYPE 2

Age at onset <40 years >50 years

Duration of symptoms Weeks Months to years

Body weight Normal or low Obese

TYPE 1 TYPE 2

Ketonuria Yes No

Rapid death without Treatment

with insulin Yes No

Auto antibodies Yes No

Diabetic complications at diagnosis No 25%

Family history of diabetes Uncommon Yes

Other autoimmune disease Yes Uncommon

The classical symptoms of thirst, polyuria, nocturia and rapid weight loss
are prominent in type 1 diabetes, many of whom are asymptomatic or have non-specific
complaints such as chronic fatigue and malaise.

Uncontrolled diabetes is associated with an increased suspectibility to

infection and patients may present with skin sepsis(boils) and genital candidiasis and
complain of pruritus vulvae and balanitis.
 Patients with type 1 diabetes often have no physical signs attributable to
diabetes, but weight loss is common.

The physical signs in patients with type 2 diabetes at diagnosis depend on

the mode of presentation. More than 70% are overweight, and obesity may be
central(truncal or abdominal). Obesity is less common in developing countries.

Hypertension is present in 50% of patients with type 2 diabetes. Although

hyperlipidaemia is also common, skin lesions such as xanthelasma and eruptive
xanthomata are relatively rare.

MAJOR MANIFESTATIONS OF DISEASE

Hyper Glycaemia:

Hyperglycaemia is a very common biochemical abnormality. It is

frequently detected on routine biochemical analysis of asymptomatic patients, and is
found during conditions which impose a burden on pancreatic beta cells, such as
pregnancy, severe illness or treatment with drugs such as corticosteriods(„stress
hyperglycaemia‟).

Pathogenesis:

Depending upon etiology of DM, hyperglycaemia may result from:

Reduced insulin secretion;

Decreased glucose use by the body; and

Increased glucose production.

Symptoms Of Hyperglycaemia Associated With Diabetes

Thirst, dry mouth.

Poly uria.

Nocturia.

Tiredness, fatigue, irritability.

Recent change in weight.

 Blurring of vision.

Pruritus vulvae, balanitis(genital condidiasis)

Nausea; headache,hyperphagia; predilection for sweet foods.

Diabetic Ketoacidosis:

Keto acidosis is caused by insulin deficiency and an increase in catabolic

hormones, leading to hepatic over-production of glucose and ketone bodies.

The cardinal biochemical features of diabetic ketoacidosis are:

Hyperglycaemia

Hyperketonaemia

Metabolic acidosis

Investigations:

The following are important but should not delay the institution of
intravenous fluid and insulin replacement:

Urea and electrolytes, blood glucose

Arterial blood gases to assess the severity of acidosis

Urinalysis for ketones

Full blood count

Infection screen: blood and urine culture, chest radiograph.

Hypoglycaemia

Hypoglycaemia (i.e. a blood glucose<3.5 mmol/l) is a result of the

treatment of diabetes rather than a manifestation of the disease itself. It occurs often in
those taking a sulphonylurea drug. Most patients recognize the symptoms of
hypoglycaemia and can take appropriate remedial action; others are less aware of these
and, if action is not taken, neuroglycopenia and reduced consciousness ensue.

Causes of Hypoglycaemia:

Errors in oral hypoglycaemic agent or insulin dose/ schedule/

administration Poorly designed insulin regimen, particularly if predisposing to nocturnal
hyperinsulnaemia.

Missed, delayed or inadequate meal

Unexpected or unusual exercise

Alcohol

Lipohypertrophy

Gastroparesis due to autonomic neuropathy

Malabsorption, e.g. celiac disease

Dumping

Unrecognised other endocrine disorder, e.g. Addison‟s disease

Factitious (deliberately induced)

Common Symptoms of Hypoglycaemia

a.Autonomic

The common autonomic symptoms of hypoglycaemia are sweating,

trembling, hunger, pounding heart, and anxiety.

b.Neuroglycopenic

The common neuroglycopenic symptoms of hypoglycaemia are confusion,

drowsiness, speech difficulty , inability to concentrate and incordination.

c.Non-Specific

The common non-specific symptoms of hypoglycaemia are nausea,

tiredness and headache.
DIAGNOSIS

Revised criteria for diagnosing DM have been issued by consensus panels

of experts from the National Diabetes Data Group and the World Health Organization

Criteria for the Diagnosis of Diabetes Mellitus

The revised criteria for the diagnosis of DM emphasize the FPG (fasting
plasma glucose) as the most reliable and convenient test for diagnosing DM in
asymptomatic individuals. A random plasma glucose concentration >11.1 mmol/L (200
mg/dL) accompanied by classic symptoms of DM (polyuria, polydipsia, weight loss) is
sufficient for the diagnosis of DM. Oral glucose tolerance testing, although still a valid
mechanism for diagnosing DM, is not recommended as part of routine screening.

Glycated Haemoglobin: HBA1C

Glycated haemoglobin provides an accurate and objective measure of

glycaemic control over a period of weeks to months. This can be utilized as an assessment
of glycaemic control in a patient with known diabetes, but is not sufficiently sensitive to
make a diagnosis of diabetes and is usually normal in patients with impaired glucose
tolerance.

Currently, laboratories report glycated haemoglobin as total glycated

haemoglobin(GHb),

Urine testing

a.Glucose

Testing the urine for glucose is the usual procedure for detecting diabetes, using
sensitive glucose-specific dipstick methods. If possible, testing should be performed on
urine passed 1-2hours after a meal since this will detect more cases of diabetes than a
fasting specimen. Glycosuria always warrants full assessment.

The greatest disadvantage of using urinary glucose as a diagnostic or

screening procedure is the individual variation in renal threshold. Apart from diabetes,
the most common cause of glycosuria is a low renal threshold for glucose, which is
common during pregnancy and in young people, and is a more frequent cause of
glycosuria than diabetes.
b.Ketones

c.Protein

d.Blood Lipids

LABORATORY EVALUATION

If the patient is a known diabetic, the following tests are to be advised

 Fasting blood sugar (FBS)

 Postprandial blood sugar (PPBS)
 Glycated haemoglobin (HbA1c)
 Blood urea
 Serum creatinine
 Urine protein
 Haemogram
 Urine complete examination
 Lipids (total cholesterol, triglycerides, HDL, LDL)
 Liver function tests (LFT)

If the patient is not a known diabetic, the following tests can be advised

 Glucose tolerance test (GTT)

 Glycated haemoglobin (HbA1c)
 Blood urea
 Serum creatinine
 Urine P/C ratio
 Urine complete examination
 Lipids (total cholesterol, triglycerides, HDL, LDL)
 Liver fun
 ction tests (LFT)
 ECG
TEST PROTOCOL FOR DIABETES FOLLOW -UP

TEST ADVICE FREQUENCY REMARKS

FBS ,PPBS Every visit -
Urea, creatinine P/C Every 3 months At every visit if renal
ratio insufficiency
Miccroalbuminuria Every 6 months Repeat if positive at previous
visit
Lipid profile Every 6 months Repeat if abnormal or on
treatment for hyperlipidaemia
HbA1c Once in 2-3 months
Liver function tests If previous LFT abnormal If patient on glitazones, lipid
(LFT) medications ,gamma GT for
those on alcohol

Serum electolytes If necessary or once in 6 If patients on ARB ACE

months inhibitors ,thiazides
Fructosamine In pregnancy ,in Type 1 -
patients
Chest X-ray If abnormal weight loss Otherwise repeat yearly
Foot X-ray If foot infection -
ECG Once every year ,once in 6 If patient has chest pain do
months if patient has during that visit
history of IHD

Doppler Once a year Repeat if indicate

biothesiometry foot
pressure study
Eyes –retinal Every year If patient has retinopathy
examination
Haemogram urine Every year Repeat if clinically indicated
complete examination
Dental check –up If required
Physiotherapy If required
Psychiatric If required
counselling
COMPLICATIONS:

COMPLICATIONS OF DIABETES MELLITUS

1. Acute Complications

a. Diabetic ketoacidosis (DKA)

b.Nonketotic hyperosmolar state(NKHS)

c.Hyper osmolar coma hypoglycemia

CHRONIC COMPLICATIONS

Chronic Complications of diabetes are due to Vascular damage from persistent

hyperglycemia. Vascular damage leads to end-organ damage. Other conditions associated
with diabetes, such as hypertension, dyslipidemia (as well as smoking) accelerate the
development of vascular damage and the chronic complications of diabetes, which are the
following:
Diabetic Ketoacidosis:

Diabetic ketoacidosis is a major medical emergency and remains a serious

cause of morbidity, principally in people with type 1 diabetes. The average mortality in
developed countries is 5-10% and is higher in the elderly.

A clear understanding of the biochemical basis and pathophysiology of

this problem is essential for its efficient treatment.

Ketoacidosis is caused by insulin deficiency and an increase in catabolic

hormones, leading to hepatic over-production of glucose and ketone bodies.

The cardinal biochemical features of diabetic ketoacidosis are:

a. hyperglycaemia

b. hyperketonaemia

c. metabolic acidosis.

Hyperglycaemia causes a profound osmotic diuresis leading to dehydration

and electrolyte loss, particularly of sodium and potassium. The metabolic acidosis forces
hydrogen ions into cells, displacing potassium ions, which may be lost in urine or through
vomiting.

About half the deficit of total body water is derived from the intracellular
compartment and occurs comparatively early in the development of acidosis with
relatively few clinical features; the remainder represents loss of extra cellular fluid
sustained largely in the later stages. It is at this time that marked contraction of the size of
the extra cellular space occurs, with haemo concentration, a decreased blood volume, and
finally a fall in blood pressure with associated renal ischaemia and oliguria.

Every patient in diabetic ketoacidosis is potassium-depleted, but the

plasma concentration of potassium gives very little indication of the total body deficit.
Plasma potassium may even be raised initially due to disproportionate loss of water and
catabolism of protein and glycogen.

However, soon after insulin treatment is started there is likely to be

precipitous fall in the plasma potassium due to dilution of extra cellular potassium by
administration of intravenous fluids, the movement of potassium into cells as a result of
treatment with insulin, and the continuing renal loss of potassium.

The severity of ketoacidosis can be assessed rapidly by measuring the

plasma bicarbonate; less than 12 mmol/l indicates severe acidosis.

Clinical features:

a. Symptoms Nausea,vomitingThirst,polyuria,Abdominal pain,Altered

mental function and Shortness of breath

b. Physical findings Tachycardia,Dry mucous membranes, reduced skin

turgor,Dehydration, hypotension,Tachypnea, Kussmaul respirations, respiratory
distress,Abdominal tenderness, (may resemble acute pancreatitis or surgical
abdomen)FeverLethargy ,obtundation , cerebral edema and possibly comac.

c. Precipitating events Inadequate insulin administration, infection

(pneumonia/UTI/gastroenteritis/sepsis), Infarction (cerebral, coronary, mesenteric,
peripheral) and drugs (cocaine)

Nonketotic Hyperosmolar State

Clinical Features NKHS is most commonly seen in elderly individuals

with type 2 DM. Its most prominent features include polyuria; orthostatic hypotension;
and a variety of neurologic symptoms that include altered mental status, lethargy,
obtundation, seizure, and possibly coma.

The prototypical patient is a mildly diabetic, elderly individual with a

several week history of polyuria, weight loss, and diminished oral intake that culminates
in mental confusion, lethargy, or coma. The physical examination reflects profound
dehydration and hyperosmolality and reveals hypotension, tachycardia, and altered
mental status.

NKHS is often precipitated by a serious, concurrent illness such as

myocardial infarction or stroke. Sepsis, pneumonia, and other serious infections are
frequent precipitants and should be sought thoroughly. In addition, a debilitating
condition (prior stroke or dementia) or social situation that compromises water intake
may contribute to the development of the disorder. Finally, the development of NKHS
can be associated with the use of certain medications (thiazide diuretics, glucocorticoids,
phenytoin).

2. Chronic Complications of Diabetes Mellitus

a. Microvascular:

Eye disease

Retinopathy(nonproliferative/proliferative)

Macular edema

Cataracts

Glaucoma

Neuropathy

Sensory and motor (mono- and polyneuropathy)

Autonomic

Nephropathy.

b. Macrovascular:

Coronary artery disease

Peripheral vascular disease

Cerebrovascular disease

c. Other:

Gastrointestinal (gastroparesis, diarrhoea)

Genito urinary (uropathy/sexual dysfunction)

Dermatologic
DIABETIC RETINOPATHY:

Diabetic retinopathy is the most common cause of blindness in adults between 30 and 65
years of age in developed countries.

Pathogenesis:

Hyperglycaemia increases retinal blood flow and metabolism and has

direct effects on retinal endothelial cells and pericytes, loss of which impairs vascular
autoregulation.the resulting uncontrolled blood flow increases production of vasoactive
substances and endothelial cell proliferation, resulting in capillary closure. This causes
chronic retinal hypoxia and stimulated production of growth factors, including vascular
endothelial growth factor (VEGF). VEGF acts via proteinkinase C to stimulate
endothelial cell growth (causing new vessel formation) and increased vascular
permeability (causing exudative damage).

Clinical Features Of Diabetic Retinopathy:

1. Microaneurysms

2. Retinal haemorrhages

3. Exudates

4. Cotton wool spots

5. Venous changes

6. Neovascularisation

7. Pre-retinal haemorrhage

8. Vitreous haemorrhage

9. Fibrosis
INTRARETINAL MICROVASCULAR ABNORMALITIES

Intraretinal microvascular abnormalities (IRMA) are dilated, tortuous

capillaries which represent the remaining patent capillaries in an area where most have
been occluded.

Neovascularisation:

This may arise from the venous circulation on the optic disc or the retina in
response to areas of ischaemic retina. retinal detachment can occur due to contraction of
adhesions between the vitreous and the retina.

Venous Changes:

These include venous dilatation (an early feature probably representing

increased blood flow), „beading‟ (sausage-like changes in calibre) and increased
tortuosity including „oxbow lakes‟ or loops.

These latter changes indicate widespread capillary non-perfusion and are a

feature of advanced pre-proliferative retinopathy.

Cataract:

Cataract is a permanent lens opacity and is the most common cause of visual
deterioration in the elderly population.

The lens thickens and opacifies with age, and the increased metabolic
insult to the lens in people with diabetes causes these changes to accelerate and occur
prematurely. Very rarely, a type of cataract specific to diabetes occurs in young patients
with poorly controlled diabetes, called a „snow-flake‟ cataract. This does not usually
affect vision but tens to make fundal examination difficult.

Renal Complications Of Diabetes Mellitus:

The nephropathy that develops in type 2 DM differs from that of type 1

DM in the following respects:

(1) microalbuminuria or over nephropathy may be present when type 2

DM is diagnosed, reflecting its long asymptomatic period;
 (2) hypertension more commonly accompanies microalbuminuria or
overt nephropathy in type 2 DM; and

(3) microalbuminuria may be less predictive of progression to overt

nephropathy in type 2 DM. Finally, it should be noted that albuminuria in type 2 DM may
be secondary to factors unrelated to DM, such as hypertension, congestive heart failure,
prostate disease, or infection.

Other renal problems may also occur in individuals with DM. Type IV
renal tubular acidosis (hyporeninemic hypoaldosteronism) occurs in many individuals
with DM

NEUROPATHY AND DIABETES MELLITUS

Diabetic neuropathy occurs in approximately 50% of individuals with

long-standing type 1 and type 2 DM. It may manifest as polyneuropathy,
mononeuropathy, and/or autonomic neuropathy.

a.Polyneuropathy/Mononeuropathy:

The most common form of diabetic neuropathy is distal symmetric

polyneuropathy. It most frequently presents with distal sensory loss. Hyperesthesia,
parathesia, and pain also occur. Any combination of these symptoms may develop as
neuropathy progresses. Physical examination reveals sensory loss, loss of ankle reflexes,
and abnormal position sense.

b.Diabetic polyradiculopathy

c.Mononeuropathy (dysfunction of isolated cranial or peripheral nerves)

d.Autonomic Neuropathy

Cardiovascular Morbidity and Mortality:

Cardiovascular disease is increased in individuals with type 1 or type 2

DM. The Framingham Heart Study revealed a marked increase in several cardiovascular
diseases in DM including peripheral vascular disease, congestive heart failure, coronary
artery disease, myocardial infarction, and sudden death (risk increase from one- to
fivefold).
 The extremely high frequency of underlying cardiovascular disease in
individuals with diabetes (especially in type 2 DM).The absence of chest pain (“silent
ischemia”) is common in individuals with diabetes.

Hypertension:

Hypertension can accelerate other complications of DM, particularly

cardiovascular disease and nephropathy. Hypertension therapy should first emphasize
life-style modifications such as weight loss, exercise, stress management, and sodium
restriction.

CLINICAL FEATURES OF THE DIABETIC FOOT

Symptoms

Neuropathy Ischaemia

None None

Paresthesia Claudication

Pain Rest pain

Numbness

Structural Damage Ischaemia

Ulcer Ulcer

Sepsis Sepsis

Abscess Gangrene

Osteomyelitis

Digital gangrene

Charcot joint
Management Of Diabetic Foot Ulcers:

Remove callus skin, treat infection, avoid weight-bearing, ensure good

diabetic control, control oedema, undertake angiogram to assess feasibility of vascular
reconstruction where indicated.

Infections:

Individuals with DM exhibit a greater frequency and severity of infection.

The reasons for this increase include incompletely defined abnormalities in cell-mediated
immunity and phagocytic function associated with hyperglycemia, as well as diminished
vascularization secondary to long-standing diabetes. Hyperglycemia likely aids the
colonization and growth of a variety of organisms (Candida and other fungal species).

Pneumonia, urinary tract infections, and skin and soft tissue infections are
all more common in the diabetic population.

Dermatologic Manifestations

The most common skin manifestations of DM are protracted wound

healing and skin ulcerations.

