WIMJ, Vol 4, Issue 2 Complete PDF

WIMJOURNAL, Volume No. 4, Issue No.
2, 2017 pISSN 2349-2910, eISSN 2395-0684

Manoorkar G S
ORIGINAL RESEARCH ARTICLE

The study of Insulin Resistance in the Off Springs of Diabetics and
Non Diabetic Patients
Ganesh Manoorkar1, Suvarna Tale 2
Associate Professor, Department of Biochemistry, Grant Government Medical College,
Mumbai1, PG student Department of Biochemistry, Grant Government Medical College,
Mumbai-400008, Maharashtra, India2
Abstract:
Introduction:
Insulin resistance is one of the main cause in the pathogenesis of the development of type- 2
diabetes mellitus. Elevated insulin levels and insulin resistance may be present several years prior to
the development of hyperglycaemia. Hence the diagnosis of insulin resistance at the initial stages in
risk group people could be used as an effective measure to prevent type 2 diabetes mellitus and its
outcome, including reduction in morbidity and mortality. Though type 2 diabetes mellitus has
multifactorial aetiology, genetic factor plays an important role in the development of diabetes
mellitus. So we have tried to establish relation between genetic factor and insulin resistance by
studying the insulin resistance in off springs of diabetics and non diabetics patients.
Aims and objectives:
Estimation of insulin levels in the off springs (non diabetics) of diabetics and non diabetics
patients.
Comparision of insulin resistance in the off springs (non diabetics) of diabetics and non
diabetics.
To find the relation between insulin resistance and genetic factor.
Material and method:
This study was carried out in the department of Biochemistry Grant Government Medical
College Mumbai. Total 100 non diabetic people were included in the study of age above 30 years.
These are divided into two groups as-
Group-I includes 50 off springs (Ist degree relatives) of non diabetic people.
Group-II includes 50 off springs (Ist degree relatives) of diabetic people.
© Walawalkar International Medical Journal 1

WIMJOURNAL, Volume No. 4, Issue No. 2, 2017 pISSN 2349-2910, eISSN 2395-0684
Manoorkar G S
The fasting plasma glucose and serum insulin levels are estimated in the above two groups.
The insulin resistance was calculated by using HOMA-IR model.
Result:
Fasting plasma glucose, serum insulin level and insulin resistance is significantly increased in
group-II people as compared to group-I people.
Conclusion:
There is a strong relation between genetic factor and insulin resistance which exist prior to
the development of diabetes mellitus. The people of group-II are susceptible for the development of
diabetes mellitus. If these people are identified and managed early we may prevent or may delay the
development of the type 2 diabetes mellitus in these people.
Key words:
Type 2 diabetes mellitus, Insulin resistance
How to cite this article: Ganesh Manoorkar and Suvarna Tale .The study of insulin resistance in the off
springs of diabetics and non diabetic patients. Walawalkar International Medical Journal 2017; 4(2):1-6.
http://www.wimjournal.com
Address for correspondence:

Dr. Ganesh. S. Manoorkar, Associate Professor, Department of Biochemistry, Grant Government
Medical College, Mumbai -400008. Maharashtra, India.
Email: drganeshmanoorkar@yahoo.in, Mobile No: 9823172
Received date: 10/12/2017 Revised date: 15/12/2017 Accepted date: 20/12/2017
DOI Link: http://doi-ds.org/doilink/12.2017-77855227/
Introduction: mellitus since it represent majority of cases.

Diabetes mellitus is a metabolic Though type 2 diabetes mellitus has
disorder as a result of either insulin resistance multifactorial aetiology, genetic factor plays
and/or insulin deficiency/ or both. It is a an important role in the development of type 2
complex disease where the carbohydrate and diabetes mellitus1. In such people elevated
fat metabolisms are affected predominantly. insulin levels and insulin resistance may be
Type 2 diabetes mellitus is considered as one present several years prior to hyperglycemia.
of the most predominant type of diabetes

Manoorkar G S
Insulin resistance: off springs of diabetics and non diabetic

Insulin resistance is defined as the patients.
diminished ability of cells to respond to the Aims and Objectives:
action of insulin in transporting glucose 1) Estimation of plasma glucose and
(sugar) from the bloodstream into muscle and insulin level in the off springs (non
other tissues. diabetics) of diabetics and non
If we eat or drink any food containing diabetics patients.
glucose (or the digestible carbohydrates) 2) Comparison of insulin resistance in the
plasma glucose level increases. In normal off springs (non diabetics) of diabetics
persons, the elevated blood glucose level and non diabetics.
stimulates beta (β) cells in the Islet of 3) To find the relation between insulin
Langerhans, of pancreas, to release insulin resistance and genetic factor.
into the blood. The insulin, in turn, makes Material and Methods:
tissues in the body (primarily skeletal muscle This study was carried out in the
cells, adipose tissue) to absorb glucose, and department of Biochemistry Grant
thereby lower the blood glucose level. When Government Medical College Mumbai.
blood glucose level decreases insulin output Total 100 non diabetic people were included
also decreases. In an insulin-resistant person, in the study of age above 30 years. These are
normal levels of insulin do not have the same divided into two groups as-
effect in controlling blood glucose levels. Group-I include 50 off springs (Ist degree
During the compensated phase of insulin relatives) of non diabetic people.
resistance insulin levels are higher, and blood Group-II includes 50 off springs (Ist degree
glucose levels are still maintained. relatives) of diabetic people.
Thus diagnosis of insulin resistance at The fasting plasma glucose and serum
the initial stages in these risk group people insulin levels are estimated in the above two
may be used as an effective measure to groups. The insulin resistance was calculated
prevent type 2 diabetes mellitus and its by using HOMA-IR model.
outcome, including reduction in morbidity and Ratio of males and females kept same
mortality. So we have tried to establish in all the groups.
relation between genetic factor and insulin Informed consent will be obtained
resistance by studying the insulin resistance in from all the study participants and the ethical

Manoorkar G S
committee of our tertiary care hospital Method:

approved the study. Serum insulin concentrations were measured
Exclusion criteria: by means of a Chemiluminescence
The people with known diabetes Immunological Assay.
mellitus, presence of risk factors of diabetes Diagnostic criteria for increase in serum
mellitus, obesity, hypertension, liver disease, Insulin:
kidney disease, thyroid disease, etc. The proposed reference interval for
Statistical analysis: normal fasting insulin levels was 6 to 27
The statistical analysis will be done uIU/ml2.
using SPSS for Windows, version 17. Assessing Insulin Resistance: HOMA-IR
Student’s t-test and Pearson correlation test (Homeostasis model assessment of insulin
will be used for the analysis of p value and resistance):
correlation of scale variables. Results with p < HOMA-IR was developed by
0.05 will be accepted as statistically Matthews3 as a method for estimating insulin
significant. Data will be expressed as mean ± sensitivity from fasting serum insulin and
SD. fasting plasma glucose.
Estimation of Fasting Plasma Glucose Insulin sensitivity was calculated by the
(mg/dl): homeostasis model assessment method
Plasma from the fluoride bulb was (HOMA-IR), which was calculated by
used for the estimation of plasma glucose. following formula:
Method: HOMA-IR = Fasting Plasma Glucose
GOD-POD method (Glucose oxidase (mg/dL) × fasting Insulin (uIU/ml) / 405.
and peroxidase method): Diagnostic criteria for Insulin resistance:
The WHO diagnostic criteria for Diabetes Subjects with a HOMA-IR
mellitus: (homeostasis model assessment of insulin
Fasting plasma glucose ≥ 126mg/dl or resistance) level above the 3.5 of the present
Post meal plasma glucose > 200 mg/dl study population were defined as having
Estimation of Serum Insulin (uIU/ml): insulin resistance (4).
Serum from the plain bulb was used Low HOMA values indicated high
for the estimation of serum Insulin. insulin sensitivity, and high HOMA values
indicated low insulin sensitivity.

Manoorkar G S
Results:
Table – 1 Table showing the comparison of all parameters in Group-I and Group-II in study
population:
Parameters Group-I Group II P value
Mean Plasma fasting glucose level (mg/dl) 73.67 + 10.23 89.16 + 17.68 P < 0.05
Mean Serum Insulin level (uIU/ml) 14.41 + 4.18 28.80 + 11.23 P < 0.05
Mean value of HOMA-IR 2.57 6.34 P < 0.05
Group-II shows significantly higher mean plasma glucose, higher mean serum insulin level and
higher insulin resistance.
Discussion: the KCNQ1 gene related to insulin secretion

We have found that mean fasting abnormality. It is an important disease-
plasma glucose is higher in group-II (89.16 + susceptible gene associated with the
17.68 mg/dl) as compared to group-I (73.67 + pathogenesis of diabetes in Asian ethnic
10.23 mg/dl). groups including the Japanese (1).
Renuka Pangaluri et al found higher Eman M et al found higher mean
mean fasting plasma glucose (109.2 ± 14.3 insulin level which is 11.2 (8.3 - 14.2) (mU/l)
mg/dl) in patients as compared to mean fasting in insulin resistance people than non resistance
plasma glucose (85.4 ± 12.4 mg/dl) in normal people in which mean insulin level is 6.1 (4.2
controls(5). They suggest glucose uptake in the - 8.4) (mU/l)(6).
muscles and adipose tissue is affected due to Richard Mack Blanche et al found
insulin resistance. lower mean fasting insulin level in control as
Eman M et al also found higher mean 15.8µIU/mL and higher in type 2 diabetes as
fasting plasma glucose as 5.7±0.8 5 (mmol/l) 29.1 µIU/mL2.
in insulin resistance people and 5.4 ± 0.7 Renuka Pangaluri et al found higher
(mmol/L) in non insulin resistance people(6). mean fasting plasma insulin level as 25.72 ±
We have found mean serum insulin is 5.29 (µIU/mL) in patients and 12.45 ± 2.2
higher in the group-II (28.80 + 11.23 uIU/ml) (µIU/mL) in controls5.
as compared to group-I (14.41 + 4.18 uIU/ml). We have also found mean HOMA-IR
Recently, a genomewide association is higher in group-II than group-I.
study (GWAS) has found that the mutation in

Manoorkar G S
Reizo Baba etal found insulin resistance in and insulin concentration in man.
(7)
non obese adolescents i.e. below 40 years . Diabetologia; 1985; 28: 412-9.
Conclusion: 4) Gokcel A, Baltali M, Tarim E, Bagis
There is a strong relation between T, Gumurdulu Y, Karakose H, et al;
genetic factor and insulin resistance which Detection of insulin resistance in
exist prior to the development of diabetes Turkish adults: a hospital-based study;
mellitus. The people of group-II are Diabetes Obes Metab; 2003; 5:126-30.
susceptible for the development of diabetes 5) Renuka Pangaluri, Shika Ann Seban,
mellitus. If these people are identified and Ebenezer William and Padmanaban;
managed early we may prevent or may delay Study of Thyroid dysfunction and
the development of the type 2 diabetes Insulin Resistance in Hemodialysis
mellitus in these people. patients; International Journal of
Conflict of interest: None to declare Research in Pharmaceutical and
Source of funding: Nil Biomedical Sciences; Oct – Dec 2012;
References: Vol. 3 (4); 1680-83.
1) Unoki H, Takahashi A, Kawaguchi T; 6) Eman M. Alissa, Suhad M. Bahijri1,
SNPs in KCNQ1 are associated with Daad H. Akbar and Tawfik M.
susceptibility to type 2 diabetes in East Ghabrah; Determination of insulin
Asian and European populations; Nat resistance in non-diabetic Saudi adults
Genet; 2008; 40: 1098–1102. by including fasting free fatty acids
2) Richard Mack, Blanche Skurnick, into QUICKI; International Journal of
Yolette Sterling-Jean; Fasting Insulin Medicine and Medical Sciences;
Levels as a Measure of Insulin September, 2009; Vol. 1 (9); pp. 365-
Resistance in American Blacks, The 369.
Journal of Applied Research; 2004, 7) Reizo Baba, Masaaki Koketsu,
Vol. 4, No.1: 90-94. Masami Nagashima; Role of Insulin
3) Matthews DR, Hosker JP, Rudenski Resistance in non obese adolescents;
AS, Naylor BA, Treacher DF, Turner Nagoys J. Med Sci; 2010; 72, 161-
RC; Homeostasis model assessment: 166.
Insulin resistance and beta-cell
function from fasting plasma glucose

Syed S A

A Retrospective Study of Screening of Common Transfusion Transmitted
Infections in the Blood Bank of a Tertiary Care Centre
Syed Sarfaraz Ali1, Rangrao Deshpande2, Saroj Deoghare3,
Vijay Dombale4 and Prajakta Chandrakant5
Senior resident, Department of Pathology, Shree Swami Samarth Blood Bank, B.K.L Walawalkar
Hospital, Sawarde1, Professor and Head, Department of Pathology, B.K.L Walawalkar Rural
Medical College, Sawarde2, Senior resident, Department of Pathology, Shree Swami Samarth
Blood Bank, B.K.L Walawalkar Hospital, Sawarde3, Principal, B.K.L Walawalkar Rural Medical
College, Sawarde4, DMLT student5
Abstract:
Background:
Blood is one of the essential components of body. The Blood Transfusion saves millions of
lives each year globally. However, there are adverse consequences associated with it.
Aim:
To study the seroprevalence of Transfusion Transmissible Infections in blood bags donated in
blood bank.
Materials and methods:
A retrospective review of donors record covering the period between 2013 to 2017 was
analysed and all blood bags were screened for HIV, HBsAg, HCV, syphilis and malaria.
Results:
The overall prevalence of HIV, HbsAg, HCV, syphilis and malaria were 0.03%, 0.80%,
0.07%, 0.05% and 0.01% respectively.
Conclusion:
All blood bags must be screened for TTI's, thus ensuring safe blood supply to the recipients. The
strict donor selection criteria by applying FDA approved IIIrd generation screening tests along with
strict guidelines for blood transfusion to reduce the incidence of TTI in recipient of blood.
Keywords:
Blood donors; Blood transfusion; Transfusion transmissible infection

Syed S A
How to cite this article: Syed Sarfaraz Ali, Rangrao H. Deshpande, Saroj B. Deoghare, Vijay Dombale, and
Prajakta Chandrakant. A Retrospective Study of Screening of Common Transfusion Transmitted Infections in the
Blood Bank of a Tertiary Care Centre. Walawalkar International Medical Journal 2017; 4(2):07-16.