Diabetic dermopathy, sometimes termed pigmented pretibial papules, or

“diabetic skin spots,” begins as an erythematous area and evolves into an area of circular
hyperpigmentation . These lesions result from minor mechanical trauma in the pretibial
region and are more common in elderly men with DM.

Acanthosis nigricans (hyperpigmented velvety plaques seen on the neck or

extensor surfaces) is sometimes a feature of severe insulin resistance and accompanying
diabetes. Generalized or localized granuloma annulare (erythematous plaques on the
extremities or trunk) and scleroderma (areas of skin thickening on the back or neck at the
site of previous superficial infections) are more common in the diabetic population.
Lipoatrophy and lipohypertrophy can occur at insulin injection sites but are unusual with
the use of human insulin. Xerosis and pruritis are common and are relieved by skin
moisturizers.
CLINICAL EXAMINATION OF THE PATIENT WITH DIABETES:

1.Examination Of The Hands:

Limited joint mobility (sometimes called cheirorthropathy) may be

present; this is the inability to extend (to 180) the metacarpophalangeal or interphalangeal
joints of at least one finger bilaterally. The effect can be demonstrated in the prayer sign.
It causes painless stiffness in the hands, and occasionally affects the wrists and shoulders.

Dupuytren‟s contracture is common in diabetes and may include nodules

or thickening of the skin and knuckle pads.

Carpal tunnel syndrome is common in diabetes and presents with wrist

pain radiating into the hand.

Trigger finger (flexor tenosynovitis) may be present in people with

diabetes.

Muscle-wasting/sensory changes may be present as features of a peripheral

sensorimotor neuropathy, although this is more common in the lower limbs.

2.Abdomen Hepatomegaly

3.Blood Pressure

4.Axilla Acanthosis nigricans

5.Neck Carotid pulses, Bruits and thyroid enlargement

6.Head Xanthelasma, Cranial nerve palsy and eye

movements/ptosis

7.Examination Of The Eyes:

Visual acuity

Distance vision using Snellen's chart at 6 metres.

Near vision using standard reading chart.

 Impaired visual acuity may indicate the presence of diabetic eye disease,
and serial decline may suggest development or progression in severity.

Lens opacification, look for the red reflex using the ophthalmoscope held
30 cm from the eye.

The presence of lens opacities or cataract should be noted.

Fundal examination:

The pupils must be dilated with a mydriatic and examined in a darkened

room.Features of diabetic retinopathy should be noted, including evidence of previous
laser treatment which leaves photocoagulation scars.

8.Legs : Muscle-wasting

Sensory abnormality

Granuloma annulare

Hair loss

Tendon reflexes

Necrobiosis lipoidica

Neuropathic foot ulcer

9.Examination Of The Feet

Inspection:

Look for evidence of callus formation on weight-bearing areas, clawing of

the toes (a feature of neuropathy, loss of the plantar arch, discolouration of the
skin,ischaemia), localised infection and the presence of ulcers. Deformity of the feet may
be present, especially in charcot neuroarthropathy.Fungal infection may affect skin
between toes, and nails.

Circulation:

Peripheral pulses, skin temperature and capillary refill should be tested.

Sensation:

Light touch: use monofilaments.

Vibration sense: use 128Hz tuning fork over big toe/malleoli.

Pin-prick: Use pin

Pain: pressure over Achilles tendon.

Proprioception test

Position of big toe

Test for distal anaesthesia/hyperaesthesia in stocking distribution.

Reflexes: Test plantar and ankle reflexes.

DIETARY MANAGEMENT:

Aims Of Dietary Management:

Abolish symptoms of hyperglycaemia

Reduce overall blood glucose and minimise fluctuations

Achieve weight reduction in obese patients to reduce insulin resistance,

hyperglycaemia and dyslipidaemia

Avoid hypoglycaemia associated with therapeutic agents

(insulin,sulphonylureas)

Avoid weight gain associated with therapeutic agents (insulin,

sulphonylureas, thiazolidinediones)

Avoid „atherogenic‟ diets or those which may aggravate diabetic

complications (e.g. high protein intake in nephropathy)

General Principles of Diet for Diabetes:

Direct sugar intake in the form of refined carbohydrates should be totally

avoided. This includes table sugar, sweets, and jaggery. The total quantity of food must
be restricted.
 There is no need to change over from rice to wheat or ragi as the
carbohydrate content of these different cereals is not significantly different. Green leafy
vegetables and other low calorie foods can be taken in unlimited quantities.

Addition of vegetable proteins in the form of bengal gram, green gram,

have multiple benefits as they:

a) Increase the protein content

b) Increase the fibre content

c) Help to flatten sudden urges of blood sugar after a meal

d) Help to reduce serum lipid (fat) levels

e) The diet should help to maintain ideal body weight.

f) The diet should also help bring down the cholesterol triglyceride
levels

Types Of Diabetic Diet

The basis for types of diet used in the treatment of diabetes;

1. Low energy, weight-reducing diets

2. Weight maintenance diets

3. Diets for insulin-treated diabetes

Low-energy, weight-reducing diets

Dietary prescriptions which cause a daily deficit of 500 kcal provide a

realistic diet and induce a weekly weight loss of around 0.5 kg. Rapid weight reduction
may provoke loss of lean body tissue, and care must be taken in the elderly to avoid the
omission of essential nutrients, vitamins and minerals. Caloric restriction is essential for
the obese diabetic patient treated with insulin and most oral agents, to try to minimise the
weight gain which these can promote. in such individuals, the omission of snacks
between meals is often necessary
Weight maintenance diets

These are necessary for individuals with a normal body mass index and
ideally should be high in carbohydrate and low in fat, with particular attention being paid
to the type of fat ingested.

Diets for Insulin-treated Diabetes

A regular pattern of meals (and snacks) is important to maintain a constant

daily intake of carbohydrate, and protects against hypoglycaemia. Simple information on
the relative carbohydrate content of foods can be provided where ever appropriate.
Carbohydrate exchanges (10 g portions) are currently not advocated as a method of
controlling carbohydrate intake, as the exchange system makes no allowance for the
glycaemic effect or for the fat content of foods. However, a good working knowledge of
the carbohydrate content of foods is essential for practical management. An insufficient
dose of insulin for a meal with a large carbohydrate content leads to post-prandial
hyperglycaemia, while inadequate carbohydrate consumption risks hypoglycaemia.

Diabetic Foods And Sweeteners:

Low-calorie and sugar-free drinks are useful for patients with diabetes.
These drinks usually contain non-nutritive sweeteners. Many „diabetic foods‟ contain
sorbitol or fructose which are relatively high in energy, may be expensive and may have
gastrointestinal side-effects. They are not recommended as part of the diabetic diet.

The non-nutritive sweeteners saccharin, aspartame, sucramate and acesulphame K are the
most widely used and provide means for reducing energy intake without loss of
palatability.

Of Energy Derived From Carbohydrate, Protein And Fat

UK national Recommended
diet diabetic diet

Energy Maintain BMI of 25 kg/m2 To approach

BMI of22 kg/m2

Carbohydrate 45 % 50 – 55%
Fat 40% 30-35%

Saturated fatty acids 17% <10%

Monounsaturated 11% 10-15%

Polyunsaturated 6% <10%

Protein 12-15% 10-15%

BMI = body mass index (weight [kg]/ height2 [m2])

Education Of The Patient About Dm And Exercise

Diabetes Education:

The diabetes educator is a health care professional (nurse, dietician, or

pharmacist). The educator is a vital member of the comprehensive diabetes care program
and educates the patient about a number of issues important for optimal diabetes care,
including self-monitoring of blood glucose; urine ketone monitoring (type 1 DM); insulin
administration; guidelines for diabetes management during illnesses; management of
hypoglycemia; foot and skin care; diabetes management before, during, and after
exercise; and risk factor-modifying activities.

Exercise:

Exercise is an integral component of comprehensive diabetes care that can

have multiple positive benefits (cardiovascular benefits, reduced blood pressure,
maintenance of muscle mass, reduction in body fat, weight loss, etc.).

For individuals with type 1 or type 2 DM, exercise is also useful for
lowering plasma glucose (during and following exercise) and increasing insulin
sensitivity.

Daily, regular physical exercise reduces insulin requirements. Sudden,

unaccustomed violent exercise, however, it likely to precipitate hypoglycemia especially
in patients on insulin and should be taken prophylactically. In the juvenile diabetic who
has omitted insulin, vigorous exercise can however precipitate ketoacidosis Skeletal
muscle is a major site for metabolic fuel consumption in the resting state, the increased
muscle activity during vigorous, aerobic exercise greatly increases fuel requirements.
Individuals with type 1DM are prone to either hyperglycemia or hypoglycemia during
exercise.

To avoid exercise – related hyper-or hypoglycemia, individuals with type 1DM should:

1 .Monitor blood glucose before, during, and after exercise.

2. Eat a meal 1 to 3 hr before exercise and the supplemental

carbohydrate feedings at least every 30min during vigorous or prolonged exercise;

3. Decrease insulin doses(based on previous experience) before

exercise and inject insulin into a non exercising area.

4. Learn individual glucose responses to different types of exercise

and increase food intake for upto 24hr after exercises, depending on intensity and
duration of exercise.

5. In individuals with type 2DM, exercise-related hypoglycemia is

less common but can occur in individuals taking either insulin or sulfonyl ureas.

ON GOING ASPECTS OF COMPREHENSIVE DIABETES CARE:

The morbidity and mortality of DM-related complications can be greatly

reduced by timely and consistent surveillance procedures. Screening for dyslipidemia and
hypertension should be performed annually.

An annual comprehensive eye examination should be performed by

qualified optometrist or ophthalmologist.

Guidelines for Ongoing Medical Care for Patients with Diabetes:

1.Self-monitoring of blood glucose (individualized frequency)

2.HbA1c testing (2-4 times/year)

3.Patient education in diabetes management (annual)

 4.Medical nutrition therapy and education (annual)

5.Eye examination (annual)

6.Foot examination (1-2 times/year by physician; daily by patient)

An annual foot examination should:

a. assess blood flow, sensation, and nail care;

b. look for the presence of foot deformities such as hammer or claw toes
Charcot foot;

c. identify sites of potential ulceration

7. Screening for diabetic nephropathy (annual)

8. Blood pressure measurement (quarterly)

9. Lipid profile (annual).

 MATERIALS AND METHODS

A Pilot Study To Evaluate The Therapeutic Efficacy Siddha Herbal Formulation Of

THETRAN VIDHAI KUDINEER For The Treatment Of Mathumegam (Type 2
Diabetes Mellitus)

Study Design & Conduct Of The Study:

Study type : An open clinical trial

Study place : OPD & IPD of ayothidass pandithar hospital, national institute of Siddha,
Tambaram sanatorium, Chennai- 47

Study period : 12 months

Sample size : 40 patients

Population And Sample:

All NIDDM patients (fasting blood sugar 110-130 mg% and PP blood
sugar 210- 280 mg%) satisfying the inclusion and exclusion criteria mentioned below will
be the population of study.NIDDM patients attending the OPD of Ayothidoss Pandithar
Hospital of National Institute of Siddha ,Chennai-47 will be enrolled for this clinical
research.

Sample size:

Sample size will be 40 patients. (30 Op & 10 Ip )

Treatment:

Medicine Name : THETRAN VITHAI KUDINEER

Dose : 30 ml every four hours before food / day

Adjuvant : cow‟s butter milk

Duration : 48 Days
Standard Operating Procedure For ‘THETRAN VITHAI KUDINEER‟ ( Internal):

Source Of Raw Drugs:

The source of raw drugs for preparation of THETRAN VITHAI KUDINEER are
purchased from a well reputed country shop and raw drugs are purified & prepared in
gunapadam lab of nNational Institute of Siddha.

Ingrdients of Thetran Vithai Kudineer:

 Thetran vithai ( Strychnous potatorum.linn )

 Kadukkai thol ( Terminalia chebula.linn )

 Avari virai ( Cassia auriculata.linn ) each 130 gms

 Vilam pisin ( Limonia acidissima.linn)

Method of purification:

Purification of thetran vidhai :

Thetran vidhai is soaked in cows milk for 3 hours and is washed with plain water.

Purification of kadukkai thol:

Kadukkai seed is removed and soaked in lime juice and dried in sunlight.

Purification of vilampisin:

Vilampisin is clean well by removing the debris which adhere with it.

Method Of Purification Of Thetran Vithai Kudineer:

Ingredients:

 Thetran vithai chooranam ( strychnous potatorum )

 Kadukkai thol chooranam ( terminlia chebula )

 Aavarai vithai chooranam (cassia auriculata) each 112 gms

 Vilampisin chooranam ( limonia acidissima )

Ingredients 1,2,3,4 are ground separately with iron martar till it attains consistency. They
are fine chooranam mixed well and preserved in a clean and dry glass.

Drug storge:

The trial drug THETRAN VIDHAI CHOORANAM is stored in a clean

and dry glass bottles.

Dispensing :

The chooranam is given in packets

Subject selection :

As and when patients with symptoms of inclusion criteria reporting at

OPD Aythidoss pandithar hospital of NIS will be subjected to screening test &
documentation will be done using screening proforma.

Inclusion criteria:

1. Age 30 to 65 yrs.

2. Patients who are willing to attend the OPD regularly for the first 15 days will be
included in the clinical trial.

3. Patients who are willing to take treatment to take as IPD will be included in the clical
trial.

4. patients who are reporting with the clinical symptoms such as polyurea, polydipsia,
polyphagia, will be included in the clinical trail.

5. blood sugar Fasting 110 mg – 130 mg % ; PP 210 mg -280mg % will be included in

the clinical trial

Exclusion criteria:

1.Blood sugar fasting > 130 mg % and or PP 280 mg %

2. Patients with diabetic complications like diabetic foot, retinopathy, etc

3. Heart disease
 4. Hyper tension

5. Hyper thyroidism

6. Diabetic ulcer

Withdrawl criteria:

1 Intolerance to the drug and development of adverse reactions during

drug trial.

2. Poor patient compliance & Defaulters.

3. Patient turned unwilling to conttinue in the course of clinical trial

4. Occurrence of any serious illness

Tests and Assessments:

a) Clinical Assessments:

Polyuria, polydypsia, polyphagia, nocturia, tiredness, fatigue ,sudden gain

in weight, blurring of vision,pricking pain in both palm and soles,burning sensation in
both soles ,and paresthesia in the feet,pruritis vulvae, balanitis.

b) Investigation:

Blood Test:

TC ,DC, ESR, Hb, sugar (Fasting ,PP) Lipid profile,Liver function test,
Renal function test.

Urine Test:

Albumin,Sugar (Fasting and PP), Deposits

Bile salt,Bile pigments, Urobilinogen.

Clinical assessment &Investigations-Siddha System:

Ennvagai thervugal –Naa,Niram ,Mozhi,Vizhi, Sparism,Malam,Moothiram ,Naadi.

Moothiram:

Neerkuri - Niram,Edai,Manam,Nurai,Enjal.

Neikuri

Motion Test: - Ova,Cyst,Occult blood.

METHODOLOGY

STUDY ENROLLMENT

 In the Phase II study, patients reporting at the OPD with the clinical symptoms of
Polyphagia, Polyurea, Polydipsia, nocturia etc.. will be examined clinically for
enrolling in the study based on the inclusion and exclusion criteria.
 The patients who are to be enrolled would be informed (Form IV-D) about the
study, trial drug, possible outcomes and the objectives of the study in the language
and terms understandable to them.

 After ascertaining the patient‟s willingness, informed consent would be obtained

in writing from them in the consent form .(Form- IVA)
 All these patients will be given unique registration card in which patients‟
Registration number of the study, Address, Phone number and Doctors phone
number etc. will be given, so as to report easily should any complications arise.
 Complete clinical history, complaints and duration, examination findings-- all
would be recorded in the prescribed Proforma in the history and clinical
assessment forms separately. Screening Form- I will be filled up; Form I-A, Form
–II and Form –III will be used for recording the patients‟ history, clinical
examination of symptoms and signs and laboratory investigations respectively.
 Patients would be advised to take the trial drug and appropriate dietary advice
(Form IV-E) would be given according to the patients‟ perfect understanding.
 CONDUCT OF THE STUDY:

The trial drug THETRAN VIDHAI KUDINEER (Internal ) is given

continuously for 48 days.
For OP Patients, they should visit the hospital once in 12 days. At
each clinical visit clinical assessment is done and prognosis is noted. For IP
Patients the drug is provided daily and prognosis is noted.

For IP patients also clinical assessment is done daily. Laboratory

investigations are done 15th day, 24th & 48 th day of the trial. For IP patients, who
is not in a situation to stay in the hospital for a long time is advised to attend the
OPD for further continuation of treatment. After the end of the treatment also, the
patient is advised to visit the OPD for another 2 months for follow-up.
If any trial patient who fails to collect the trial drug on the prescribed day
but wants to continue in the trial from the next day or two, he/she will be allowed ,
but defaulters of one week and more will not be allowed to continue and be
withdrawn from the study with fresh case being inducted.

DATA MANAGEMENT

 After enrolling the patient in the study, a separate file for each patient will be
opened and all forms will be filed in the file. Study No. and Patient No. will be
entered on the top of file for easy identification. Whenever study patient visits
OPD during the study period, the respective patient file will be taken and
necessary recordings will be made at the assessment form or other suitable form.
 The screening forms will be filed separately.
 The Data recordings will be monitored for completion by HOD and adverse event
by Sr.Research Officer (Statistics). All forms will be further scrutinized in
presence of Investigators by Sr.Research Officer (Statistics) for logical errors and
incompleteness of data to avoid any bias. No modification in the results is
permitted for unbiased reports.

OUT COME
1.Before treatment
2.After treatment
 ADVERSE EFFECT / SERIOUS EFFECT MANAGEMENT:

If the trial patient develops any adverse reaction ,he/she would be

immediately withdrawn from the trial and proper management will be given in OPD of
National institute of Siddha.