Dr. Syed Sarfaraz Ali, Department of Pathology, Shree Swami Samarth Blood Bank, B.K.L
Walawalkar Hospital, Sawarde-415606, Tal. Chiplun, Dist. Ratnagiri, Maharashtra, India,
E-mail: sarfarazhayaz@gmail.com, Mobile No.:918147756719
Introduction: been fully screened & is not contaminated by

Blood Transfusion is a life saving any blood-borne disease such as HIV,
intervention and millions of lives are saved Hepatitis B & Hepatitis C, Malaria,
each year globally through this procedure.(1) Syphilis.(3,4) .
A crucial requirement in the
However, blood transfusions are also procurement of safe blood is to have a
associated with certain risks which can lead to National program for donor selection,
adverse consequences. It may cause acute or recruitment, retention, and education; this will
delayed complications and carries the risk of minimize donations from donors who might
(2)
the transmission of infections. transmit diseases to the recipients.
Globally, more than 81 million units of An unsafe blood transfusion is very
(3)
blood are donated each year. More than 18 costly both from human and economic point
million units of blood are not screened for of view. Morbidity and mortality resulting
transfusion-transmissible infections. Unsafe from the transfusion of infected blood have far
blood remains a major threat for the global reaching consequences, not only for the
spread of transfusion transmissible infections. recipients themselves but also for their
(1)
families, their communities and the wider
According to WHO, safe blood is a society .The economic cost of the failure to
universal right, which means blood that will control the transmission of infection includes
not cause any harm to the recipient & that has increase requirement for medical care, higher

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level of dependency, loss of productive labour Study population:

force and placing heavy burden on already Total 7939 blood bags were collected
overstretched health and social services on through voluntary blood donations in blood
national economy.(3) bank as well as in the camps organized by
The improved screening and testing hospital. The male and female donors between
of the donors have significantly reduced the age group of 19 to 50 years having weight
transfusion transmitted diseases in most of the more than 45 kg were included while persons
developed countries. However, the scenario in having history or in treatment of TTI's,
developing countries is not so. Many studies hypertension, diabetes, epilepsy were
have also shown that seroprevalence of these excluded. Lactating and pregnant females
diseases is very low or negligible in case of were also excluded.
voluntary donors as compared to replacement Methods:
donors. (5) The blood from voluntary donors were
The aim of present study was to know collected according to WHO guidelines (3) and
the status of Transfusion Transmissible detailed past history of immunization was
infection in blood samples donated from 2013 taken. In the blood bank sera were separated
to 2017 and to compare the seroprevalence in and all the units were screened for HIV, HBV,
the donors in remote areas of Ratnagiri and HCV by NACO approved IIIrd generation
District. ELSA kits using immunochromatographic
sandwich assay principle; while for testing of
Material and Methods: syphilis Rapid plasma Reagin method and for
Study design: Malaria Rapid Malarial Antigen Card Test
This is blood bank based retrospective was used.
study conducted in Swami Samarth blood All the reactive/positive blood bags
bank of B.K.L. Walawalkar Hospital, Dervan. were analyzed within 7 days of collection. All
The records of blood bags that were donated the bags in grey zone were discarded as per
to blood bank from 2013 to 2017 were the WHO guidelines. Validity of test was
analyzed. The permission from head of the assured as per given criterion.
Institution and B.T.O. (Blood Transfusion Statistical analysis:
Officer) was obtained. The data entry was carried out using
Microsoft Office Excel 2007 worksheet and

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percentage and proportions for each variable positive blood bags for TTI’s were displayed
was calculated. in table 3. The age wise seroprevalence of
Results: HIV, HBV, HCV, Malaria and syphilis were
A total of 7939 records were reviewed summarized in (Table 4) and the sex wise
and it is found that maximum blood bags were distribution of TTI was explained in (Table 3).
received in year 2013 (i.e. 2205 blood bags) The Taluka wise distribution of blood bags
and minimum in 2017 (i.e. 1148 blood bags) received in depicted in Table 5.
(Table 1) .The age and sex wise contribution
was elaborated by table 2 while the reactive/
Table 1. Year wise distribution of Blood Bags received.
Year No. of Blood Bags received
2013 2205
2014 1587
2015 1452
2016 1547
2017 1148
Table 2. The age and sex wise contribution of donors

Sr. No Age group Total blood bags Male Female
1 19 – 20 1118 1029 [12.96% ] 89 [1.12% ]
2 21 – 30 3449 3291 [41.45% ] 158 [1.99% ]
3 31 – 40 2096 2008 [25.29% ] 88 [1.10% ]
4 41 – 50 1019 971 [12.23% ] 48 [0. 60% ]
5 51 – 60 254 243 [3.06% ] 11 [0.13% ]
6 61 – 70 3 3 [0.03% ] 0 [ 0.00% ]
Total 7939(100%) 7545 [ 95.03 ] 394 [ 4.96% ]
The majority of donation was done by male 7545 (95.03%) followed by females 394 (4.96%)
with maximum donors (3449) were in the age group of 21 – 30 years (Table 2 )

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Table 3. Distribution of reactive/ positive and safe blood bags.

Total no. of blood bags Total no. of Reactive/Positive blood Total no. of Safe blood bags
collected bags
7939 78 [0.98%] 7862 [99.03%]
Out of total 7939 blood bags 78(0.98%) bags were found to be reactive/ positive for
Transfusion transmissible infections (Table 3).
Table 4. The age wise seroprevalence of TTI’s

Age Total blood HIV HBsAg HCV VDRL M.P
Group bags
19 - 20 1118 0 4[0.05%] 1[0.08] 0 0
21 - 30 4349 2[0.02%] 29[0.36%] 3[0.03%] 2 [0.02%] 1[0.01%]

31 - 40 2096 0 22[0.27%] 2[0.02%] 2 [0.02%] 0
41 - 50 1019 1[0.01%] 8[0.1%] 0 0 0
51 - 60 254 0 1[0.01%] 0 0 0
61 - 70 3 0 0 0 0 0
Total 7939 3[ 0.03%] 64[0.80%] 6[0.07%] 4[0.05%] 1[0.01]
Among 78 TTIs reactive/ positive bags Out of 7939 blood bags maximum
the majority were of HBsAg reactive/positive donation was done in Chiplun Taluka (3238
(64 bags (0.80%)) and the maximum donors bags) followed by Dapoli, Ratnagiri,
are within the age group of 21 to 40 years. Ghuhagar, Khed and Sangmeshwar (Table 5).
Whereas HCV, VDRL, Malaria and HIV The others include Sindhudurga, Malvan,
blood bags were reactive/positive within the Raigadh etc. which contributes 7.9% of total
age group ranging from 21 to 30 years (Table blood bags.
4)

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Table 5. Taluka wise distribution of donors
Sr. Region Total blood HIV HBsAg HCV VDRL MP

No. bags.
Chiplun 3238[40.78%] 0 28[0.35 %] 2[0.02%] 3[0.03%] 1[0.01%]
1
Khed 670[8.43%] 0 4[0.05%] 0 0 0
2
Dapoli 981 [0.10%] 1[0.01%] 7[0.08%] 1[0.01%] 0 0
3
Guhagar 738 [9.29%] 1[0.01%] 8[0.1%] 1[0.01%] 0 0
4
Sangmeshwar 619 [7.79%] 0 5 [0.06%] 0 0 0
5
Ratnagiri 740 [9.32%] 0 5 0 0 0
6 [0.06%]
7 Lanja 211 [2.65%] 0 0 0 0 0
Rajapur 110 [1%] 1[0.01%] 1[0.01%] 1[0.01%] 1[0.01%] 0
8
Others 632 [7.96%] 0 5[0.0%] 0 1[0.01%] 0
9
Total [7939] 3[0.03%] 64[0.80%] 6[0.07%] 4[0.05%] 1[0.01%]
Discussion: recipient. In developing countries the

Transfusion of blood and blood prevalence of TTIs is much higher and quite
components is a life saving measure and help far from attending a zero risk level at the
the patient worldwide. At the same time present moment.6
however blood transfusion is an important This study showed that 7939 blood
mode of transmission of infections to the bags donated from the year 2013 to 2017. Out
of total, 78 blood bags had serological

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evidence of TTI’s; most frequently being Kirana Pailoor et.al(9) and Varsha G
Hepatitis B. The results of this study when Sul et.al(11), they also found higher prevalence
compared with the studies conducted by P. of HBsAg followed by HCV, Syphilis, HIV
Pallavi et.al(8) , R .H. Deshpande et al(5), and Malaria in there respected area.(Table 6)
Table 6. Comparison of our study with others.

Sangeet P. Pallavi R. H Kirana Dharmesh Varsha Our
a et.al Deshpande Pailoor et Sharma G Sul et Study
Puhuja Mysore et.al Latur Karnataka Gwalior al Dervan
et.al (2004 - (2007 - al.(2008 - et.al (2009 Solapur (2013 -
Delhi 2008)(8) 2011)(5) 2012)(9) 2013)(10) (2012 - 2017)
(2002 - 2014)(11)
2005)(7)
years 4 5 5 5 5 3 5
cases 28,956 39060 83,245 27,990 6,7123 33,783 7939
positive 1000 4273 3088 160 2747 922 78
cases
HIV 646 170 329 17 91 227 03
HBsAg 163 497 2368 87 601 64
HCV 191 90 193 18 161 145 06
VDRL 111 198 35 114 49 04
MP 03 21 01
In this study the Total 7939 blood bags HCV 0.5 to 1.5%, HIV 0.08% to 3.87% and
were donated out of which 78 bags are Syphilis 0.85% to 3.0% .The data providing a
reactive/ positive for TTIs. The prevalence of picture of TTIs burden from the different parts
TTIs among Indian blood donors are reported of India has also come from various
to be ranging as follows; HBV 0. 66% to 12%, seroprevalence studies (Table 7)

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Table No.7: Comparison of transfusion transmitted infections: Prevalence rate in different

parts of India.
Place Bags HIV HbsAg HCV VDRL MP positive
tested reactive reactive reactive reactive
(6)
Mangalore 9599 6 33 6 11 1
(12)
Dehradun 6751 9 67 13 42 0
Ahmednagar(13) 5661 4 62 42 4
Bhopal(14) 5008 26 149 29 12
Lucknow (15) 39060 170 497 9 111
New Delhi(7) 28966 163 646 192
Ludhiyana(16) 44064 37 290 483 373
Gwalior(10) 67132 91 2360 161 114
Ratnagiri 7939 03 64 6 04 21
(Our study)
Conclusion: Conflict of interest: None to declare

Thus the present concluded that Source of funding: Nil
Hepatitis B infection still continues to be a References:
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of the disease is still very high in the general Safety Appia, CH-1211 Geneva 27,
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Syed S A
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057&Id=31

Pundkar R D

Risk Factors for Anemia in Pregnancy: A Case Control Study
Rutuja Pundkar 1, Jagdish Powar 2, Swapnil Sonar3, Maruti Desai4
Assistant professor, Department of community medicine SMBT Medical college, Nashik 1,
Statistician cum tutor, SMBT Medical College, Nashik 2 , Junior resident, SMBT Medical
College,Nashik3, Statistician, Department of Preventive & Social Medicine,
B.K.L Walawalkar Rural Medical College, Sawarde, Tal- Chiplun, Dist.- Ratnagiri,
Maharashtra , India4
Abstract:
Background:
Aim of the study was to find the risk factors leading to Anemia in pregnancy. The main
objective was to study the various sociodemographic factors leading to anemia. And to assess the
knowledge about anemia among study participants.
Material and methods:

The present Case control study was carried out at Primary Health Centre, to determine the
risk factors leading to anemia in pregnancy. A total of 308 pregnant females were registered. Among
them two groups were made, group I cases and group II controls. Each group had 50 cases each.
Laboratory test were done and females having hemoglobin less than 11mg/dl were considered
anemic. Anemic females were considered cases and females having Hb >11mg/dl were considered
controls. Data analysis was done using SPSS software.
Results:
The overall mean haemoglobin (Hb) was 11.55g/dL in controls, whereas it was seen that
among the cases it was 9.58g/dL.It would seem that diet, family size, education, social class, gravida
and parity are associated with anemia in pregnancy.
Conclusion:
After adjusting for all the possible covariates there seems to be significant association
between Hb levels and age group, education level, family size, diet, gravida and parity.
Keywords:
Anemia, pregnancy, knowledge, sociodemographic.
How to cite this article: Dr Rutuja D Pundkar, Mr Jagdish D Powar, Dr Swapnil V Sonar and Mr Maruti B Desai.
Risk Factors for Anemia in Pregnancy: A Case Control Study. Walawalkar International Medical Journal 2017;
Address for http://www.wimjournal.com
4(2): 17-25. correspondence:

Pundkar R D
Dr. Rutuja Dinkar Pundkar, Assistant professor, Department of community medicine, SMBT
Medical College, Nashik. Maharashtra, India.
Email: rutujapundkar83@gmail.com, Mobile No: 7709036129
Introduction: health, integrated management of childhood

The nutritional status of the expectant illness, adolescent health, making pregnancy
mother is the most important determinant of safer/safe motherhood, roll-back malaria,
pregnancy outcomes, including the birth deworming (including routine antihelminthic
weight of the newborn.(1) Anemia is control measures) and stop-tuberculosis(3).
particularly high for women with no Anemia is considered a severe public health
education, women from scheduled tribes, and problem by World Health Organization when
women in the two lowest wealth anemia prevalence is equal to or greater than
quantiles(2).Anemia is an indicator of both 40% in the population. Anemia prevalence’s
poor nutrition and poor health. Iron deficiency during pregnancy differed from 18% in
in its most severe form results in anaemia – developed countries to 75% in South Asia(4).
IDA – and since haemoglobin concentration is The demand for iron increases about six to
relatively easy to determine, the prevalence of seven times from early pregnancy to the late
(5)
anaemia has often been used as a proxy for pregnancy .Besides poor nutrition, frequent
IDA. Food-based approaches to increase iron labour, multiparity, abortions, parasitic
intake through food fortification and dietary infestations, consuming excess tea or coffee
diversification are important sustainable after meals determined as the predictors of
strategies for preventing iron deficiency and anemia in reproductive age women
(6)
IDA in the general population. However, .Worldwide, anemia contributes to 20% of
approaches that combine iron interventions all maternal deaths(7).The World Health
with other measures are needed in settings Organisation defines a non-pregnant woman
where iron deficiency is not the only cause of with haemoglobin of less than 12 g/dl at sea
anaemia. Strategies should be built into the level as likely to be anaemic. Accounting for
primary health care system and existing the physiological changes in pregnancy, the
programmes such as maternal and child equivalent value for pregnant women is 11

Pundkar R D
g/dl or a haematocrit less than 33% (WHO, Study area:

1972)(8). This study used 11.0 g/dl as the Carried out at Primary Health Centre
criteria for anaemia in pregnancy following (Takali Khatgoan) Ahmednagar.
(8)
the WHO recommendations .Knowledge of The PHC was located 12 km from
the sociodemographic factors associated with Ahmednagar on Kalyan Road. Total
anemia in pregnancy can be used to formulate population covered by the PHC was
a multipronged strategy to attack this approximately 35,066 people. It had 13
important public health problem. Hence, a villages & 6 subcentres. Total population of
case control study was undertaken to know the Takali Khatgoan is 5,959 people. The Ante
various risk factors leading to anemia in Natal Clinic (ANC) is held every 1st& 3rd
pregnancy. Wednesday of the month.
Aim: Sample size:

To find the risk factors leading to Pregnant women visiting the ANC
Anemia in pregnancy. clinic were enrolled by health worker
separately for the first & the subsequent visit
Objectives: of pregnant women. A total 308 pregnant
• To study the various women visiting the health center were
sociodemographic factors leading to enrolled.
anemia. 2 groups were made by systematic
• Find the association between random sampling. Among 2 groups 50 were
sociodemographic factors and anemia. cases and 50 were controls.
• To assess the knowledge about anemia
among study participants. Inclusion criteria:
For cases were, hemoglobin count
Material & methods: less than 11gm% & for controls was
Study design: hemoglobin count more than 11gm%.
The present was a Case control study
Study procedure:
Informed consent was obtained &
explanation as to the purpose of study was

Pundkar R D
offered. Thus, pregnant women were Ethical approval:

interviewed with predesigned, pretested, semi Ethical approval for the study was
structured questionnaire. A detailed obtained from the ethical committee at the
demographic profile of the women, that is, Medical College, Ahmednagar.
age, age at first pregnancy, religion, family
size, education, and occupation was collected. Data analysis:
Socioeconomic classification suggested by Data analysis was performed using
B.G. Prasad was adopted & updated(9). SPSS 21. Descriptive statistics, including
mean, range, & standard deviations, were
Laboratory method: calculated for all variables. Proportions were
Hemoglobin level was estimated by compared using Chi-square tests & chi square
Sahli’s acid hematin method of hemoglobin for trend at 0.05 level significance.
estimation(10). According to World Health
Organization (WHO), hemoglobin level below Results:
11g/dL is labeled as anemia during pregnancy. The present study revealed that the
The same criteria were used for diagnosing age of the respondents ranges from 19 to 29
(11)
anemia in pregnancy . years. It was seen that majority of the age of
study participants ranged from 20 to 25 years.
With mean age being 22 years.

WIMJOURNAL,
URNAL, Volume No. 4, Issue No. 22, 2017 pISSN 2349-2910, eISSN 2395-0684
2395
Pundkar R D
Table 1: Association between

en Sociodemographic factors and anemia among the
study population.
Information Cases (50) Contr Significa
acquired ols nce
retrospectively (50)
Maternal Age 21.92+2.3 21.86+ n.s

(mean) 5 2.1
Education 41 30 p<0.0076
(literate)
Occupation 39 44 n.s
(unemployed)
spacing 2 or <2 18 16 n.s

years
Family size (>3) 39 27 p=0.0056
Diet (non veg) 15 5 p=0.0062
Figure 2: Knowledge abo

about Anemia Among Controls & Case
60
50
40 17
30 34 no
20 yes
33
10 16
0
controls cases

WIMJOURNAL,
2395
Pundkar R D
Figure 3: Family Size and anemia among the study population
40 39
27
30 23
20 11 cases
10 controls
0
<3
>3
Figure 4: Diet and Anemia among the study population
normal
anemic
15

Pundkar R D
Table 2: Assessment of knowledge among the study population
Assessment Cases Controls Significance

of (n=50) (n=50)
knowledge
Knowledge 34 17 p=0.00033
(present )
Discussion: gestational age, gravida and parity are also

The overall mean haemoglobin (Hb) associated with anemia in pregnancy.
(13)
was 11.55g/dL in controls, whereas it was seen Study by Taner et al also showed
that among the cases it was 9.58g/dL.It would that 41.6% had hemoglobin levels <11g/dl.
seem that diet, family size, education, social This high prevalence of anemia among
class, gravida and parity are associated with pregnant women in Taner’s study was
anemia in pregnancy. Resent study showed that explained by the distribution of socioeconomic
as the level of education goes on increasing the status of the population. It showed that low
percentage of anemia in pregnant women goes socioeconomic status had more anemic cases.
(8)
on decreasing. The study also showed that as Ahmad Z et al in their study stated that the
the family size increased the percentage of age of the mother is significantly associated
anemia also increased. The pregnant women with anaemia, with the majority of mothers
having vegetarian diet were more prone to the (56.6%) who are more than 40 years old being
disease as compared to those having mixed anaemic at the first anatenatal visit. By parity,
diet. Table no 1 show that factors like 37.5% of the primigravida, 47.1% of the
education, family size, diet, knowledge are multigravida, 52.9% of the grandmultipara
associated significantly. Whereas factors like and 64.0% of the great grandmultipara were
maternal age, occupation, previous obstetrics anaemic. Again, parity is shown to be
history, etc are not significant. significantly associated with anaemia.
As compared to other studies like; A study in Pakistan showed that
(12)
Haniff et al , they found that age, ethnicity, anemic subjects were slightly older than
education, social class, urban rural residence, nonanemic subjects; whereas nonanemic