ETHICAL ISSUES

1 .To prevent any infection while collecting the blood sample from the
patient only disposable syringes , gloves with proper sterilization of lab equipments
will be used.

2 . No other external & internal medicines will be used. There will be no

infringement on the rights of patient.

3 .The data collected from the patient will kept confidently. The patient will
be informed about the diagnosis, treatment and follow up.

4. After the consent of the patient (through consent form) they will be
enrolled in the study.

5. Informed consent will be obtained from the patient explaining

understandable language to the patient.

6. Treatment would be provided free of cost.

7. In condition of treatment failure, any other adverse reactions

developed, patient will be given alternative treatment at the National Institute of
Siddha with full care through the end.

ASSESSMENT FORM

FORM I SCREENING & SELECTION PROFORMA

FORM I A HISTORY PROFORMA ON ENROLLMENT

FORM II CLINICAL ASSESSMENT ON ENROLLMENT

FORM II A CLINICAL ASSESSMENT DURING & AFTER TRIAL

FORM III LABORATORY INVESTIGATION ON ENROLLMENT &
CONCLUSION OF TRIAL

FORM IV A CONSENT FORM

FORM IV B WITHDRAWAL FORM

FORM IV C DRUG COMPLIANCE FORM

FORM IV D PATIENT INFORMATION SHEET

FORM IV E DIETARY ADVICE FORM

FORM IV F ADVERSE REACTION FORM.

 OBSERVATION AND RESULTS

For the clinical study 30 out patients and 10 inpatients were selected and treated in
PG Maruthuvam Department, National Institute of Siddha hospital,Chennai-47.

Results were observed with respect to the following criteria.

1. Age distribution

2. Sex distribution

3. Yaakai

4. Kosangal

5. Neer Kuri,Neikuri

6. Family history

7. Food habits

8. Personal habits

9. Socio-economic status

10. Mukutram

11. Udal Thathukkal

12. En Vagai Thervu

13. Clinical manifestations

14. Chronicity of illness

15. Results
1.AGE DISTRIBUTION:

Age between 30 and 60 were selected for this study

Table:1

Age
Op/Ip Cases Sex
30-40 41-50 51-60

Male 03 04 16
OP
Female 01 02 04

Male - - 01
IP
Female - - 09

Total/percentage 4/10% 6/15% 30/75%

Most of the cases were between age group of (51-60) i.e. 75%.and age group of 41-50
were 15% and 30-40 age group were 10%.
2.SEX DISTRIBUTION:

Table:2

Patients OP IP percentage

Male 23 01 60

Female 07 09 40

40 Patients of both sexes were selected for this study. Among these 24 cases (60%)were
Male and 16 cases( 40%) were Female. Madhumegam can affect both sexes.
3.YAAKKAI:

Table:3

S. No Yakkai No. of cases Percentage (%)

1 Vaatham
2 Vaatha pittham
3 Vaatha kapham
4 Pittham
5 Pittha vaatham
6 Pitha Kapham
7 Kapham
8 Kapha vadham
9 Kapha pittham
0 -
12 30
10 25
0 -
4 10
5 12.5
0 -
7 17.5
2 5

Most of the patients affected in madhumegam were vatha udalina22 cases (55% )
and pitha udalinar9 cases( 22.5%) and kapha udalinar9 cases( 22.5%.)
4.KOSANGAL:

Table:4

Kosam No of Cases Peercentage of cases

Annamaya kosam 20 50

Pranamayakosam - -

Manomayakosam 4 10

Aanandha mayakosam 10 25

Vignanamayakosam 5 12.5

50% of the cases(20) were affected in Annamayakosam. Anandha maya kosam

were affected 25% of cases,(10), 10% of cases (4) were affected Manomayakosam,and
12.5% cases(5) were affected in Vignanamayakosam.
5.FAMILY HISTORY:

Table:5

Family history No family history

No of patients 15 25

percentage 37% 63%

Out of 40 Patients 15 cases (37%) had positive family history of type 2

diabetes. From the above study hereditary plays an important role in this disease .
6.NEIKURI:

Table:6

SPREADING NO OF PERCENTAGE(%)
PATTERN CASES

Aravena neendathu (vatha 22 55

neer -
lengthening like a snake )

Aazhi pol paraviathu 9 22.5

(pitha neer – spreading
like a ring )

Muththu pol ninrathu 9 22.5

(kaba neer – appears like a
pearl )

Total 40 100

NEER KURI NEIKURI

Muththu pol
ninrathu
22%

Aravena
neendathu
Aazhi pol 55%
paraviyathu
23%

Most of the cases had vaatha neer ie. 22 cases ( 55 % ),9 cases ( 22.5 % ) had pitha
neer,and 9 cases ( 22.5 % ) had kaba neer.
7.FOOD HABITS:

Table:7

Food habits No of patients Percentage

Vegetarian 13 32.5

Non vegetarian 27 67.5

Only 32.5% (13 cases) were vegetarians and the rest were found to be taking
mixed diet, i.e 67.5% of cases(27). It clearly showed that non vegetarian diet is more
prone to Madhumegam.
8.PERSONAL HABITS:
table:8

Personal habits No of cases percentage

Smokers 7 17.5

Alcoholic 12 30

Out of 40 cases 17.5% of patients(7) were smokers30%(12) patients were

alcoholic.
9.SOCIO- ECONOMIC STATUS:

Table: 9

S.No Economic status No of cases Percentage(%)

1. Poor 11 27.5

2. Middle class 23 57.5

3. Rich 6 15

Total 40 100

Among 40 patients 27.5% of cases(11) were under poor socio- economic

status and 57.5% of cases(23) were from middle class family and 15% of cases(6)
were from Rich.
10.Incidence according to Mukkutrangal:

Table: 10

(i)Vaatham:

Sl. no Vaatham No.of cases Percentage (%)

1 Praanan 0 0
2 Abaanan 22 55
3 Udhaanan 15 37.5
4 Viyaanan 17 42.5
5 Samaanan 22 55
6 Naagan 8 20
7 Koorman 7 17.5
8 Kirukaran 12 30
9 Devathaththan 5 12.5
10 Thananjeyan 0 0

Viyaanan (pain present in the both upper and lower limbs,burning

sensation present in the both soles) was affected in 42.5% cases(17). Udhanan
(tiredness,drowsiness) was affected 37.5% (15 cases) and abaanan (poly
uria,constipation,nocturia,sexual disturbance) was affected in 55%cases(22). Samaanan
(indigestion,) was affected 55%(22cases) and kirukaran (polyphagia)was affected in 30%
cases(12) and nagan (burning sensation present in both eyes) was affected 20%(8) and
Deva thaththan (tiredness,anxity) was affected in 12.5% cases(5 cases). Finally koorman
was affected in 17.5% ( 7)cases.

(ii)Piththam

Table:11

S.no Piththam No. of cases out of 40 Percentage (%)

1 Anal 15 37.5
2 Ranjagam 11 27.5
3 Pirasagam 7 17.5
4 Saathagam 35 87.5
5 Aalosagam 4 10

Saathaga pittham was affected in 87.5%(35) cases. Anal pittham was

affected in 37.5% of cases(15). Ranjaga pitham was affected in 27.5%(11) cases,pirasaga
pittham was affected in 17.5% cases(7).Aalosaga pitham was affected in 10% of cases(4).
iii) Kabam:

Table:12

S.No Kapham No. of cases out of 40 Percentage (%)

1. Avlambagam 10 25
2. Kilethagam 12 30
3. Pothagam 7 17.5
4. Tharpagam 4 10
5. Santhigam 20 50

Avalambagam was affected in 25%(10 cases), kilethagam was affected in

30% (12 cases) and Tharpagam affected in10%.(4 cases) Santhigam was affected in
50%(20) cases.many cases affected in santhigam.
11.Ezhu udal thaathukkal:

Table:13

S.no Udal thaathukkal No .of cases out of 40 Percentage

1. Saaram 40 100
2. Chenneer 15 37.5
3. Oon 0 0
4. Kozhuppu 7 17.5
5. Enbu 20 50
6. Moolai - -
7. Sukilam/Suronitham 7 17.5

In
Udal Thathukkal Saarm was affected in all cases. Chenneer was affected in 37.5% (15) of
cases Kozhuppu was affected in 17.5%(7) of cases. Enbu was affected in 50%(20) of
cases.sukilam was affected 17.5%(7) of cases.
12.Enn vagai thervugal:

Table:14

S.no Enn vagai thervugal No. of cases out of 40 Percentage (%)

1. Sparisam 20 50
2. Naa 7 17.5
3. Niram 3 7.5
4. Mozhi - -
5. Vizhi 4 10
6. Malam 03 7.5
7. Mooththiram
i) slowly spread 36 90
ii)Fastly spread 4 10
8. Naadi
i)Vaatha piththam 10 25
ii)Piththa vaatham 07 17.5
iii)Piththa kapham 06 15
iv)Kapha piththam 06 15
v) kappa vadham 11 27.5
 In enn vagai thervugal moothiram slowly spread in 90% (36)cases.fastly
spread in 10% (4) cases vizhi affected (burning sensation of both
eyes,cataract,diminished vision) in 10% (4) of cases and naa was affected in 17.5%(7) of
cases. Naadi was vaatha piththam in 25%(10) cases, piththa vaatham in 17.5% (7)cases
and piththa kapham in 15% (6)cases and kapha vatham in 27.5%(11) cases, kapha pitham
was noted in 15% (6) cases.

13.Showing the clinical features:

Table:15

S. no Clinical features No. of cases out of Percentage

40

1. Polyuria 25 62.5
2. Polydypsia 10 25
3. Polyphagia 12 30
4. Nocturia 10 25
5. Tirdness 32 80
6. Pain in the limbs 20 50
7. Pain and burning sensation in the 18 45
both sole
8. Pruritis Vulvae 3 7.5
9. Balanitis 4 10

62.5 % (25 cases) patients complained of polyuria and 25%(10 cases)

complained of Polydypsia.30%(12 cases) complained of polyphagia,25%(10 cases)
complained nocturia, 80%(32 cases) complained tirdness,50%(20 cases) complained
pain in limbs.45%(18 cases) complained pain and burning sensation in the both sole,and
7.5% (3 cases) complained pruritis vulvae, 10% (4 cases) complained Balanitis.
14.Chronicity of illness:

Table:16

S.No Duration of illness No of cases Percentage(%)

1. 0-1 years 5 12.5

2. 1-3 years 12 30

3. 3-5 years 14 35

4. 5-10 years 6 15

5. 10-20 years 3 7.5

Total 40 100

12.5% (5)patients had the history of this disease up to 0-1 yrs only. 30%
(12)of patients suffered for1-3 yrs and 35 % (14)patients for3-5 yrs.and 15%(6) patients
for 5-10 yrs,and 7.5%(3) patients suffered for 10-20 yrs.

15.Results: Blood sugar:

Table:17

S.No Gradation of results No of cases Percentage(%)

1. Good 24 60

2. Moderate 10 25

3. Poor 6 15

Total 40 100

Good result range:Fasting 70-110mgs%,Post prandial-120-140mgs%.24cases 60%.

Moderate result range: Fasting 110-120mgs%,Post prandial-140-170mgs%.10cases

ie., 25%

Poor result range: fasting above 120mgs%,post prandial-above 180mgs%.6 cases,

ie.,15%.
 Diagram shows that 60% (24)of cases had good clinical improvement,
25% (10)of cases had moderate and 15% (6)of cases had poor improvement.

Results- urine sugar:

Table:18

S.No Gradation of results No of cases Percentage(%)

1. Good 24 60
2. Moderate 10 25
3. Poor 6 15
Total 40 100

Good result range:-urine sugar nil

Moderate result range: urne sugar level + to ++

Poor result range: urine sugar level above ++.

Blood sugar and urine sugar before and after treatment results:

GOOD RESULTS
S. Name OP/IP Age/ Before After before after
No No Sex treatment treatmen treatment treatment
t
B.Sugar B.Sugar urine urine
mg/dl mg/dl sugar sugar
FA PP FA PP F PP F PP
1 Mr.Lakshman B3454 60/ 117 269 88 130 Nil ++ Nil +
an 5 M
2 Mr.Sundar A165 54/ 109 245 88 132 Nil + Nil Nil
71 M
3 Mr.Natarajan B9950 53/ 120 217 102 126 Nil + Nil Nil
3 M
4 Mr.Ilango A323 45/ 122 240 109 130 Nil + Nil Nil
12 M
5 Mr.Gopal B6922 55/ 125 263 98 128 Nil ++ Nil Nil
3 M
6 Ms.Manjula C1569 53/F 120 240 88 132 Nil + Nil Nil
5
7 Mr.Ashok C171951/ 130 253 97 134 Nil ++ Nil Nil
kumar 2 M
8 Mr.Bakthavac C176957/ 110 240 82 122 Nil + Nil Nil
hlam 9 M
9 Mr.Baskar C397169/ 119 230 103 130 Nil ++ Nil Nil
M
10 Mr.Ismayil B6466 54/ 127 260 98 132 Nil ++ Nil Nil
2 M
11 Mr.Ramasund A512 59/ 120 236 97 128 Nil + Nil Nil
ar 65 M
12 Mr.Venkatesa B9360 55/F 126 225 86 122 Nil + Nil Nil
n 7
13 Mr.Saravanan C2450 29/ 122 265 94 128 ++ +++ Nil Nil
M
14 Mr.Raja AH93 40/ 119 249 96 126 ++ +++ Nil Nil
25 M
15 Mr.Saravanan C4742 42/ 127 206 106 120 Nil + Nil Nil
M
16 Mrs.Lakshmi A419 43/F 130 260 86 130 Nil + Nil Nil
84
17 Mrs.Lurdu C996 60/F 129 220 97 128 Nil Nil Nil Nil
flora
18 Mrs.Tamilsel A702 40/F 128 251 100 130 Nil + Nil Nil
vi 98
19 Mrs.Kasthuri 3039 56/F 127 223 101 126 Nil + Nil Nil
20 Mrs.Zeenath 3137 56/F 128 240 92 126 Nil + Nil Nil
nisha
21 Mrs.Sumathi 3212 55/F 121 220 96 121 Nil Nil Nil Nil
22 Mrs.Anbu 3058 60/F 121 230 101 122 Nil + Nil Nil
23 Mrs.Abitha 2993 55/F 111 239 98 136 ++ +++ Nil Nil
begam
24 Mrs.Sumathi 3212 55/F 120 210 92 124 Nil + Nil Nil

MODERATE RESULTS
S.N Name OP/I Age/ Before After before after
o P Sex treatment treatment treatment treatment
No B.Sugar B.Sugar urine sugar urine sugar
mg/dl mg/dl
FA PP FA PP F PP F PP
1 Mr.Amirtahalin AJ38 60/ 126 290 110 146 Nil + Nil Nil
gam 59 M
2 Mr.Alakapuri B558 58/F 119 229 116 148 Nil + Nil +
39
3 Mr.Selvan C874 57/ 130 239 115 150 Nil ++ Nil +
21 M
4 Mr.Ramanujam C711 58/ 129 278 118 154 + +++ Nil +
3 M
5 Mr.Mohamed B910 38/ 117 210 114 152 Nil + Nil +
yusuf 80 M
6 Mr.Rajendran B935 48/ 129 277 112 159 Nil ++ Nil +
20 M
7 Mr.Dhamothar B572 50/ 127 276 118 156 ++ +++ Nil +
an 12 M
8 Mrs.Sumathi 3178 53/F 125 274 113 154 Nil Nil Nil +
9 Mrs.Leelavathi 3097 58/F 122 237 112 151 ++ +++ + +
10 Mr.Rajasekar 4052 56/ 127 272 117 156 Nil ++ Nil +
M
 POOR RESULTS
S.N Name OP/I Age Before After before after
o P / treatment treatment treatment treatment
No Sex B.Sugar B.Sugar urine urine
mg/dl mg/dl sugar sugar
FA PP FA PP F PP F PP
1 Mr.Rajendran B648 51/ 130 216 126 200 Nil + + ++
39 M
2 Mr.Adhirayan B593 60/ 130 277 124 221 ++ +++ ++ ++
92 M
3 Mr.Sabapathy AL87 49/ 130 274 122 246 Nil + + ++
56 M
4 Mrs. karhikayini AL87 51/F 130 245 122 210 Nil ++ + ++
57
5 Mrs.Malathy A531 42/F 129 260 125 240 Nil + + ++
67
6 Mrs.Marivarathar 2966 65/F 131 244 124 226 Nil + + ++
ajam

Showing the clinical features results:

No of cases
Clinical features
Before After Percentage(%)
treatment treatment
Polurea 25 25-20 = 5 80
Polydypsia 10 10-8 = 2 80
Polyphagia 12 12-10 = 2 83.3
Nocturia 10 10-7 = 3 70
Tiredness 32 32-18 = 14 56.25
Pain in the limbs 20 20-8 = 12 40
Pain and burning in the 18 18-10 = 8 55.5
both sole
Pruritis vulvae 3 3-1 = 2 33.3
Balanitis 4 4-1 = 3 25

Polurea, Polydypsia, Polyphagia, Nocturia-

Good result ( 70 – 85 % )

Tiredness, pain in the limbs, pain an burning in the both sole

Moderate result ( 40 -60 % )

Pruritis vulvae, balanitis

Poor result ( 0 – 30 % ).
Statistical Analysis:

All collected data were entered into computer using MS Excel software. The data
entry was cross-checked manually with CRF. The data was analysed using SPSS version
18.0 software. The probability value 0.05 was taken as significant level. Paired „t‟ test
was employed to determine the significance of blood sugar at before and after treatment.

Mean ±Standard deviation of Blood sugar at FA- Before and After treatment

FA – before 123.98 ±5.87 t = 11.29, p <0.0001

FA – after 104.58 ±12.67 Significant

The average blood sugar at the start of treatment and after the treatment were
123.98 and 104.58 respectively.