Pundkar R D
women were significantly taller and heavier, • Future studies are needed to look into
and a lower proportion were underweight the cutoff levels of Hb associated with
(BMI < 18.5). In addition, anemic women the relative risks & odds ratio.
were more likely to have no formal education
and to be employed outside the home.The Conflict of interest: None to declare
number of prior pregnancies was inversely Source of funding: Nil
related to mean hemoglobin level. Women References:
who reported consumption of red meat or 1. National Nutrition Survey, 2001-2002
chicken two or more times per week before revealed that anemia, especially iron
pregnancy had higher hemoglobin deficiency remains a major problem,
concentrations, but only the differences in 45% of women suffer from iron
mean hemoglobin concentrations associated deficiency anemia during pregnancy.
with consumption of red meat were significant 2. United Nations International
(14)
(10.03 vs. 9.87 g/dL,p = .004). Children’s Education Fund, World
(15)
In a study by Leyla K it was seen Food Programme Ministry of Health
that the mean ages of anaemic and nonanemic and Non Governmental Organization
women were similar, 26.9 and 26.4 years partners. The State of the world's
respectively (p > 0.05).Of the women, 10.2% children: Literature review on
were illeterate, 55.1% were primary school maternal anemia and iron
graduates. Anemia was majorly seen in supplementation. Islamabad. :
vegetarian (37.0%) (p < 0.05). Ministry of Health and Non
Conclusion: Governmental Organizations, 2000.
• After adjusting for all the possible 3. http://whqlibdoc.who.int/hq/2004/anae
covariates there seems to be miastatement.pdf.
significant association between Hb 4. Wang S, An L, Cochran SD: Women.
levels and age group, education level, In Oxford textbook of public health
family size, diet, gravida and parity. Fourth edition. Edited by: Detels R,
• A study is in progress to ascertain the McEwen J, Beaglehole R, Tanaka H.
outcome of anemia in pregnancy in the United States: Oxford University
Primary Health Centre. Press; 2002:1587-601.

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5. Christensen RD, Ohls RK: Anaemias Delhi: Indian Council of Medical

unique to pregnancy and the perinatal Research; 2004.
period. In Wintrobe's clinical 12. Haniff J, Das A, Onn LT, Sun CW,
hematology Volume 2. 11th edition. Nordin NM, Rampal S, Bahrin S,
Edited by: Greer JP, Foerster J, Ganeslingam M, Kularatnam KI, Zaher
Lukens NJ, Rodgers GM, Paraskevas ZM.Anemia in pregnancy in Malaysia:
F, Glader B. USA: Lippincott a cross-sectional survey.Asia Pac J Clin
Williams and Wilkins; 2004:1467- Nutr. 2007;16(3):527-36.
1486. 13. Cüneyt Eftal Taner, Atalay Ekin, Ulaş
6. Nutritional anaemia Solmaz, Cenk Gezer, Birgül Çetin,
[http://www.sightandlife.org/pdf/NAb Mustafa Keleşoğlu, Merve Bayrak
ook.pdf] Erpala, and Mehmet Özeren.
7. Micronutrient deficiencies iron Prevalence and risk factors of anemia
deficiency anaemia among pregnant women attending a
[http://www.who.int/nutrition/topics/id high-volume tertiary care center for
a/en/index.html] delivery. J Turk Ger Gynecol Assoc.
8. Zulkifli Ahma, Rogayah Jaafar, M 2015; 16(4): 231–236.
Hashim Mohd Hassan, Mohd Shukri 14. Naila Baig-Ansari. Anemia prevalence
Othman, Azmi Hashim. Anaemia and risk factors in pregnant women in
during pregnancy in rural Kelantan. an urban area of Pakistan. Food Nutr
Mal J Nutr 3:83-90, 1997. Bull. 2008 Jun; 29(2): 132–139.
9. Baride JP, Kulkarni AP. Text book of 15. Leyla Karaoglu, Erkan Pehlivan,
community medicine. 3rd ed. Mumbai, Mucahit Egri, Cihan Deprem, Gulsen
India: Vora Medical publications; Gunes, Metin F Genc, and Ismail
2006. p.12- 35. Temel. The prevalence of nutritional
10. Sanyal S. Clinical Pathology: Prep anemia in pregnancy in an east
manual for undergraduates. New Anatolian province, Turkey. BMC
Delhi: Elsevier India private limited; Public Health. 2010; 10: 329.
2005. p.25.
11. Toteja GS. Singh P. Micronutrient
profile of Indian Population. New

Deoghare S B

Study of Estrogen Receptor, Progesterone Receptor and Human Epidermal
Growth Factor Receptor Expression by Immunohistochemistry in Breast
Carcinoma
Saroj Deoghare1, Vijay Dombale2, Syed Sarfaraz Ali2 and Anam Dalwai4
Senior resident, Department of Pathology, B.K.L Walawalkar Rural Medical College, Sawarde 1,
Principal, B.K.L Walawalkar Rural Medical College, Sawarde2, Senior resident, Department of
Pathology, B.K.L Walawalkar Rural Medical College, Sawarde 3, DMLT student4
Abstract:
Introduction:
Over the last few decades there have been outstanding advances in breast cancer management
leading to early detection and treatment of disease. Recent attention has been directed to
immunohistochemistry (IHC) based classification of Estrogen Receptor (ER) / Progesterone
Receptor (PR) and Human epidermal growth factor receptor/neu (HER2-neu) status which provides
prognostic and therapeutic information and is inexpensive and readily available.
Aim:
The present study was undertaken with the view of correlating the histopathology of the
tumor by way of tumor grade, various traditional prognostic markers and its immunohistochemistry
profile with respect to Estrogen/Progesterone hormone receptors and Human epidermal growth factor
receptor/neu status.
Material and Methods:
An observational study was conducted in the Department of Pathology, BKL Walawalkar
Rural Medical College for two and half year from January 2015 to June 2017 including all the cases
of breast carcinoma diagnosed on histopathology on Modified Radical Mastectomy (MRM)
specimens and needle core biopsy. The cases with no prior oncological treatment and having
complete clinical data were included and the cases with non-malignant conditions of breast were
excluded. A total of 134 cases were studied. The surgical specimens were then evaluated
immunohistochemically for ER, PR, HER2-neu markers.