Mean ±Standard deviation of Blood sugar at PP- Before and After treatment

PP – before 245.7 ± 22.27 t = 17.8, p <0.0001

PP – after 148.3 ±34.6 Significant

The average blood sugar at the start of treatment and after the treatment were 245
and 148 respectively.

There is statistically significant difference between before and after treatment on average
blood sugar of FA and PP (p<0.0001).
 OBSERVATION OF CLINICAL LABORATORY EXAMINATIONS

At the time of admission to the trial, in all the 40 patients the following parameters
observed,

I.Routine blood investigations,

1.Haemoglobin estimation ,

2.Total WBC count,

3.total RBC count

4.Differential count,

5.Erythrocyte sedimentation Rate,

II.Blood sugar

1.Fasting

2.Post prandial

III.Liver function test,

IV.Renal function test,

V.Serum Lipid Profile

VI..Motion test,

VII. Urine examination

1.Albumin

2.Sugar

3.deposit

VIII.Neer kuri,Nei kuri also observed.

Before treatment- Haematology

TC ESR
OP/IP Age/ B.Sugar mg/dl Hb DC-% T.RBC
S.No Name cu/m mm/hr
No Sex gms% million
FA PP m P L E M 1/2 1
1. Mr.Lakshmanan B34545 60/M 117 269 13.6 7400 61 34 03 - 6 12 3.1
2. Mr.Amirtahalingam AJ3859 60/M 126 290 14.6 8300 55 40 05 - 10 20 3.4
3. Mr.Sundar A16571 54/M 110 245 15.5 7900 55 40 03 - 08 16 3.2
4. Mr.Rajendran B64839 51/M 130 216 14.5 7400 60 36 04 - 12 24 3.6
5. Mrs.Alakapuri B55839 58/F 119 229 12.0 8200 65 37 04 - 04 08 3.4
6. Mr.Natarajan B99503 53/M 120 217 13.5 8500 61 35 02 01 12 24 4.0
7. Mr.Ilango A32312 45/M 122 240 14.6 8600 54 45 03 - 08 16 3.1
8. Mr.Gopal B69223 55/M 125 263 11.2 7900 55 44 03 - 12 24 3.4
9. Ms.Manjula C15695 53/F 120 240 11.0 7500 55 42 02 - 04 08 3.5
10. Mr.Selvan C87421 57/M 130 239 13.0 8200 64 34 02 - 04 08 4.2
11. Mr.Ashok kumar C17192 51/M 130 253 11.9 7600 50 46 04 - 04 08 3.9
12. Mr.Bakthavachlam C17699 57/M 110 240 11.5 7400 56 43 03 - 08 16 3.2
13. Mr.Ramanujam C7113 58/M 129 278 11.7 7800 55 40 04 - 04 08 3.6
14. Mr.Baskar C3971 59/M 119 230 11.0 8200 60 35 04 - 10 20 3.4
15. Mr.Ismayil B64662 54/M 127 260 11.4 7900 55 44 02 - 02 04 3.6
16. Mr.Adhirayan B59392 60/M 130 277 11.3 7200 55 40 04 - 08 16 3.8
17. Mr.Ramasundar A51265 59/M 120 236 9.1 7400 61 36 03 - 04 08 3.0
18. Mr.Sabapathy AL 8756 49/M 130 274 10.3 7600 56 42 02 - 04 08 3.4
19. Mr.Venkatesan B93607 55/M 126 225 13.6 7900 58 40 02 - 12 24 3.6
20. Mr.Mohamed yusuf B91080 38/M 117 210 10.3 7600 55 43 02 - 06 12 3.4
Before treatment- Haematology

TC ESR
OP/IP Age/ B.Sugar mg/dl Hb DC-% T.RBC
S.No Name cu/m mm/hr
No Sex gms% million
FA PP m P L E M 1/2 1
21 Mr.Rajendran B93520 48/M 129 277 13.0 7200 50 37 02 - 08 16 3.4
22. Mr.Saravanan C2450 29/M 122 265 11.3 7500 54 41 02 - 10 20 3.3
23. Mr.Dhamotharan B57212 50/M 127 276 11.0 8000 66 32 04 - 04 08 4.8
24. Mr.Raja AH9325 40/M 119 249 10.7 8200 52 44 03 01 20 40 3.5
25. Mr.Saravanan C4742 42/M 127 206 11.5 7000 64 34 02 - 40 80 4.5
26 Mrs.Lakshmi A41984 43/F 130 260 15.4 7600 60 36 04 - 10 20 4.1
27. Mrs. karhikayini AL8757 51/F 130 245 12.3 7200 58 38 04 - 08 16 3.3
28. Mrs.Lurdu flora C996 60/F 129 220 15.9 8100 66 40 05 - 10 20 4.1
29. Mrs.Malathy A53167 42/F 129 260 13.2 6900 54 44 04 - 4 8 4.0
30 Mrs.Tamilselvi A70298 40/F 128 251 9.9 7000 58 36 04 02 16 32 3.9
31. Mrs.v.Sumathi 3178 53/F 125 274 11.2 7600 65 34 04 - 10 20 3.2
32. Mrs.Kasthuri 3039 56/F 127 223 13.0 8000 54 44 02 - 12 24 4.3
33. Mrs.Zeenath nisha 3137 56/F 128 240 11.5 1800 56 42 02 - 10 20 4.2
34. Mrs.Leelavathi 3097 58/F 122 237 11.6 7900 66 36 04 - 04 08 3.8
35. Mrs.J.Sumathi 3212 55/F 121 220 8.7 8400 65 30 05 - 40 80 3.0
36. Mrs.Anbu 3058 60/F 121 230 12.0 7900 54 42 04 - 20 40 3.6
37. Mrs.Abitha begam 2993 55/F 111 239 11.4 7600 60 37 03 - 04 08 3.5
38. Mrs.Marivaratharajam 2966 60/F 130 244 9.2 8000 60 36 03 01 26 52 3.1
39. Mrs.Balkis 3136 59/F 120 210 12.5 9600 67 25 06 02 08 16 4.1
40. Mr.Rajasekar 4052 56/M 127 272 7.5 8000 64 30 05 01 08 16 2.5
After treatment- Haematology

S.No OP/IP Age/ B.Sugar mg/dl Hb TC DC-% ESR T.RBC

Name No Sex gms% cu/m mm/hr million
FA PP m P L E M 1/2 1
1. Mr.Lakshmanan B34545 60/M 88 130 12.8 7200 58 32 01 - 05 11 3.0
2. Mr.Amirtahalingam AJ3859 60/M 110 146 13.0 8200 54 43 03 - 07 13 3.2
3. Mr.Sundar A16571 54/M 88 132 15.0 8300 56 42 03 - 05 12 3.1
4. Mr.Rajendran B64839 51/M 126 200 13.5 7600 63 38 02 - 09 18 3.3
5. Mr.Alakapuri B55839 58/F 116 148 13.0 8400 67 36 05 - 03 06 3.5
6. Mr.Natarajan B99503 53/M 102 126 13.0 8700 65 33 04 - 09 18 4.2
7. Mr.Ilango A32312 45/M 109 130 14.6 8400 58 44 03 - 07 14 3.2
8. Mr.Gopal B69223 55/M 98 128 12.4 8100 53 47 03 - 11 22 3.2
9. Ms.Manjula C15695 53/F 88 132 11.8 7300 52 41 01 - 03 06 3.7
10. Mr.Selvan C87421 57/M 115 150 13.7 8500 65 36 03 - 04 08 4.1
11. Mr.Ashok kumar C17192 51/M 97 134 12.8 7500 49 51 04 - 04 08 3.6
12. Mr.Bakthavachlam C17699 57/M 82 122 12.4 7600 52 47 06 - 06 12 3.6
13. Mr.Ramanujam C7113 58/M 118 154 11.5 7400 45 42 05 - 03 06 3.4
14. Mr.Baskar C3971 59/M 103 130 11.7 8300 56 37 05 - 06 12 3.7
15. Mr.Ismayil B64662 54/M 98 132 11.6 7800 52 46 03 - 03 06 3.2
16. Mr.Adhirayan B59392 60/M 124 221 11.8 7600 52 45 02 - 06 12 3.2
17. Mr.Ramasundar A51265 59/M 97 128 9.6 7600 56 37 02 - 04 08 3.6
18. Mr.Sabapathy AL 8756 49/M 122 246 10.2 7700 58 41 04 - 03 06 3.2
19. Mr.Venkatesan B93607 55/M 86 122 13.0 8200 56 42 01 - 08 16 3.2
20. Mr.Mohamed yusuf B91080 38/M 114 152 10.5 8200 52 46 04 - 04 08 3.7
After treatment - Haematology

S.No OP/IP Age/ B.Sugar mg/dl Hb TC DC-% ESR T.RBC

Name No Sex gms% cu/m mm/hr million
FA PP m P L E M 1/2 1
21 Mr.Rajendran B93520 48/M 112 159 13.2 7600 52 36 04 - 06 12 3.6
22. Mr.Saravanan C2450 29/M 94 128 11.6 7800 56 42 03 - 06 12 3.2
23. Mr.Dhamotharan B57212 50/M 118 156 12.6 9000 62 37 05 - 04 08 4.2
24. Mr.Raja AH9325 40/M 96 126 10.2 8500 57 41 06 - 10 20 3.8
25. Mr.Saravanan C4742 42/M 106 120 13.2 7600 55 37 03 - 20 40 3.2
26 Mrs.Lakshmi A41984 43/F 86 130 11.6 7400 58 37 02 - 08 16 4.2
27. Mr. karhikayini AL8757 51/F 122 210 12.5 7500 56 34 02 - 05 10 3.2
28. Mrs.Lurdu flora C996 60/F 97 128 13.2 8200 60 41 05 - 05 10 3.8
29. Mrs.Malathy A53167 42/F 125 240 13.6 7400 56 42 02 - 04 08 4.2
30 Mrs.Tamilselvi A70298 40/F 100 130 10.1 7200 58 34 03 01 08 16 4.1
31. Mrs.V.Sumathi 3178 53/F 113 154 11.7 7800 62 31 03 - 05 10 3.3
32. Mrs.Kasthuri 3039 56/F 101 126 13.3 8200 51 32 02 - 11 22 4.4
33. Mrs.Zeenath nisha 3137 56/F 92 126 12.6 1800 52 44 03 - 06 12 4.1
34. Mrs.Leelavathi 3097 58/F 112 151 13.1 8200 65 37 04 - 02 04 3.1
35. Mrs.J.Sumathi 3212 55/F 96 121 9.8 8100 54 31 02 - 09 18 3.2
36. Mrs.Anbu 3058 60/F 101 122 12.6 7400 52 41 03 - 11 22 3.6
37. Mrs.Abitha begam 2993 55/F 98 136 11.8 7800 61 36 02 - 04 08 3.2
38. Mrs.Marivartharajam 2966 60/F 124 226 10.2 8200 57 36 04 - 06 12 3.8
39. Mrs.Balkis 3136 59/F 92 124 13.2 9200 61 32 04 01 08 16 4.2
40. Mr.Rajasekar 4052 56/M 117 156 9.8 8200 53 30 04 - 06 12 3.5
Before treatment- Haematology
Lipid profile Liver Function Test RFT
Al Gl
S. OP/IP Age/ T.Ch HD LD VL TG T. D. T.P Cal U.
I.B AL b o P U Cr
No No Sex o L L DL L Bm Bm PT G Mg A
mg OT K G G Mg mg Mg
Mg/ Mg Mg/ Mg Mg/ g/d g/d u/l ms / Mg
/dl u/l u/l ms ms /dl /dl /dl
dl /dl dl /dl dl l l % dl /dl
% %
1. B34545 60/M 190 53 110 27 139 0.6 0.2 0.4 36 24 236 8.6 4.4 4.2 8.2 3.5 5.0 26 0.6
2. AJ3859 60/M 165 40 95 30 186 0.5 0.3 0.2 30 26 216 8.2 4.6 3.6 8.4 3.6 4.9 38 0.6
3. A16571 54/M 146 28 92 26 197 0.6 0.2 0.4 34 27 195 7.9 4.8 3.1 8.2 3.4 4.7 18 0.8
4. B64839 51/M 140 24 90 36 169 0.5 0.3 0.2 36 28 217 8.6 5.2 3.4 7.8 3.4 3.9 26 0.7
5. B55839 58/F 176 46 100 36 157 0.4 0.2 0.2 45 43 232 7.8 4.8 3.0 8.4 3.4 5.5 20 0.7
6. B99503 53/M 186 36 110 40 187 0.6 0.3 0.3 38 30 197 8.6 4.8 3.8 7.8 3.6 5.6 28 0.6
7. A32312 45/M 172 38 102 30 196 0.6 0.3 0.3 34 48 235 8.6 4.8 3.8 8.4 3.4 4.9 18 0.6
8. B69223 55/M 194 42 127 25 126 0.5 0.3 0.2 20 19 275 7.6 4.4 3.2 9.2 3.3 4.4 20 0.7
9. C15695 53/F 190 45 110 35 210 0.9 0.3 0.6 36 42 235 8.4 4.6 3.8 8.0 3.2 4.8 26 0.6
10. C87421 57/M 159 35 100 24 124 1.2 0.7 0.5 24 18 190 7.8 3.9 3.9 9.0 4.5 3.6 18 0.9
11. C17192 51/M 108 24 66 18 169 0.5 0.3 0.2 36 24 210 8.1 5.9 2.2 7.6 3.5 4.3 43 1.0
12.. C17699 57/M 195 45 115 35 217 0.6 0.2 0.4 37 19 189 8.2 3.8 4.2 8.4 3.4 5.2 16 0.6
13. C7113 58/M 238 48 172 18 193 0.6 0.3 0.3 36 38 235 8.7 4.4 4.0 9.2 3.8 5.8 24 0.8
14. C3971 59/M 207 49 135 28 141 0.8 0.4 0.4 30 25 216 7.8 4.6 3.2 8.3 4.0 3.8 21 0.7
15. B64662 54/M 181 42 118 21 201 0.5 0.3 0.2 38 32 221 8.4 4.8 3.6 7.9 3.4 5.6 19 0.7
16. B59392 60/M 162 36 92 34 190 0.5 0.2 0.3 24 20 217 8.2 4.2 4.0 7.8 3.4 4.9 23 0.5
17. A51265 59/M 192 46 110 36 211 0.7 0.4 0.3 43 34 235 7.6 4.3 3.3 8.2 3.7 5.2 21 0.7
18. AL 8756 49/M 207 43 138 36 219 0.5 0.2 0.3 46 40 241 8.6 5.2 3.4 8.8 3.4 4.9 23 0.8
19. B93607 55/M 152 38 96 28 191 0.6 0.4 0.2 36 30 215 7.8 4.2 3.6 8.6 3.9 4.1 20 0.7
20. B91080 38/M 215 45 117 63 187 0.8 0.5 0.3 36 28 247 8.6 4.6 4.0 9.2 3.8 5.4 30 0.6
Before treatment- Haematology

S. Age/ Lipid profile Liver Function Test RFT

No Sex T.Ch HDL LDL VL TG T. D I.B PT AL T. Al Glo Cal P U. U Cr
OP/IP o Mg/ Mg/ DL L Bm B mg OT u/l K P b Gm Mg/ Mg/ A mg M
No Mg/d dl dl Mg Mg/ g/d mg /dl u/l u/l G G s dl dl M /dl g/d
l /dl dl l /dl ms ms % g/d l
% % l
21. B93520 48/M 190 45 110 35 210 0.8 0.6 0.2 34 28 216 8.2 4.8 3.4 7.6 3.1 4.7 36 0.8
22. C2450 29/M 230 55 130 45 197 0.5 0.3 0.2 24 20 217 7.6 4.2 3.4 8.4 3.6 4.9 21 0.7
23. B57212 50/M 123 32 65 26 185 0.8 0.4 0.4 28 21 211 8.4 4.8 3.6 7.8 3.2 5.1 27 0.7
24. AH9325 40/M 230 55 116 59 295 0.6 0.3 0.3 26 19 270 7.4 4.3 3.1 9.2 3.6 4.5 26 0.6
25. C4742 42/M 150 40 90 20 210 0.9 0.5 0.4 34 26 230 8.0 4.6 3.4 8.5 4.1 5.2 24 1.0
26. A41984 43/F 209 38 109 36 120 0.8 0.4 0.4 28 30 252 7.8 5.0 2.8 8.2 3.2 5.4 34 0.8
27. AL8757 51/F 180 44 110 26 187 0.5 0.2 0.3 42 28 198 8.8 4.8 4.0 9.0 3.8 5.0 30 0.6
28. C996 60/F 210 56 124 30 166 0.9 0.5 0.4 23 33 234 8.0 4.2 3.8 8.6 3.5 5.9 40 1.0
29. A53167 42/F 145 40 85 20 189 0.7 0.4 0.3 28 32 201 8.2 4.6 3.6 8.2 4.2 5.0 26 0.6
30. A70298 40/F 195 55 115 35 234 0.6 0.3 0.3 38 22 231 7.9 4.1 3.8 8.3 3.0 4.9 18 0.7
31. 3178 53/F 183 50 104 29 147 0.6 0.3 0.3 48 33 389 5.5 3.6 1.9 8.3 3.9 4.5 19 0.6
32. 3039 56/F 269 56 145 58 223 0.6 0.4 0.2 41 51 268 8.2 4.0 4.2 8.8 3.1 5.1 16 0.7
33. 3137 56/F 171 45 95 31 187 0.5 0.3 0.2 33 42 213 8.9 4.8 4.1 7.6 3.8 5.8 21 0.9
34. 3097 58/F 213 37 139 37 189 0.6 0.3 0.3 24 28 317 6.9 4.2 2.7 8.7 3.1 5.5 19 0.7
35. 3212 55/F 190 35 138 77 186 0.8 0.4 0.4 24 28 216 5.4 3.8 1.6 8.6 4.5 3.9 24 0.8
36. 3058 60/F 150 42 80 28 132 0.8 0.5 0.3 20 29 198 6.9 4.3 3.6 8.9 3.0 5.2 35 0.8
37. 2993 55/F 228 39 158 31 155 0.7 0.3 0.4 30 16 310 7.6 4.5 3.1 8.9 4.0 4.8 37 0.9
38. 2966 60/F 156 36 90 30 152 0.6 0.3 0.3 23 16 288 6.2 2.3 3.9 9.2 4.0 5.2 20 0.7
39. 3136 59/F 206 50 121 35 173 0.5 0.2 0.3 24 17 231 8.1 4.0 4.1 9.8 3.1 3.2 26 0.8
40. 4052 56/M 152 34 52 57 271 0.5 0.3 0.2 16 18 212 7.6 4.3 3.3 8.9 3.2 3.1 22 0.7
After treatment - haematology

S. Age/ Lipid profile Liver Function Test RFT

No Sex T.Ch HD LD VL TG T. DB IB OT P AL T.P Al Glo Cal P U. U Cr
OP/IP o L L DL L Bm mg mg u/l T K G b Gm Mg/ Mg/ A mg M
No Mg/ Mg/ Mg/ Mg/ Mg/ g/d /dl /dl u/l u/l ms G s dl dl M /dl g/d
dl dl dl dl dl l % ms % g/d l
% l
1. B34545 60/M 183 46 110 27 167 0.8 0.6 0.2 36 22 240 8.4 4.2 4.2 8.0 3.2 5.1 26 0.6
2. AJ3859 60/M 160 45 90 35 192 0.5 0.2 0.3 34 24 215 8.6 4.6 3.8 8.6 3.4 5.0 30 0.9
3. A16571 54/M 150 32 90 28 187 0.6 0.3 0.3 28 26 210 8.0 4.8 3.2 8.2 3.2 5.1 20 0.6
4. B64839 51/M 150 30 92 38 175 0.5 0.3 0.2 34 30 215 8.4 5.0 3.4 8.0 3.6 4.2 26 0.8
5. B55839 58/F 180 44 102 34 160 0.4 0.2 0.2 46 30 240 8.0 4.2 3.8 8.7 3.9 4.5 18 0.7
6. B99503 53/M 170 26 116 38 190 0.8 0.4 0.4 38 32 195 8.4 4.8 3.6 8.4 3.6 5.8 30 0.6
7. A32312 45/M 179 38 104 37 210 0.6 0.3 0.3 36 44 217 8.3 4.3 4.0 8.2 3.5 5.2 18 0.8
8. B69223 55/M 180 40 112 38 135 0.6 0.3 0.3 26 22 260 8.2 4.8 3.4 9.0 3.4 4.2 26 0.6
9. C15695 53/F 193 46 112 35 205 0.8 0.4 0.4 32 36 210 8.4 4.6 3.8 8.2 3.4 5.0 20 0.6
10. C87421 57/M 180 45 110 35 139 1.0 0.5 0.5 26 20 215 8.2 4.2 4.0 9.2 4.2 4.0 22 0.7
11. C17192 51/M 108 24 66 18 169 0.5 0.3 0.2 36 24 210 8.1 5.9 2.2 7.6 3.5 4.3 40 0.9
12.. C17699 57/M 185 40 120 35 215 0.6 0.3 0.3 34 28 235 8.0 4.2 3.8 8.2 3.6 5.4 18 0.6
13. C7113 58/M 250 55 170 35 210 0.6 0.3 0.3 30 26 215 8.6 4.6 4.0 8.9 3.2 5.0 20 07
14. C3971 59/M 210 50 135 30 148 0.8 0.4 0.4 36 24 235 8.4 4.4 4.0 8.6 4.2 4.5 26 0.5
15. B64662 54/M 190 46 115 29 205 0.6 0.4 0.2 26 34 225 8.0 4.8 3.2 8.0 3.6 5.5 22 0.6
16. B59392 60/M 180 40 155 35 186 0.6 0.3 0.3 26 18 210 8.4 4.6 3.8 8.4 3.9 4.7 16 0.8
17. A51265 59/M 186 44 112 30 207 0.6 0.3 0.3 40 32 232 7.8 4.2 3.6 8.2 3.0 5.0 29 0.6
18. AL 8756 49/M 196 46 118 32 211 0.5 0.3 0.2 38 28 225 8.0 4.8 3.2 8.4 3.3 5.2 24 0.7
19. B93607 55/M 150 36 93 33 185 0.6 0.4 0.2 36 32 245 8.2 4.6 3.6 8.4 3.4 5.4 18 0.6
20. B91080 38/M 202 44 120 38 190 0.6 0.3 0.3 30 24 240 8.0 4.8 3.2 9.0 4.6 5.6 28 0.4
After treatment - haematology

S. OP/IP No Age/ Lipid profile Liver Function Test RFT

No Sex T.Cho HDL LD VL TG TB DB I.B OT PT AL T.P Al Glo Cal P U. U Cr
Mg/dl Mg/d L DL mg/ mg mg mg u/l u/l K G b Gms Mg/ Mg A m M
l Mg/ Mg dl / /dl /dl u/l ms G % dl /dl M g/ g/d
dl /dl dl % ms g/ dl l
% dl
21. B93520 48/M 185 40 115 35 205 0.8 0.6 0.2 32 34 210 8.0 3.8 4.2 7.5 3.2 4.9 34 0.6
22. C2450 29/M 218 58 126 34 180 0.5 0.3 0.2 26 24 225 8.2 4.2 4.0 8.0 3.6 5.2 26 0.6
23. B57212 50/M 140 36 74 30 192 0.6 0.4 0.2 28 21 215 8.4 4.2 4.2 7.6 3.4 5.4 30 0.5
24. AH9325 40/M 153 41 92 20 103 0.6 0.3 0.3 30 26 280 8.6 5.0 3.0 8.3 3.4 5.4 24 0.7
25. C4742 42/M 208 46 135 37 187 0.7 0.4 0.3 18 38 224 9.0 4.8 4.2 8.0 3.9 4.8 16 0.9
26. A41984 43/F 220 45 115 30 135 0.8 0.4 0.4 30 34 250 8.2 4.2 4.0 8.5 3.0 5.1 36 0.6
27. AL8757 51/F 145 34 93 18 194 0.9 0.5 0.4 24 46 312 7.8 4.6 3.2 9.2 4.2 5.8 18 0.8
28. C996 60/F 221 56 130 35 213 0.6 0.3 0.3 42 26 204 8.6 4.8 3.8 8.6 3.9 4.2 37 0.5
29. A53167 42/F 190 52 108 30 188 0.5 0.3 0.2 22 38 197 9.0 5.2 3.8 7.9 3.8 5.2 26 0.8
30. A70298 40/F 168 36 102 30 211 0.4 0.2 0.2 44 24 231 8.4 4.2 4.2 8.8 3.1 5.0 35 0.6
31. 3178 53/F 159 39 93 27 137 0.6 0.3 0.3 34 28 324 7.4 3.2 4.2 7.8 3.6 5.3 20 0.6
32. 3039 56/F 198 49 101 48 157 0.6 0.4 0.2 47 44 207 7.9 5.0 2.9 8.0 4.0 5.4 17 0.6
33. 3137 56/F 152 46 87 19 157 0.6 0.4 0.2 40 32 310 7.4 3.2 4.2 8.2 3.2 5.2 19 0.6
34. 3097 58/F 215 37 139 39 195 0.6 0.2 0.4 28 30 315 7.5 4.3 3.2 8.5 3.1 4.8 19 0.7
35. 3212 55/F 166 36 100 30 149 0.5 0.2 0.3 26 25 213 6.5 4.0 2.5 8.5 3.9 3.3 25 0.6
36. 3058 60/F 156 33 95 28 139 0.5 0.3 0.2 26 22 201 7.8 4.6 2.2 6.8 4.0 8.2 31 0.8
37. 2993 55/F 151 37 75 39 194 0.5 0.3 0.2 27 20 308 8.0 4.9 3.1 8.8 3.1 2.9 16 0.6
38. 2966 60/F 153 39 82 32 162 0.6 0.3 0.3 22 18 284 7.9 4.6 3.3 8.6 3.9 5.7 25 0.8
39. 3136 59/F 265 52 157 56 281 0.6 0.3 0.3 19 10 165 7.4 4.3 3.1 8.8 3.2 4.9 28 0.8
40. 4052 56/M 166 40 65 55 277 0.6 0.3 0.3 26 22 222 7.4 4.6 3.4 9.0 4.6 3.6 18 0.7
Before treatment – Urine analysis

S.NO OP/IP No Age/ Alb Sugar Deposit Neerkkuri Neikkuri Bs Bp Uro.bil Ova Cyst Occult
Sex blood
F PP
1. B34545 60/M Nil ++ +++ 1-2Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
2. AJ3859 60/M Nil +++ +++ 1-2Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
3. A16571 54/M Nil + ++ 2-3Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
4. B64839 51/M Nil +++ ++ 2-4Pc,2-6Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
5. B55839 58/F Nil ++ + 2-4Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
6. B99503 53/M Nil ++ ++ 1-2Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
7. A32312 45/M Nil ++ ++ 1-2Pc,1-3Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
8. B69223 55/M Nil ++ +++ 2-5Pc,1-6Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
9. C15695 53/F Nil + ++ 2-4Pc,2-6Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
10. C87421 57/M Nil +++ ++ 3-4Pc,2-3Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
11. C17192 51/M Nil +++ ++ 2-4Pc,2-4Ec Pale Yellow Fastly spread Nil -Ve Normal Nil Nil Nil
12.. C17699 57/M Nil + ++ 4-5Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
13. C7113 58/M Nil +++ +++ 1-3Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
14. C3971 59/M Nil ++ ++ 3-5Pc,2-3Ec Pale Yellow Fastly spread Nil -Ve Normal Nil Nil Nil
15. B64662 54/M Nil ++ +++ 4-6Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
16. B59392 60/M Nil +++ +++ 3-5Pc,1-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
17. A51265 59/M Nil ++ ++ 2-3Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
18. AL 8756 49/M Nil +++ +++ 2-3Pc,1-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
19. B93607 55/M Nil ++ ++ 1-2Pc,2-3Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
20. B91080 38/M Nil + ++ 4-5Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
Before treatment – Urine analysis

S.NO OP/IP No Age/ Alb Sugar Deposit Neerkuri Bs Bp Uro.bil Ova Cyst Occult
Sex Neikkuri blood
F PP
21. B93520 48/M Nil ++ ++ 1-4Pc,2-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
22. C2450 29/M Nil ++ +++ 2-3Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
23. B57212 50/M Nil +++ +++ 4-6Pc,2-4Ec Pale Yellow Fastly spread Nil -Ve Normal Nil Nil Nil
24. AH9325 40/M Nil ++ ++ 2-4Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
25. C4742 42/M Nil ++ ++ 1-5Pc,2-3Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
26. A41984 43/F Nil +++ +++ 1-2Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
27. AL8757 51/F Nil +++ ++ 3-5Pc,2-3Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
28. C996 60/F Nil +++ ++ 1-4Pc,4-6Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
29. A53167 42/F Nil ++ +++ 2-4Pc,3-5Ec Pale Yellow Fastly spread Nil -Ve Normal Nil Nil Nil
30. A70298 40/F Nil ++ +++ 1-2Pc,2-8Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
31. 3178 53/F Nil ++ ++ 2-3Pc,1-4Ec Pale Yellow Fastly spread Nil -Ve Normal Nil Nil Nil
32. 3039 56/F Nil +++ ++ 3-4Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
33. 3137 56/F Nil ++ ++ 5-6Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
34. 3097 58/F Nil ++ +++ 2-4Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
35. 3212 55/F Nil ++ ++ 2-5Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
36. 3058 60/F Nil +++ ++ 4-5Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
37. 2993 55/F Nil + ++ 1-2Pc,2-6Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
38. 2966 60/F Nil +++ +++ 2-3Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
39. 3136 59/F Nil +++ ++ 2-4Pc,8-9Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
40. 4052 56/M Nil +++ +++ 1-2Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
Afetr treatment – Urine analysis

S.NO OP/IP No Age/ Alb Sugar Deposit Neerkuri Bs Bp Uro.bil Ova Cyst Occult
Sex Neikkuri blood
F PP
1. B34545 60/M Nil Nil Nil 1-2Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
2. AJ3859 60/M Nil + + 1-2Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
3. A16571 54/M Nil Nil Nil 2-3Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
4. B64839 51/M Nil ++ +++ 1-2Pc,2-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
5. B55839 58/F Nil Nil Nil 2-5Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
6. B99503 53/M Nil Nil Nil 1-3Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
7. A32312 45/M Nil Nil Nil 3-4Pc,1-3Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
8. B69223 55/M Nil Nil Nil 1-2Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
9. C15695 53/F Nil Nil Nil 3-4Pc,2-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
10. C87421 57/M Nil ++ ++ 2-5Pc,2-3Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
11. C17192 51/M Nil Nil Nil 1-2Pc,2-5Ec Pale Yellow Fastly spread Nil -Ve Normal Nil Nil Nil
12.. C17699 57/M Nil Nil Nil 2-4Pc,2-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
13. C7113 58/M Nil + ++ 1-3Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
14. C3971 59/M Nil Nil Nil 1-2Pc,2-4Ec Pale Yellow Fastly spread Nil -Ve Normal Nil Nil Nil
15. B64662 54/M Nil Nil Nil 6-8Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
16. B59392 60/M Nil +++ +++ 4-5Pc,1-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
17. A51265 59/M Nil Nil Nil 4-5Pc,2-6Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
18. AL 8756 49/M Nil ++ +++ 1-4Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
19. B93607 55/M Nil Nil Nil 1-2Pc,2-3Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
20. B91080 38/M Nil + + 4-5Pc,1-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
Afetr treatment – Urine analysis

S.NO OP/IP No Age/ Alb Sugar Deposit Neerkuri Bs Bp Uro.bil Ova Cyst Occult
Sex Neikkuri blood
F PP
21. B93520 48/M Nil + ++ 1-4Pc,2-3Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
22. C2450 29/M Nil Nil Nil 2-4Pc,1-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
23. B57212 50/M Nil + ++ 3-5Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
24. AH9325 40/M Nil Nil Nil 2-4Pc,4-6Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
25. C4742 42/M Nil Nil Nil 4-6Pc,4-8Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
26. A41984 43/F Nil Nil Nil 2-8Pc,4-6Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
27. AL8757 51/F Nil ++ ++ 1-2Pc,2-3Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
28. C996 60/F Nil Nil Nil 1-4Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
29. A53167 42/F Nil + +++ 2-5Pc,2-3Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
30. A70298 40/F Nil Nil Nil 1-2Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
31. 3178 53/F Nil ++ ++ 1-4Pc,4-5Ec Pale Yellow Fastly spread Nil -Ve Normal Nil Nil Nil
32. 3039 56/F Nil Nil Nil 2-4Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
33. 3137 56/F Nil Nil Nil 5-6Pc,6-9Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
34. 3097 58/F Nil + ++ 3-5Pc,1-2Ec Pale Yellow Fastly spread Nil -Ve Normal Nil Nil Nil
35. 3212 55/F Nil Nil Nil 2-5Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
36. 3058 60/F Nil Nil Nil 2-4Pc,4-5Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
37. 2993 55/F Nil Nil Nil 1-4Pc,2-6Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
38. 2966 60/F Nil ++ +++ 2-5Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
39. 3136 59/F Nil Nil Nil 1-2Pc,1-2Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
40. 4052 56/M Nil ++ ++ 2-4Pc,2-4Ec Pale Yellow Slowly spread Nil -Ve Normal Nil Nil Nil
 DISCUSSION

Madhumegam is one of a common metabolic disorder characterized by excessive

urine excretion and hyperglycemia. The signs and symptoms of Madhumegam are well
distinct in Yugi Vaidya Chinthamani. If ignored to treat Madhumegam produces various
complications.so the investigator had chosen the disease Madhumegam to find a solution
and prevent the complications of Madhumegam through siddha system of medicine.
"Madhumegam" which is mentioned in Siddha literatures is almost correlated with type 2
Diabetes mellitus (Non -insulin dependent diabetes mellitus NIDDM) as in modern
science.

The present study is a preliminary case study of which 40 cases were selected
according to the clinical features mentioned in Yugi Vaidhya Chinthamani. Siddha
method of diagnosis was carried out for all the patients and also modern investigations
were done as per the protocol.

Institutional animal ethical committee( IAEC) as well as institutional ethical

committee of NIS was obtained for this study.

The drug thetran vithai kuidineer posses anti – diabetic property as per Siddha
literature ( Gunapada – muthal pagam mooligai vaguppu ) 7 th edition 2003)

As per Standard operative procedure the drug was prepared at NIS,

Medicine Name : THETRAN VITHAI KUDINEER

Dose : 30 ml every four hours before food / day

Adjuvant : cow‟s butter milk

Duration : 48 Days

 Haematological and Urine examination were done for the patients at NIS
laboratory before the treatment and as well as after the treatment.

 The drug was subjected to quantitative and qualitative Biochemical analysis in

NIS and IIT Chennai.

 The following minerals were found in this drug by analysis

  Sulphate,phosphate, aluminium, iron,magnesium, calcium, ammonium, starch,
tannic acid, silicate, sodium, carbonate,

 This drug was subjected to safety studies in animal models. acute and chronic
study was done by under the WHO guidliness.

 It was found that the drug was safe in toxicity studies and harmless to the testing
animals.

 Histopathological studies was done in madras medical college lab, it shows that
there is no abnormalities in the studies.

Incidence with reference to age disribution:

Most of the cases were between the age group of (51-60) i.e. 75%.age of 41-50
were 15% and 30-40 age group were 10%.

Incidence with reference to sex distribution:

40 Patient of both sexes were selected for the study. Among these 23 cases were
Male and 17 cases were Female. Madhumegam can affect both sexes.