Deoghare S B
Results:
Out of 134 cases studied, majority of the cases (92.5%) were of Invasive Breast carcinoma,
No special type. Women of 31-50 years are more prone to the risk of the development of breast
carcinoma. Grade III tumors were seen predominant with 56.67%. implying a poor prognosis.
Percentage of ER positivity was 41.04%, PR positivity was 24.6%, Her2-Neu positivity was 26.9%
and triple negative was 41.04%. Grade 3 tumor and triple negative cases indicate poor prognosis and
poor outcome.
Conclusion:
From the present study it was concluded that with incorporation of immunohistochemistry
based classification of both ER/PR and HER2-neu status into the histopathology report along with
the traditional TNM staging and histological grading of breast carcinoma help in better therapeutic
management and increases prognostic accuracy and is inexpensive and readily available.
Keywords:
Breast cancer, Immunohistochemistry, Estrogen receptor, Human epidermal growth factor
receptor, Progesterone receptor, Triple negative.
How to cite this article: Saroj B. Deoghare, Vijay Dombale, Syed Sarfaraz Ali and Anam Dalwai. Study of
Estrogen Receptor, Progesterone Receptor and Human Epidermal Growth Factor Receptor Expression by
Immunohistochemistry in Breast Carcinoma. Walawalkar International Medical Journal 2017; 4(2):26-39.

Dr. Vijay Dombale, Department of Pathology, B.K.L Walawalkar Hospital, Sawarde-415606, Tal.
Chiplun, Dist. Ratnagiri, Maharashtra, India,
E-mail: drvijaydombale@gmail.com, Mobile No.: 9148372687
DOI Link: http://www.doi-ds.org/doilink/12.2017-11974847/
Introduction: constituting over 20% of all malignancies

Breast Cancer is the commonest among females. (1)
cancer in women worldwide. About one Worldwide, the incidence of cancer has been
million new cases diagnosed every year and observed increasing. Based on the reports of

Deoghare S B
WHO Cancer Control and Prevention While molecular and genetic testing is very
Programme for breast cancer, it is the most elegant, prognostic and predictive, it is
common cancer in women, accounting 16% expensive and not yet widely available. (6)
of all female cancers. Breast cancer is known In general, tumor size, nuclear grade,
as cancer of developed world but majority of mitotic activity, lymphatic and vascular
breast cancer deaths occur in developing invasion and lymph node involvement are
(2)
countries. In 2008, India recorded more common clinical pathological features of
deaths due to breast cancer than the USA. breast cancer that can be detected by routine
WHO forecasts that, by 2020, 70% of all light microscopy. These parameters associated
breast-cancer worldwide will be in with the grading and staging of breast cancer
developing countries. (3) are helpful in cancer treatment, clinical
Breast cancer is the most common management and prognostic assessment. (7)
cancer in women, in urban areas of Immunohistochemical (IHC)
developing countries due to increase in life assessment of hormonal markers such as ER
expectancy, urbanization and western and PR are important and useful predictive
lifestyles. Most women with breast cancer factor in breast carcinoma. In invasive breast
are diagnosed in late stages in low and carcinoma whose tumor cells lack Estrogen
middle income countries due to lack of Receptor/Progesterone Receptor, they do not
awareness on early detection and barriers to respond to hormonal therapy. Their status also
health services. In India, more than 100,000 has a prognostic value. Patients with ER/PR
new breast cancer patients are estimated to be positivity have low risk of mortality in
(4)
diagnosed annually. comparison to the patients with ER+/PR- or
Over the last few decades there have ER-/PR+ or both negative. (8,9)
been outstanding advances in breast cancer HER2-neu is also known as Epidermal
management leading to early detection of growth factor receptor 2. It has gained an
disease and the development of more effective importance as a significant prognostic marker.
(10)
treatments resulting in significant decline in Its amplification and over expression is
breast cancer deaths and improved outcome associated with the poor prognosis in breast
(5)
for women living with the disease. Recent carcinoma patients with axillary lymph node
attention has been directed singularly at metastases but there is no association with
molecular classification of breast cancer.

Deoghare S B
(11)
negative lymph nodes. HER2-neu can also which includes 134 cases of breast carcinoma
(12)
be a predictive marker. diagnosed on histopathology including all the
Currently, neo-adjuvant chemotherapy like needle core biopsies and MRM
has become the standard approach for locally specimens. The patients should not have any
advanced breast tumors as it helps to shrink prior oncological treatment and have complete
the tumor in the early stage of carcinoma and clinical data. The cases with non-malignant
make it convenient for breast conservative conditions of breast were excluded.
surgery. Tissue processing was done by fixing
Chemotherapy is also the mainstay in the tissues in 10% buffered formalin
the treatment for almost all patients of overnight. The tissues were grossed and
(13)
metastatic breast carcinoma. Several representative sections were taken and
markers such as Estrogen receptor, submitted for processing. Sections taken from
Progesterone receptor and Human epidermal paraffin embedded tissues were stained with
growth factor receptor 2-neu (HER2-neu) and hematoxylene and eosin and were examined.
their expressions have been used to study the Grading was done according to modified
breast carcinoma. Assessment of the status of Bloom Richardson grading system of WHO.
(14)
these tumor markers has significant role in Most suitable tissue block were selected for
accessing the diagnosis, treatment and ER, PR and HER2-neu markers and were sent
prognosis of breast carcinoma in patients. (8 , 9) to Tata Memorial Hospital, Mumbai. The
Thus this study was carried out with ER/PR expression shows the amount of
the aim of helping to correlate IHC and estrogen receptors (ER) and progesterone
histopathological grade of breast carcinomas receptors (PR) present in tumor cells. HER2-
using the modified Bloom-Richardson system neu assay measures the amount of HER2-neu
and hence, help in therapeutic management staining present on the membrane of tumor
(15)
and prognosis of breast carcinomas. cells. Allred’s scoring was used for IHC.
Statistical Analysis was done, the data were
Material and methods: tabulated and expressed as percentages.
This Observational study was Results:
conducted in the Department of Pathology, Out of 134 cases diagnosed, majority
BKL Walawalkar Rural Medical College, of specimens received were Modified Radical
Chiplun from January 2015 to June 2017 Mastectomy (MRM) i.e 103 and rest were