Incidence with reference to yakkai:

Most of the patients affected in madhumegam were vatha udalina22 cases (55% )
and pitha udalinar9 cases( 22.5%) and kapha udalinar9 cases( 22.5%.)

Incidence with reference to kosam

50% of the cases(20) were affected in annamayakosam, anandha maya kosam

were affected 25% of cases,(10), 10% of cases (4) were affected manomayakosam,12.5%
cases(5) were affected in vignanamayakosam.

Incidence with reference to family history:

Out of 40 Patients 15 cases had positive family history of type 2 diabetes. From
the above study hereditary plays an important role in this disease .

Neerkuri,neikuri:

Most of the cases had vaatha neer ie. 22 cases ( 55 % ),9 cases ( 22.5 % ) had
pitha neer, 9 cases ( 22.5 % ) had kaba neer.
Incidence with reference to food habits:

Only 32.5% were vegetarians and the rest were found to be taking mixed diet, i.e
67.5% of cases. It clear shows that mixed diet is more prone to Madhumegam.

Personal habits:
Out of 40 cases 17.5% of patients were smokers30% patients were alcoholic.

Incidence with reference to socio- economic status:

Among 40 patients 27.5% of cases poor socio- economic status 57.5% of cases
were from middle class family and 15% of cases were from Rich. Affected cases were
mostly from middle class.

Incidence with reference to vatham:

Viyaanan (pain present in the both upper and lower limbs,burning sensation
present in the both soles) was affected in 42.5% cases(17). Udhanan
(tiredness,drowsiness) was affected 37.5% (15 cases) and abaanan (poly
uria,constipation,nocturia,sexual disturbance) was affected in 55%cases(22). Samaanan
(indigestion,) was affected 55%(22cases) and kirukaran (polyphagia)was affected in 30%
cases(12) and nagan (burning sensation present in both eyes) was affected 20%(8) and
koorman was affected in 17.5% ( 7)cases.Finally deva thaththan (tiredness,anxity) was
affected in 12.5% cases(5 cases).

Incidence with reference to pitham:

Saathaga pittham was affected in 87.5% cases. Anal pittham was affected in
37.5% of cases. Ranjaga pitham was affected 27.5%,pirasaga pittham was affected in
17.5% cases.Aalosaga pitham was affected 10%.

Incidence with reference to kabham:

Kapham was not affected as much as vaatham and piththam. Avalambagam was
affected in 25%, kilethagam was affected in 30% Santhigam was affected in
50%cases.many cases affected in santhigam.
Incidence with reference to ezhu udal thathukkal:

In Udal Thathukkal Saarm was affected in all cases. Chenneer was affected in
37.5% of cases Kozhuppu was affected in 17.5% of cases. Enbu was affected in 50% of
cases.sukilam was affected 17.5% of cases.

Incidence with reference to envagai thervugal:

In enn vagai thervugal moothiram slowly spread in 90% (36)cases.fastly spread in

10% (4) cases vizhi affected (burning sensation of both eyes,cataract,diminished vision)
in 10% (4) of cases and naa was affected in 17.5%(7) of cases. Naadi was vaatha
piththam in 25%(10) cases, piththa vaatham in 17.5% (7)cases and piththa kapham in
15% (6)cases and kapha vatham in 27.5%(11) cases, kapha pitham was noted in 15% (6)
cases.

Incidence with reference to clinical menifestation:

62.5 % (25 cases) patients complained of polyuria and 25%(10 cases)

complained of Polydypsia.30%(12 cases) complained of polyphagia,25%(10 cases)
complained nocturia, 80%(32 cases) complained tirdness,50%(20 cases) complained
pain in limbs.45%(18 cases) complained pain and burning sensation in the both sole,and
7.5% (3 cases) complained pruritis vulvae, 10% (4 cases) complained Balanitis.

chronicity of illness.

12.5% (5)patients had the history of this disease up to 0-1 yrs only. 30% (12)of
patients suffered for1-3 yrs and 35 % (14)patients for3-5 yrs.and 15%(6) patients for 5-10
yrs,and 7.5%(3) patients suffered for 10-20 yrs.

Gradation of results:

Diagram shows that 60% (24) of cases had Good clinical improvement, 25% (10)
of cases had Moderate and 15% (6) of cases had Poor improvement.
Blood sugar levels:

Good result range: Fasting 70-110mgs%, P#ost prandial-120-140mgs%. (24 cases ie,
60%)

Moderate result range: Fasting 110-120mgs%,Post prandial-140-170mgs% (10 cases ie,

25%)

Poor result range: Fasting above 120mgs%,Post prandial-above 180mgs%. 6 cases.ie,

15%

Urine sugar levels:

Good result range: Urine sugar nil 24 cases ie, 60%

Moderate result range: Urine sugar level + to ++ 10 cases ie,25%

Poor result range: Urine sugar level above ++ 6 cases ie,15%

 SUMMARY

 This study has been approved by IAEC and IEC of NIS

 60 cases were screened by using screening form.

 40 cases of madhumegam were diagnosed clinically 10 cases were treated as

IPD,and 30 cases were treated as OPD in branch I..National Institute of Siddha.

 Treatment and prevention were carried out at the OPD and IPD of Ayothidoos
Pandithar Hospital of National Institute of Siddha, Chennai-47.

 All the patients were treated with Thetran Vidhai Kudineer before Meals in 48
days.

 This study shows that 60% (24) of cases had good clinical improvement, 25%
(10) of cases had moderate and 15% (6) of cases had poor improvement.

 Haematological and Urine examination were done before and after treatment.

 The Biochemical analysis of the trial drug was done in the National Institute Of
Siddha and IIT Chennai.

 Histopathological studies was done in Madras Medical College lab, it shows that
there is no abnormalities in the studies.

 Toxicological study of the trial drugs carried out no toxic effect were reported.

 The clinical and labarotary Obserevation in the mathumegam patient treated with
trial drug thetran vidhai kudineer showed significant control in their blood
glucose level and upgrading with in general health.
 CONCLUSION

 To bring to a close Siddha way of approach is certainly the best treatment of

Madhumegam in all aspects as trial drug Thetran vidhai kudineer could keep
away from diabetic complications.

 It is undoubtedly marked that the medicine used in the siddha system do not have
any harmful side effects.

 The trial drug illustrated no toxic effects in animal models.toxic dose Acute study-
72 mg,chronic study-3600 mg.

 With the evidence of statistical report, It shows the average blood sugar at the start
of treatment and after the treatment were 245 and 148 respectively.

 There is a significant difference between before and after treatment in the level of
blood sugar at Fasting and Postprandial [ P < 0.0001 ].

 Clinical study revealed that the trial drug posses good clinical improvement in 60
% of cases.25 % of cases had moderate results and 15% of cases had poor results.

 Because of the hopeful results clinically , the study may be undertaken with the
same drug for a prolonged period of time in more number of cases and it may
throw new lights in the managemet of Madhumegam.
 ANNEXURE-I-PROFORMA
NATIONAL INSTITUTE OF SIDDHA
CHENNAI -47
DEPARTMENT OF MARUTHUVAM
A CLINICAL TRIAL TO ASSESS THE THERAPEUTIC EFFICACY OF THETRAN VITHAI
KUDINEER (Internal) IN TREATMENT OF MATHUMEGAM ( DIABETES MELLITUS )

FORM l A - HISTORY PROFORMA ON ENROLLMENT

REG NO: 32091208/2011-12

1. Serial No of the case: _______________ 2. OP/IP No:----------

3. Name: ________________ 4. Gender: Female/male

5. Age (years): _________ DOB

Date Month Year

6.Address: --------------------------------------
-------------------------------------
--------------------------------------

7.A.Occupation: ----------------------------- B. Nature of work-----------------

8. Educational Status: A) Illiterate B)Literate

9.Height: cms 10.Weight: kg

11. Complaints and Duration:

________________________________________________________________________

________________________________________________________________________

________________________________________________________________________

________________________________________________________________________

12. Habit of
A) Smoking 1. Yes; duration ________ years; Number- 2.No
B) Alcoholism 1. Yes; duration ________ years; Quantity- ml 2.No
C) Tobacco chewing 1. Yes; duration ________ years 2.No
D) Betel chewing 1. Yes; duration ________ years 2.No

13.Dietry style: A.Pure vegetarian B.Non-vegetarian C. Mixed diet

14. Drug History: Had the patient been treated before with allopathy drug? A) Yes 2) No
15 MARITAL STATUS 1.Married 2.Unmarried

16. FAMILY HISTORY

Whether this problem runs in family? 1. Yes 2.No

If yes, mention the relationship of affected person(s) - -------------------------

-------------------------

17. MENSTRUAL HISTORY:

18. BOWEL HABITS & MICTURITION: Normal

History of habitual constipation 1.Yes 2.No

History of frequent diarrhoea 1.Yes 2.No

History of frequent dysuria 1.Yes 2.No

19. PSYCHOLOGICAL STATE

Normal Anxiety Depression

Date:
Station:

Signature of the Investigator:

Signature of the Lecturer: Signature of the HOD

3
 NATIONAL INSTITUTE OF SIDDHA
AYOTHIDASAR PANDITHAR HOSPITAL
CHENNAI -47
DEPARTMENT OF MARUTHUVAM

FORM II AND II-A CLINICAL ASSESSMENT ON ENROLLMENT AND ON VISITS

1. S NO ----------- 2. OP/IP NO ------------ REG NO: 32091208/2011-12

3. NAME-------------------------------------- 4.GENDER -------------

5. DATE OF ASSESSMENT : ----------------------

Initial (0th day) 12th day 24th day 36th day 48th day

SIDDHA SYSTEM OF EXAMINATION

1. Envagai Thervu: [Eight-Fold Examination]

I. Naadi: [Pulse Perception]

0th 12th 24th 36th 48th 0th 12th 24th 36th 48th
day day day day day day day day day day
Vali Iyya vali

Azhal Vali
Iyyam
Iyyam Azhal
Iyyam
Vali Iyya
Azhal Azhal
Azhal vali
II. NAA:[TONGUE]

0th Day 12th Day 24th Day 36th Day 48th Day
Colour Dark / Yellow Dark/Yellow/ Dark/Yellow/ Dark/Yellow/ Dark/Yellow
Red / Pale Red/Pale Red/Pale Red/Pale Red/Pale
Taste Sweet/Bitter/ Sweet/Bitter/ Sweet/Bitter/ Sweet/Bitter/ Sweet/Bitter/
Sour/Pungent/ Sour/Pungent/ Sour/Pungent/ Sour/Pungent/ Sour/Pungent/
None None None None None
coting Present Present/ Present/ Present/ Present/
/Absent Absent Absent Absent Absent
Fissure Present/ Present/ Present/ Present/ Present/
Absent Absent Absent Absent Absent
Saliva Normal/ Normal/ Normal/ Normal/ Normal/
Increased/ Increased Increased/ Increased/ Increased/
Decreased Decreased Decreased Decreased Decreased
Dryness Present Present Present/ Present/ Present/
/Absent /Absent Absent Absent Absent
Glossitis Present/ Present/ Present/ Present/ Present/
Absent Absent Absent Absent Absent
Baldness Present/ Present/ Present/ Present/ Present/
Absent Absent Absent Absent Absent

III.NIRAM: [COMPLEXION]

0th Day 12th day 24th Day 36th Day 48nd Day
Dark/Yellow Dark/Yellow Dark/Yellow Dark/ Yellow Dark/ Yellow
tinted/ Pale tinted / Pale tinted / Pale tinted / Pale tinted/ Pale

IV.MOZHI: [VOICE]

0th Day 12th day 24th Day 36th Day 48nd Day
Medium/High Medium/High/ Medium/High/ Medium/High/ Medium/High/
Low pitched Low pitched Low pitched Low pitched Low pitched
V.VIZHI: [EYES] (Lower palpabrel conjunctiva)

0th Day 12th day 24th Day 36th Day 48nd Day
Dark/Yellow Dark/Yellow Dark/Yellow Dark/Yellow Dark/Yellow
Red/ Pale Red/ Pale Red/ Pale Red/ Pale Red/ Pale

VI. MALAM; [BOWEL HABITS / STOOLS]

0th Day 12th Day 24 th Day 36nd Day 48th day

Dark/ Yellow/ Dark/ Yellow/ Dark/ Yellow/ Dark/ Yellow/ Dark/ Yellow/
Colour
Red/Pale Red/Pale Red/Pale Red/Pale Red/Pale
Solid/Semi Solid/Semi Solid/Semi Solid/Semi Solid/Semi
Consistency
Solid/Watery Solid/Watery Solid/Watery Solid/Watery Solid/Watery

Normal/ Normal/ Normal/ Normal/ Normal/

Stool bulk
Reduced Reduced Reduced Reduced Reduced

Present/ Present/ Present/ Present/ Present/

Constipation
Absent Absent Absent Absent Absent

Present/ Present/ Present/ Present/ Present/

Diarrhoea
Absent Absent Absent Absent Absent

VII. URINE EXAMINATION:

NEER 0th Day 12th Day 24 th Day 36nd Day 48th day
KURI
Niram White/Yellowi White/Yellowi White/Yellowi White/Yellowis White/Yellowis
Colour) sh/ sh/ sh/Straw h/Straw h/Straw
Strawcoloured Strawcoloured coloured/ coloured/ coloured/
/Crystal clear Crystal clear Crystal clear Crystal clear Crystal clear
Manam Present Present Present Present Present
[Odour] Absent Absent Absent Absent Absent
Nurai Nil/Reduced/ Nil/Reduced/ Nil/Reduced/ Nil/Reduced/ Nil/Reduced/
[Froth] Increased Increased Increased Increased Increased
Edai Normal Normal Normal Normal Normal
[Sp.gra] Increased/ Increased/ Increased/ Increased/ Increased/
Reduced Reduced Reduced Reduced Reduced
Enjal Present/ Present/ Present/ Present/ Absent Present/ Absent
Deposit Absent Absent Absent
Volume Normal Normal Normal Normal Normal
Increased/Red Increased/Red Increased/Red Increased/Redu Increased/Redu
uced uced uced ced ced

V11.NEIKURI

0th day 12th day 24th day 36th day 48th day
Serpentine fashion
Annular/Ringed
fashion
Pearl beaded fashion
Mixed fashion
Other fashion

VIII. SPARISAM: [PALPATORY PERCEPTION]

0th Day 12th Day 24th Day 36th Day 48nd Day
Warmth/Cold Warmth/ Cold Warmth/ Cold Warmth/ Cold Warmth/ Cold
Sweat Sweat Sweat Sweat Sweat
5. THEGI: [ TYPE OF BODY CONSTITUTION]

Vatham predominant Kabam predominant

Pitham predominant Thondha udal

6.NILAM: [ LAND WHERE PATIENT LIVED MOST]

Kurinji Mullai Marutham Neithal Palai

(Hilly terrain) (Forest range) (Plains) (Coastal belt) (Arid regions)

7. KAALAM

Kaarkalam- Pinpanikalam

Koothirkalam- Ilavenil

Munpanikalam - Muthuvenil
8. GUNAM

Sathuvam Rasatham Thamasam

9. IMPORIGAL (SENSORY ORGANS)

0th day 12th day 24th day 36th day 48th day
Mei
(Skin)
Vai
(Buccal Cavity)
Kann
(Eye)
Sevi
(Ear)
Mooku
(Nose)

10. KANMENDRIYAM ( MOTOR ORGANS)

0th day 12th day 24th day 36th day 48th day
Kai (upper limb)

Kaal (lower limbs

Vai (buccal cavity)

Eruvai (excretory
organs)
Karuvai
(reproductive
organs)

11. KOSANGAL(Sheath)

0th day 12th day 24th day 36th day 48th day
Annamaya kosam

Pranamaya kosam

Manomaya kosam

Vignanamaya kosam
Ananthamaya
kosam
12. MUKKUTRAM:[AFFECTION OF THREE HUMORS]

A)VATHAM:

0th day 12th day 24th day 36th day 48th day

Praanan
Abaanan
Samaanan
Udhaanan
Viyaanan
Naagan
Koorman
Kirukaran
Devathathan
Dhananjeyan

B) PITHAM:

0th day 12th day 24th day 36th day 48th day
Analapitham
Prasakam
Ranjakam
Aalosakam
Saathakam

C) KABAM:

0th day 12th day 24th day 36th day 48th day
Avalambagam
Kilethagam
Pothagam
Tharpagam
Santhigam

13. SEVEN DHATHUS: (7 SOMATIC COMPONENTS)

0th day 12th day 24th day 36th day 48th day

Saaram[Chyme]

Senneer[Blood]
Oon[Muscle]

Kozhuppu[Fat]

Enbu[Bones]

Moolai
[Bonemarrow]
Sukkilam/Suroni
tham[Genital
discharges]

14. SYSTEMIC EXAMINATION:

0th day 12th day 24th day 36th day 48th day
Locomotor system
Cardio Vascular System

Respiratory system
Gastro Intestinal system
Central Nervous System
Urogenital system

Endocrine System

15. GENERAL EXAMINATION:

0th day 12th day 24th day 36th day 48th day
Height (cms)
Weight (kg)
Temperature(°F)
Pulse rate (pe rmin)
Heart rate (per min)
Respiratoryrate(permin)
Blood pressure(mm/Hg)
Pallor
Jaundice
Cyanosis
Lymphadenopathy
Pedal edema
Clubbing
Jugular vein pulsation
 16. CLINICAL SYMPTOMS

S.no Clinical symptoms 0 th day 12th day 24th day 36th day 48th day
1. poly urea
2. Polydypsia
3. Polyphagia
4. Nocturia
5. Tiredness
6. Pain in the limbs
7. Pain &burning sensation
in the both sole
8. Parasthesia in the feet
9. Pruritis vulvae
10. Balanitis
11 Asymptomatic

Date :

Station:

Signature of the Investigator:

Signature of the Lecturer: Signature of the HOD

 NATIONAL INSTITUTE OF SIDDHA
AYOTHIDASAR PANDITHAR HOSPITAL
CHENNAI -47
DEPARTMENT OF MARUTHUVAM
FORM III-LABORATORY PARAMETERS-CHART

1. OP/IP No: ________ 2.S. No: 3.Reg no: 32091208/2010-11

4. Name: ________________ 5. Age: _______ years 6. Gender: M/F

Before
Blood investigation Normal values tmt 24thday After tmt

M:13-18
HB( gms%)
W:11-16
M:4.5-6.5
T.RBC(milli/cu.mm) W:3.5-5.5
½ hr. -
ESR (mm) M:0-10
1 hr.
W:0-20
T.WBC (/cu.mm) 4000-11000
Polymorphs 40-75
Lymphocutes 20-35
DIFFERENTIAL
Monocytes 2-10
COUNT (%)
Esonophils 1-6
Basophiles 0-1

Normal Before TMT(with After TMT

Blood Investigation 24th day
Values Date) (With Date)
1,50000-
Platelets ;(lak/ cubic mm)
500000
Fasting 80-120
Blood glucose
(mg/dl) PP <130
Random <140
Serum
150-250
cholesterol
Lipid profile HDL 30-60
(mg/dl) LDL Upto 130
VLDL 40
TGL Upto 160
Blood urea 16-50
Serum
0.6-1.2
RFT (mg/dl) creatinine
M:3-9
Serum
W: 2.5-
Uric acid
7.5
 Total
0.3-1
bilirubin
Direct
0.1-0.3
bilirubin
Indirect
0.2-0.8
bilirubin
Serum
total 6-8
protein
Serum
3.5-5.5
Albumin
Serum
2-3.5
globulin
Fibrinoge
LFT (mg/dl) 0.2-0.4
n(g/dl)
Serum
9-11
calcium
Serum
phosphoro 2-5
us
SGOT
6-18
(IU/L)
SGPT
3-26
(IU/l)
Alkaline
phosphata
3-12
se (kingÅ
units)
Before TMT(with After TMT (With
Urine investigation 24THDAY
Date) Date)

Neer kuri

Niram

Manam

Nurai

Edai

Enjal

Nei kuri

Albumin

Fasting sugar

PP sugar

Random Sugar
Deposits

Bile salts

Bile pigments

Urobilinogen

Motion test

Ova

Cyst

Occult blood

Specific Before TMT 24THDAY After TMT

investigation Date: Date: Date:
HbA1c

Date :

Station:

Signature of the Investigator:

Signature of the Lecturer: Signature of the HOD

 NATIONAL INSTITUTE OF SIDDHA
AYOTHIDASAR PANDITHAR HOSPITAL
CHENNAI -47
DEPARTMENT OF MARUTHUVAM

A Clinical Trial To Assess The Therapeutic Efficacy Of Thetran Vithai

Kudineer (Internal) In Treatment Of Mathumegam ( Diabetes Mellitus )

FORM IV-B ----WITHDRAWAL FORM

S. NO: -------------------- OPD/ IPD NO: -------- REG NO: 32091208/2011-12

NAME: ------------------ AGE: -------- GENDER: M/F

Date of trial commencement: -----------------------

Date of withdrawal from trial: -------------------

Reasons for withdrawal:

Long absence at reporting : Yes/ No

Irregular treatment: Yes/ No

Shift of locality : Yes/No

Increase in severity of symptoms: Yes/No

Development of severe adverse drug reactions: Yes/No

Date :

Station:

Signature of the Investigator:

Signature of the Lecturer: Signature of the HOD

 NATIONAL INSTITUTE OF SIDDHA
AYOTHIDASAR PANDITHAR HOSPITAL
CHENNAI -47
DEPARTMENT OF MARUTHUVAM
A Clinical Trial To Assess The Therapeutic Efficacy Of Thetran Vithai Kudineer
(Internal) In Treatment Of Mathumegam ( DiabetesMellitus)
FORM IV –C (DRUG COMPLIANCE FORM)
S. NO: OPD/IPD NO : NAME :
REG NO: 32091208/2011-12
Name Of The Drug : THETRAN VIDHAI KUDINEER (Internal)
Drugs issued: (Nos) Drugs issued: (Nos)
Drugs returned: (Nos) Drugs returned: (Nos)
DRUG TAKEN TIME
S.NO DATE
MORNING/TIME EVENING/TIME
Day 1
Day 2
Day 3
Day 4
Day 5
Day 6
Day 7
Day 8
Day 9
Day 10
Day 11
Day 12

Date :
Station:
Signature of the Investigator:

Signature of the Lecturer: Signature of the HOD

 NATIONAL INSTITUTE OF SIDDHA
AYOTHIDASAR PANDITHAR HOSPITAL
CHENNAI -47
DEPARTMENT OF MARUTHUVAM
FORM IV –C (DRUG COMPLIANCE FORM)
S. NO: OPD/IPD NO : NAME :
REG NO: 32091208/2011-12
Name Of The Drug : THETRAN VIDHAI KUDINEER (INT)
Drugs issued: (Nos) Drugs issued: (Nos)
Drugs returned: (Nos) Drugs returned: (Nos)
DATE DRUG TAKEN TIME
DAYS
MORNING/TIME EVENING/TIME
Day 13
Day 14
Day 15
Day 16
Day 17
Day 18
Day 19
Day 20
Day 21
Day 22
Day 23
Day 24

Date :
Station:
Signature of the Investigator:
Signature of the Lecturer: Signature of the HOD
 NATIONAL INSTITUTE OF SIDDHA
AYOTHIDASAR PANDITHAR HOSPITAL
CHENNAI -47
DEPARTMENT OF MARUTHUVAM
FORM IV –C (DRUG COMPLIANCE FORM)
S. NO: OPD/IPD NO : NAME :
REG NO: 32091208/2011-12
Name Of The Drug : THETRAN VIDHAI KUINEER (INT)
Drugs issued: (Nos) Drugs issued: (Nos)
Drugs returned: (Nos) Drugs returned: (Nos)

DRUG TAKEN TIME

S.NO DATE
MORNING/TIME EVENING/TIME
Day 25
Day 26
Day 27
Day 28
Day 29
Day 30
Day 31
Day 32
Day 33
Day 34
Day 35
Day 36

Date :
Station:
Signature of the Investigator:

Signature of the Lecturer: Signature of the HOD

 NATIONAL INSTITUTE OF SIDDHA
AYOTHIDASAR PANDITHAR HOSPITAL
CHENNAI -47
DEPARTMENT OF MARUTHUVAM
FORM IV –C (DRUG COMPLIANCE FORM)
S. NO: OPD/IPD NO : NAME :
REG NO: 32091208/2011-12
Name Of The Drug : THETRAN VIDHAI KUINEER (INT)
Drugs issued: (Nos) Drugs issued: (Nos)
Drugs returned: (Nos) Drugs returned: (Nos)
DRUG TAKEN TIME
DAYS DATE
MORNING/TIME EVENING/TIME
Day 37
Day 38
Day 39
Day 40
Day 41
Day 42
Day 43
Day 44
Day 45
Day 46
Day 47
Day 48

Date :
Station:
Signature of the Investigator:

Signature of the Lecturer: Signature of the HOD

 , - 47

( )

: ______________________

, - 47

___________________________________
.

, , , ,
..

,
.

30 4
48 , 12
.

_________________ (
) . ____________

IEC

..
, .
.
 NATIONAL INSTITUTE OF SIDDHA
AYOTHIDASAR PANDITHAR HOSPITAL
CHENNAI -47
DEPARTMENT OF MARUTHUVAM
FORM IV –D (INFORMATION SHEET)

Name of Principal Investigator:…………………………………..…………………………..

I, ________________________Studying as PG Scholar at National Institute of

Siddha,Tambaram Sanatorium is doing a trial on the study diabetic. Diabetic is a most common
clinical syndrome characterized by hyperglycaemia due to deficiency of insulin occurring
throughout the world.

In this regard, I am in a need to ask you few questions.I will maintain

confidentiality of your comments and data obtained . There will be no risk of disclosing your
identity and no physical, psychological or professional risk is involved by taking part in this
study.

Taking part in this study is voluntary. No compensation will be paid to you for taking part in this
study.

You can choose not to take part. You can choose not to answer a specific question. There is
no specific benefit for you if you take part in the study. However, taking part in the study may be
of benefit to the community, as it may help us to understand the problem of defaulters and
potential solutions.

If you agree to be a participant in this study, you will be included in the study primarily
by signing the consent form and then you will be given the internal medicine THETRAN VITHAI
KUDINEER 30 ml every 4 hours in a duration of 48 days.

The information I am collecting in this study will remain between you and the principal
investigator(myself). I will ask you few questions through a questionnaire. I will not write your
name on this form. I will use a code instead. The questionnaire will take approximately 20
minutes of your time.

If you wish to find out more about this study before taking part, you can ask me
all the questions you want or contact ____________-PG Scholar cum principal
investigator of this study,attached to National Institute of Siddha,Chennai-47. Ph no ------
 , - 47

( )

: :

: :

: :

NATIONAL INSTITUTE OF SIDDHA, CHENNAI – 47

AYOTHIDASAR PANDITHAR HOSPITAL

DEPARTMENT OF POTHUMARUTHUVAM
 FORM IV A CERTIFICATE OF CONSENT

“I have read the foregoing information, or it has been read to me. I have had the opportunity to
ask questions about it and any questions I have asked have been answered to my satisfaction.

I consent voluntarily to participate as a participant in this study and understand that I

have the right to withdraw from the study at any time without in any way it affecting my
further medical care”.

"I have received a copy of the information sheet/consent form".

Date:

Signature of the participant

In case of illiterate participant

“I have witnessed the accurate reading of the consent form to the potential
participant, and the individual has had the opportunity to ask questions. I confirm that the
individual has given consent freely.”

Date:

Signature of a witness

Left thumb Impression of the

Participant

(Selected by the participant bearing no connection with the survey team)

 ANNEXURE-II
PREPARATION OF TRIAL DRUG

§¾üÈ¡ý Å¢¨¾ ÌÊ¿£÷ :

§ºÕõ ºÃì̸û:

1. §¾üÈ¡ý Å¢¨¾,
2. ¸Î측ö §¾¡ø,
3. ¬Å¡¨Ã Å¢¨¾,
4. ŢǡõÀ¢º¢ý.

¦ºöÓ¨È:

“§¾üÈ¡ý Å¢¨Ã¸Î측ö ¦ºôÀâ šš¨Ã

§ÂüÈ Å¢Ç¡õÀ¢º¢§É¡ Êò¾¨ÉÔí - §¸¡ü¦È¡Ê¡ö
Àí¸¡ ÂÚ¸¡ü ÀÍÅ¢ý§À¡ â¦ÈÀÕ¸ô
¦À¡í¸¢ ÅÕ ¿£Ã¢Æ¢× §À¡õ”.

Ingredients 1,2,3,4 are ground separately with iron martan till it attains consistency. They
are fine chooranam mixed well and preserved in a clean and dry glass.

¾£Õõ §¿¡ö¸û:

¿£Ã¢Æ¢×.
¬¾¡Ãõ:
̽À¡¼õãÄ¢¨¸ÅÌôÒ,Àì¸õ±ñ:551
 ANNEXURE-III- RAW DRUGS REVIEW

1.§¾üÈ¡ý ¦¸¡ð¨¼:strychnos potatorum linn.

Other names:þøÄõ,¸¾¸õ,º¢øÄõ,§¾Ú.
Parts used:ÀÆõ,Å¢¨¾.
Taste:¨¸ôÒ
Quality:¦ÅôÀõ
Division:¸¡÷ôÒ
Action:
Alterative,tonic demulcent,mild expectorant.

¦À¡Ð̽õ:
'þøÄ¡ Áĸ Á¢ÃñÎ Á¢ýÈ¡§É¡
¢øÄ¡ Áĸ Á¢Õì̧Á-þøÄ¡Áø
Å¡¨Æì ¸É¢Ôõ Ũ¼Ô Á¢ØÐÓñÀ¡ñ
Å¡¨Æì ¸É¢Ôý¨Åò ¾Åý'
Medicinal uses:

 venereal sores,

 dysuria,

 polyuria,

 urolithiasis,

 burning micturation,

 anemia,

 ascities.

 It also cures dysmennorhea.

2.¬Å¡¨Ã Å¢¨¾ -Cassia auriculata

Other names: Å¢¨Ã,²ÁÒðÀ¢,§Á¸¡Ã¢,¬ÌÄ¢,¾Ä§À¡¼õ.

Parts used::þ¨Ä.â,Àð¨¼,Å¢¨¾,§Å÷,À¢º¢ý.
Taste :ÐÅ÷ôÒ
Quality:¾ðÀõ
Division:þÉ¢ôÒ

Action:
Astrigent
Alterative
Tonic
¦À¡Ð̽õ:
“¦º¡øÖ¾üÌ Á𧼡 ¦¾¡¨Ä¡¾ §Á¸¿£÷
±øÄ¡ ¦Á¡Æ¢ìÌ ¦ÁâŸüÚ - ¦ÁøÄź
Á¡Å¡¨Ãô ÀõÀÃõ§À¡ Ä¡ðÎó ¦¾¡Æ¢Ä½í§¸ !
¡š¨Ã ãÄ¢ ÂД
Medicinal used:

 It is used to cure diabetes,

 urinary tract disorders,

 leucorrhea,

 bone fever .
3.¸Î측ö:

Other names:
ƒ£ÅÉ¢¸¡, «Ó¾õ, «õ¨Á, «Ã¢¾¸¢, «ÀÂý, â¾É¡, §Á¸õ,
Parts used :À¢ïÍ, ÀÆõ,
Taste : ÐÅ÷ôÒ, «òмý ÒÇ¢ôÒ, ¸¡÷ôÒ, ¨¸ôÒ,

¦À¡Ð̽õ:
'¾¡¨¼ ¸Øò¾ì¸¢ ¾¡Ö ÌȢ¢Ţ¼ô
À£¨¼ º¢Ä¢À¾Óü §À¾¢Ó¼õ - ¬¨¼¦Âð¼¡ó
àÄÁ¢Ê ÒñÅ¡¾ §º¡½¢¸¡ Á¡Ä¢Ãñ
¼¡ÄÁ¢Ê §À¡õÅâ측 ¡ø'
Medicinal uses:

 it cures anemia,

 heart disease,

 anorexia,

 excessive secretion of mucus,

 useful in the treatment of diarrhea and dysentery

 it has a nourishing, restorative effect on the central nervous

system.

 It Cures the Tingling in feet [diabetic neuropathy] and poly urea.

4.ŢǡõÀ¢º¢ý: limonia acidissima

Other names:
¸ÊôÀ¨¸,¸À¢ò¾õ,Å¢Ç×,¦ÅûÇ¢ø.
Parts used::À¢º¢ý,ÀÆõ,þ¨Ä,¸¡ö.
Taste ::ÐÅ÷ôÒ
quality:¾ðÀõ
Division: ¸¡÷ôÒ
Action:
Demulcent.
¦À¡Ð̽õ:
'¿øÄ Å¢Ç¡õÀ¢º¢¨É ¿üÀ¡¸ï ¦ºö¾Õó¾ò
¦¾¡ø¨Ä¾¢ º¡Ãó ¦¾¡¨ÄŦ¾¡ý§È¡-¦ÁøÄ¢Âáø
Åó¾¦Åû¨Ç ¾ýÛ¼§É Á¡¾÷ ¦ÀÕõÀ¡Îõ
¯óп£÷ô §À¡ì̧Á¡õ ¯ý'
Medicinal uses:

 Plant treats diarrhea,

 anorexia,

 anemia,

 useful in diarrhea, and dysentery

 The spines are crushed with those of other trees and an infusion taken as a
remedy for menorrhagia and leucorrhea.

 It cures diabetes.
 DRUG PHOTOS

Thetran vidhai Aavarai viddhu

Kadukkai Vilampisin

Thetran vidhai choornam Thetran vidhai kudineer

 ANNEXURE-IV-PRE CLINICAL STUDY

BIO -CHEMICAL ANALYSIS OF THETRAN VIDHAI KUDINEER - ANALYSED

AT NATIONAL INSTITUTE OF SIDDHA

OBSERVATI
S.No EXPERIMENT INFERENCE
ON

1. Appearance of sample Brown in

colour

2. Solubility:
Sparingly
a. A little(500mg) of the sample soluble
is shaken well with distilled water.
Presence of Silicate
b. A little(500mg) of the sample
is shaken well with con. HCl/Con.
H2So4

3. Action of Heat:
Presence of Carbonate
A small amount(500mg) of the White fumes
sample is taken in a dry test tube and evolved
heated gently at first and then strong.

4. Flame Test:

A small amount(500mg) of the No Bluish

sample is made into a paste with con. green flame Absence of Copper
HCl in a watch glass and introduced appeared.
into non-luminous part of the Bunsen
flame.

5. Ash Test:s A filter paper is soaked

into a mixture of sample and dil. Yellow
Presence of sodium
cobalt nitrate solution and introduced colour flame
into the Bunsen flame and ignited
Preparation of Extract:5gm Of thetran vidhai kudineer is weighed accurately and
placed in a 250ml clean beaker and added with 50ml of distilled water. Then it is boiled
well for about 10 minutes. Then it is cooled and filtered in a 100ml volumetric flask and
made up to 100ml with distilled water.

OBSERVA
S.No EXPERIMENT INFERENCE
TION
I.Test For Acid Radicals
1. Test For Sulphate: Presence of Sulphate
Cloudy
a. 2ml of the above prepared extract
appearance
is taken in a test tube to this added 2ml of
present
4% dil ammonium oxalate solution.
2. Test For Chloride:
No cloudy
2ml of the above prepared extracts is
appearance Absence of Chloride
added with 2ml of dil-HCl is added until
present
the effervescence ceases off..
3. Test For Phosphate: Mild
2ml of the extract is treated with 2ml of Yellow
Presence of Phosphate
dil.ammonium molybdate solution and appearance
2ml of con.HNo3 present
4. Test For Carbonate: Cloudy
2ml of the extract is treated with appearance Presence of carbonate
2mldil. magnesium sulphate solution present
C Test For Nitrate:
1gm of the substance is heated with No Brown
copper turning and concentrated H2So4 gas is Absence of Nitrate
and viewed the test tube vertically down. evolved
6. Test For Sulphide: NoRotten
1gm of the substance is treated with 2ml Egg
Absence of Sulphide
of con. HCL Smelling
eggs evolved
7. Test For Fluoride & Oxalate:
2ml of extract is added with 2ml of dil. No Cloudy Absence
Acetic acid and 2ml dil.calcium chloride appearance of fluoride and oxalate
solution and heated.
8. Test For Nitrite:
3drops of the extract is placed on a filter No
paper, on that-2 drops of dil.acetic acid Characteristi Absence of Nitrite
and 2 drops of dil.Benzidine solution is c changes
placed.
9. Test For Borate:
2 Pinches(50mg) of the substance is Bluish green
made into paste by using dil.sulphuric colour flame Absence of borate
acid and alcohol (95%) and introduced not appeared
into the blue flame.
II. Test For Basic Radicals
1. Test For Lead: NoYellow
2ml of the extract is added with 2ml Precipitate is Absence of Lead
of dil.potassium iodine solution. obtained.
2. Test For Copper: No Blue
a. One pinch(50mg) of substance is colour flame
made into paste with con. HClin a watch No Blue Absence of copper
glass and introduced into the non- colour
luminuous part of the flame. precipitate
formed.
3. Test For Aluminium: Yellow
To the 2ml of extract dil.sodium colour Presence of aluminium
hydroxide is added in 5 drops to excess. appeared
4. Test For Iron:
a. To the 2ml of extract add 2ml of mild red
dil.ammonium solution colour Presence of Iron
b.To the 2ml of extract 2ml thiocyanate appear
solution and 2ml of con HNo3 is added

5. Test For Zinc:

To 2ml of the extract dil.sodium
White
hydroxide solution is added in 5 drops to Absence of Zinc
precipitate is
excess and dil.ammonium chloride is
not formed
added.
6. Test For Calcium:
Cloudy
2ml of the extract is added with 2ml of appearance
4% dil.ammonium oxalate solution and white Presence of calcium
precipitate is
obtained
c7. Test For Magnesium:

To 2ml of extract dil.sodium hydroxide White Presenceof Magnesium

solution is added in drops to excess. precipitate is
obtained
8. Test For Ammonium:

To 2ml of extract 1 ml of Nessler's Brown

Presence of ammonium
reagent and excess of dil.sodium colour
hydroxide solution are added. appeared

9. Test For Potassium:

A pinch(25mg) of substance is treated of No

with 2ml of dil.sodium nitrite solution and Yellowish
Absence of Potassium
then treated with 2ml of dil.cobalt nitrate precipitate is
in 30% dil.glacial acetic acid obtained.
10. Test For Sodium:
yellow
2 pinches(50mg) of the substance is made
colour flame Presence of sodium
into paste by using HCl and introduced appeared
into the blue flame of Bunsen burner.
11. Test For Mercury:
No yellow
2ml of the extract is treated with 2ml of Absence of mercury
precipitate is
dil.sodium hydroxide solution.
obtained
12. Test For Arsenic:
No brownish
2ml of the extract is treated with 2ml of
red Absence of arsenic
dil.sodium hydroxide solution.
precipitate is
obtained
 III. Miscellaneous
1. Test For Starch:

2ml of extract is treated with weak Red colour

Presence of starch
dil.iodine solution developed

2. Test For Reducing Sugar:

5ml of Benedict's qualitative solution is
taken in a test tube and allowed to boil for Brick red Absence of reducing
2 minutes and added 8 to 10 drops of the colour not sugar
extract and again boil it for 2 minutes. The developed
colour changes are noted.
3. Test For The Alkaloids:

a) 2ml of the extract is treated with 2ml .

of dil.potassium lodide solution.
b) 2ml of the extract is treated with 2ml Yellow Absence of Alkaloid
of dil.picric acid. colour
c) 2ml of the extract is treated with 2ml developed
of dil.phosphotungstic acid.
4. Test For Tannic Acid:
No block Presence of Tannic
2ml of extract is treated with 2ml of precipitate is acid
dil.ferric chloride solution obtained
5. Test For Unsaturated Compound:
Potassium
To the 2ml of extract 2ml of permanganat Absence of unsaturated
dil.Potassium permanganate solution is e is not compound
added. decolourised
6. Test For Amino Acid:

2 drops of the extract is placed on a violet colour Absence of amino

filter paper and dried well. 20ml of developed acids
Biurette reagent is added.
7. Test For Type Of Compound: green colour
Presence of oxy
2ml of the extract is treated with 2 ml developed
quinole pinephrine and
of dil.ferric chloride solution. red colour
pyro catechol
developed
Anti pyrine, Aliphatic
amino acids and
meconic acid are
No violet
present
colour
Apomorphine
developed
salicylate and
Resorcinol are absent.
Morphine, Phenol
No blue
cresol and hydrouinone
colour
are absent.
developed
Preliminary Qualitative phyto chemical tests procedure and interpretation of results

S.NO PROCEDURE INFERENCE

1. Calcium Presence of calcium

2. Sulphate presence of Sulphate

3. Chloride absence of Chloride

4. Carbonate presence of carbonate

5. Starch presence of of starch

6. Iron Presence of iron

7. Phosphate Presence of phosphate

8. Tannic acid Presence of Tannic acid

9. Aluminium Presence of Aluminium

10. Magnesium Presence of Magnesium

11. Ammonium presence of Ammonium

12. Mercury Absence of Mercury

13. Alkaloids Absence of Alkaloids

14. Reducing Absence of reducing sugar

Sugar

15. Silicate Presence of Silicate

16. Copper Absence of Copper

17. Sodium Presence of Sodium

18. Lead Absence of Lead

19. Fluoride And Absence of Fluoride and Oxalate

Oxalate
 QUANTITATIVE ANALYSIS REPORT

SOPHISTICATED ANALYTICAL INSTRUMENT FACILITY

IITM,CHENNAI-36

PERKIN ELMER OPTIMA 5300DV ICP-OES

SampleID-Thetranvidai Kudineer

Analyte Mean

Al 308.215 1.842mg/L

As193.696 BDL

Ca 317.933 25.415
mg/L

Cd 226.502 BDL

Hg 253.652 BDL

Fe 238.204 8.653 mg/L

Mg279.079 9.356 mg/L

Na 589.592 18.245mg/L

P 213.617 17.201 mg/L

Pb 230.204 BDL

Si 288.15 81.869mg/L

(BDL=Below detection limit )

 TOXICOLOGICAL EVALUVATION OF THETRAN VIDHAI KUDINEER

ACUTE TOXICITY STUDY OF THETRAN VIDHAI KUDINEER

[WHO GUIDELINES,1993]

Principle:

Acute toxicity was carried out in Swiss albino mice with a single exposure of 10
times of the recommended therapeutic dose of test compound the study duration will be
14 days.

Animal species : Swiss albino mice

Age / Weight / Size : 6 weeks. Mice-20-25 gms.

Gender : Both male and female

Number of Animals : Mice: 20

Acclimatization Period : 7 Days

Clinical dose : 2000 mg\day

S.No Group No of mice

1 Vehicle control 10 (5 male, 5 female)

Toxic dose 10X therapeutic dose 10 (5 male, 5 female)

2 (720 mg)

Test Animals

Test animals were obtained from the animal laboratory of the King institute, Chennai
and stocked at National institute of siddha, Chennai.All the animals were kept under
standard environmental condition (27+ or – 2 degree c).The animals had free access to
water and standard pellet diet(Sai meera foods pvt.ltd, Bangalore).The principles of
laboratory animal care were followed and the Institutional ethical committee approved
the use of animals and the study design. (1248/ac/09/CPCSEA/June/ 2011)
Route of administration: oral route was selected, because it is the normal route of
clinical administration.

Test substance and vehicle

The thetran vidhai kudineer is brown in colour with mild astringent taste .The test
substance is soluble in water, in order to obtain and ensure the uniformity in drug
distribution, the drug is dissolved by aqueous Tween 80 solution (10%).

Administration of doses

Thetran vidhai kudineer was suspended in aqueous Tween 80 solution (10%),with

uniform mixing and it was administered to the group‟s in a single oral dose The control
groups were received equal volume of the vehicle. The animals were weighed before
giving the drug. The dose level was calculated according to body weight, and surface
area. Since the clinical dose was 4000mg\day It was converted to animal dose (720mg)
and then administered. The principle of laboratory animal care was followed.

Observations

Observations were made and recorded systematically and continuously observed as per
the guideline after substance administration. Animals were observed individually (visual
observations included skin changes, alertness, grooming, aggressiveness, sensitivity to
sound,touch and pain,restlessness,tremors,convulsion,righting reflex,gripping reflex,pinna
reflex,corneal reflex,writhing reflex,papillary reflex,urination,salivation,lacrimation for
first 4 hrs, then periodically during the first 24 hrs. Animals were observed for body
weight and mortality for 14 days. If animals dying during the period of study, the animals
were sacrificed. At the end of the 14th day all animals were sacrificed and necroscopy was
done.

Body Weight

Individual weight of animals were determined before the test substance was administered
and daily for 14 days. Weight changes were calculated and recorded. At the end of the
test surving animals were weighed and sacrificed.
Results: Thetran vidhai kudineer at the dose 720mg/kg/bw did not exhibit any mortality
in mice.

No behavior changes were noted for the first 4 hours and for the next 24 hours and
throughout the study period of 14 days.No weight reduction was noted before and after
the acute study duration.Reflexes were found to be normal before and after the studyAll
other observations were found to be normal before and after the study.In Necropsy,the
organs of the animal such as,Liver,Heart,Lungs, Pancreas,Spleen, Stomach,Intestine,
Kidney,Urinary bladder,Uterus all appeared normal.

LONG TERM TOXICITY STUDY OF THETRAN VIDHAI KUDINEER:

Animals : Male and Female wistar albino rats

Age : 6-8 weeks

Weight : 150-200 gms

Gender : Both male and female

Number of animals : Rat: 40

Acclimatization period : 7 Days

Clinical dose : 4000mg\day

Clinical duration : 48 days

S.No Group No of Rats

1 Vehicle control 10 (5male,5 female)

2 1XTherapeutic dose (1.728 g) 10 (5male,5 female)

3 5XTherapeutic dose (8.640g) 10 (5male,5 female)

4 10XTherapeutic dose(17.280g) 10(5male, 5 female)

Animal source:

Test animals were obtained from the animal laboratory of the King institute, Chennai, and
stocked at national institute of siddha, chennai. All the animals were kept under standard
environmental condition (27+ or – 2 degree c) .The animals had free access to water and
standard pellet diet(Sai meera foods pvt.ltd, Bangalore). The principles of laboratory
animal care were followed and the Institutional ethical committee approved the use of
animals and the study design. (1248/ac/09/CPCSEA/June/IAEC 2011)

Identification of animal: By cage number, animal number and individual marking on fur
.

Housing & Environment: The animals were housed in polypropylene cages provided
with bedding of husk .Dark and light cycle each of 12 hours.

Administration period:

The period of administration of the test substance to animals are depending on the
expected period of clinical use. Since the clinical dose of the test drug is 48 days and as
per WHO guidelines the administration period is reported to be 3 months.

Dose selection:

The results of acute toxicity studies in swiss albino mice indicated that Thetran vidhai
kudineer was non toxic and no behavioral changes, mortality was observed. On the basis
of these results, the doses were selected for the study as per WHO guidelines.

Preparation and administration of dose:

Thetran vidhai kudineer was suspended in aqueous twin 80 solution(10%). It was

administered to animals at dose levels of 1Xtherapeutic dose (1.728gms), 5XTherapeutic
dose (8.640gms) and 10XTherapeutic dose (17.280gms).The control animals were
administered vehicle only. Administration was by oral (gavage) once a day for 90 days.

METHODOLODY:

Randomization, numbering and grouping of animal:

The animals were randomly divided into four groups for dosing up to 90 days. Each
group consist of 10 animals (5 per sex in each group) were allowed acclimatization period
of 7 days to laboratory conditions prior to the initiation of treatment. Each animal was fur
marked with picric acid. The females were nulliparous and non pregnant.

OBSERVATION:

Experimental animals were kept under observation throughout the course of study for the
following:

Body weight:

Weight of each rat was recorded on day 1 and at weekly intervals throughout the course
of study and at termination to calculate relative organ weights. From the data mean body
weights and percent body gain were calculated.

Food and water consumption:

The quantity of food consumed by groups consisting of an animal for different doses were
recorded at weekly intervals. food consumed per animal was calculated for control and
the treated dose groups

Clinical sings

All animals were observed daily for clinical sings. The time of onset intensity and
duration of this symptom if any were recorded

Mortality:

All animals were observed twice daily for mortality during entire course of study.

TERMINAL STUDIES:

LABORATORY INVESTIGATIONS:

Following laboratory investigations were carried out on day 91 in animals fasted

over night .Blood samples were collected by cardiac puncture using sodium heparin
(200IU\ml) for blood chemistry and potassium EDTA (1.5 mg/ml) for hematology
anticoagulant. Blood sample were centrifuged at 3000 r. p .m for 10 minutes.
Hematological investigations:

Hematological parameters were determined by manual methods at uma clinical

lab in Chennai.

Biochemical investigations:

The effect of thetran vidhai kudineer on certain biochemical parameters were

examined and compared with those of the control group. The blood samples collected
with heparinized bottles were centrifuged at 5000 rpm for 10 minutes to obtain clear
serum for the following investigation. Glucose was estimated using commercial Glucose
estimation kit (Span Diagnostics) by the method of Barham et al., (1972) and Tenscher. et
al., (1971).Haemoglobin PCV,RBC,Erythocyte count was estimated by Hemocytometer
method of Ghai (1995). Total Leukocyte Count was estimated by Hemocytometer method
of John (1972).Total (bilirubin test kid- malloy& evelyn 1937) direct and indirect
bilirubin were determined.Alkaline phosphatase,Alanine amino tranferase (ALT) and
Aspartate amino transferase (AST) were measured by using ALT and AST test kit (kind
& king) .Total protein TP concentration was determined.Albumin was determined based
on its reaction with bromocresol green (binding method) .Urea was determined according
to urease –berthelot method and plasma creatinine was estimated using jaffe
rection.Results of biochemical investigations conducted on day 91 revealed significant
changes in the values of different parameters studied when compared with those of
respective controls.

NECROPSY:

All the animals were sacrificed on day 91 under ether anesthesia. Necropsy of all
animals was carried out and the weights of the organs including liver, kidneys, brain,
heart, and lungs were recorded.

HISTOPATHOLOGY:

Tissue samples of organs from control and treated animals were preserved in 10%
formalin for preparation of sections using microtome. The organs included liver, kidneys,
heart, lungs and stomach of the animals were preserved and they were subjected to
histopathological examination.

The organ pieces (3-5 micron ) were fixed in 10% formalin for 24 hours and washed in
running water for 24 hours .Samples were dehydrated in tissue processor and then cleaned
in benzene to remove absolute alcohol .Embedding was done by passing the cleared
sample through three cups containing molten paraffin at 50 degree c and then a cubical
block of paraffin made by the L moulds it was followed by microtome and the slides were
stained with haematoxylin–eosin stain .Stained sections of each organ were examined
under light microscope at high (40X) power magnification. All the histo pathological
slides were prepared at Dept .of. Pathology, madras medical college, Chennai.

Results:

Control animals

Liver: Shows central veins with rows of radiating heapatocytes,Portal triads and cells
appear normal.

Kidney : Shows glomeruli tubules,interstitial cells of normal histology

Heart: Shows normal appearing myocardial fibres with patent coronaries.

Lung : Shows bronchioles,alveoli,widened alveolar septa and chronic inflammatory cells.

Stomach : Shows gastric mucosal glands lined by columnar cells.

Impression : Normal study

Test group animals

Liver : shows central veins with radiating cords of hepatocytes,portal trials and kupfer
cells appear normal.

Kidney : shows normal appearing tubules and glomeruli.

Heart : shows normal appearing myocardial fibres wit patent coronaries.

Lungs: Shows bronchioles, alveoli and focal lymphoid aggregates,the alveolar septa are
thickened and contained chronic inflammatory cells.

Stomach : Shows gastric mucosa with glands lined by tall columnar cells

Impression : Normal study

HISTOPATHOLOGY SLIDES

Figure 1: Histopathology of Liver

Plate A – Control group
Plate B – Treated on 5 X
Plate c – trated on 10 X
Plate A,B & C shows normal
hepatocytes, sinusoids.

Figure2: Histopathology of Lungs

Plate A – Control group
Plate B – Treated on 5X
Plate C—Treated on 10X
Plate A,B & C shows normal
alveoli, bronchiole and lymphoid
follicles

Figure3: Histopathology of Stomach

Plate A – Control group
Plate B – Treated on 5X
Plate C—Treated on 10X
Plate A, B & C shows gastric
mucosa with glands lined by tall
columnar cells.
Figure4: Histopathology of Heart
Plate A – Control group
Plate B – Treated on 5X
Plate C—Treated on 10X
All 3 plates shows normal
myocardial fibres.

Figure5: Histopathology of Kidney

Plate A – Control group
Plate B – Treated on 5X
Plate C—Treated on 10X
All 3 plates shows normal a
ppearing glomeruli tubules and
interstitium.
ANNEXURE-V-CERTIFICATES
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38.Web Hosting : Wikipedia.com

39.www.pubmed.com