Deoghare S B
needle core biopsies. The age of the patients case each of Mucinous and Medullary
ranged from 27 to 83 with mean age being carcinoma. (Table 3). On extensive dissection
50.4 years (SD ±13.3years). Most of the cases of adjacent beast tissue and axillary tail,
belonged to the age group of 31-50 years with lymph nodes were retrieved in MRM, out
total of 74 cases, followed by 26 cases which 48 cases showed positive metastatic
(19.40%) from 51-60 years, 25 (18.65%) from deposits.
61-70 years (Table 1). All were females Modified Bloom Richardson scoring
except one which was male. Right breast was was done for all breast carcinoma cases (Table
more prone comprising of 76 (56.7%) cases. 4) and graded accordingly. Grade III was
Upper outer quadrant of breast was present in 62%, followed by 23% of Grade II
predominantly involved in 63 (47.01%) cases and 15% of Grade I (Table 5). On
(Table 2). histopathlogical examination, perineural
The size of tumor in MRM specimen invasion was noted in 38% of cases and
were measured between 2.0-5.0 cm in 67 lymphovascular invasion in 64.92% cases.
cases (50%), followed by >5cms in 21 cases In our study 41.04% cases showed ER
(27.6%) and ≤2cms in 15 cases (22.4%). The positivity, 24.6% showed PR positivity and
most common histologic type is Invasive 26.9% showed HER2-neu positivity. Only
Breast Carcinoma, No special type (IBC-NST) 2.2% cases showed triple positivity. However
accounting to 124 cases followed by 3 case triple negative cases were 55 (41.04%) (Table
each of Invasive Lobular Carcinoma (ILC) 6). 21.6% belonged to luminal A group and
and Ductal Carcinoma in situ (DCIS) and 2 2.2% belonged to luminal B group (Table 7).
Table 1 - Age Distribution of carcinoma breast

Age No. of cases
21-30 2 (1.5%)
31-40 37 (27.6%)
41-50 37 (27.6%)
51-60 26 (19.4%)
61-70 25 (18.6%)
71-80 6 (4.4%)
81-90 1 (0.7%)
Total 134

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Table 2 – Quadrant Distribution

Quadrant No of Cases
UOQ 63 (47.01%)
UIQ 37 (27.7%)
LOQ 19 (14.2%)
LIQ 10 (7.3%)
Central 5 (3.7%)
Total 134
Table 3 - Types of Carcinomas on histopathological diagnoses
Histological diagnosis No.of cases

IBC-NST 124 (92.5%)
DCIS 3 (2.2%)
ILC 3 (2.2%)
Medullary C 2 (1.5%)
Mucinous C 2 (1.5%)
Total 134
Table 4 – RB Scoring and case distribution

Score Tubule Nuclear Mitotic rate
formation grading
1 4 (3%) 11 (8.2%) 24 (17.9%)
2 24 (17.9%) 32 (23.9%) 82 (61.2%)
3 106 (79.1%) 91 (67.9%) 28 (20.9%)
Total cases 134 134 134
Table 5 – Histologic grading in various types of carcinoma

Histological Grade No of cases
I 20 (15%)
II 31 (23%)
III 83 (62%)
Total 134

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Table 6 – IHC Status of cases under study

IHC Marker status No of cases(out of
134)
ER positive 55 (41.04%)
PR positive 33 (24.6%)
HER2neu positive 36 (26.9%)
Triple positive 3 (2.2%)
Triple negative 55 (41.04%)
Table 7 – Luminal Classification of cases under study

Types No of cases (out
of 134)
Luminal A 29 (21.6%)
(ER+/PR+, HER2neu -)
Luminal B 3 (2.2%)
(ER+/PR+, HER2neu +)
HER2neu positive 23 (17.2%)
(ER-/PR-, HER2neu +)
Triple negative 55 (41.04%)
(ER-/PR-, HER2neu -)
Discussion: respect to ER, PR hormone receptors and

The use of IHC in breast cancer has Her2-neu. (16)
become an integral part of a complete and Estrogen receptors:
comprehensive histopathology report. In terms There are two forms of ER, ERα and
of prognosis and prediction of response to ERβ which together mediate downstream
treatment, in addition to histological grade and events. ERα (classical ER), the major player in
tumor subtype, hormone markers, ER/ PR and breast cancer is analyzed in clinical practice.
HER2-neu have become the mainstay ERβ on the other hand is a relatively newly
requirement for the oncologist. The present recognized ER and its function particularly its
study was undertaken with the view of role in breast cancer is poorly understood.
correlating the histopathology of the tumor by ER-positive cells in the normal breast
way of tumor grade, various traditional does not indicate proliferative activity whereas
prognostic markers and its IHC profile with ER-positive cells in atypical ductal
hyperplasia and in invasive and in in-situ

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carcinoma, show proliferative activity. The HER2-neu:

transformation from an ER-positive non The HER2-neu gene is located on the
proliferating cell phenotype into an ER- long arm of chromosome 17 (17q12-21.32). It
positive proliferating cell phenotype appears encodes p185 oncoprotein which is a receptor
to be a critical switch and is one of the tyrosine kinase that can be associated with
characteristic events of malignancy. The exact multiple signal transduction pathways. It has
mechanism that is responsible for this switch been found to be overexpressed in many types
is as yet not explained, although deregulation of human malignancies, notably breast,
of transforming growth factor beta signaling is ovarian, gastric, pancreatic, prostatic,
considered as the main culprit. Estrogen colorectal, cancers of the female genital tract
receptor (ER) positive tumors are and lung cancer. HER2-neu, also known
heterogeneous and the efficacy of hormonal as erbB-2 oncoprotein is overexpressed in 25
therapy depends on status of multiple other to 30 per cent of breast cancers. HER-2/neu
proteins along with other transcription factors overexpression in patients with breast cancer
such as FOXA1, GATA-3, growth factors and and positive lymph nodes is linked to poor
co-activator and co-repressorproteins. (17) prognosis with a reduced disease-free interval
Progesteron receptors: and shortened survival time, and similar
These are an estrogen-regulated linkage may exist in node-negative cases.
protein found in the cells of breast tissue. HER2-neu gene expression level seems to be a
Therefore its expression is believed to significant predictor for response to some
(18)
function as in ER pathway. Assessment of therapeutic agents.
both ER and PR is helpful in predicting Trastuzumab (Herceptin), a
response to hormonal therapy more accurately. humanized monoclonal anti HER2-neu
There are few proposals which indicate that antibody, was approved by the US Food and
PR positive tumors are more likely to respond Drug Administration as an adjuvant
(19)
to tamoxifen. The predictive value of PR therapeutic agent for patients with metastatic
positivity in the absence of ER is breast cancer overexpressing HER-2/neu
controversial. Breast tumors which are ER+ protein. As a result, evaluation of HER-2/neu
and ⁄or PR+ show low mortality risk in status has become pivotal in determining
comparison with ER- and ⁄or PR- tumors. (20) patient’s eligibility for trastuzumab treatment.
(21)

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A significant relationship between constituted to 63.2% and 62.5% respectively

amplification of the HER2-neu (c-erbB-2) which shows concordance with the present
oncogene and adverse clinical outcome in study.
(32)
patients with breast cancer was first noted by Kumar A et al and Varughese AA
Slamon et al1 in 1987. Panjwani et al showed et al (23) observed that IBC -NOS type was the
positive correlation of grade III with HER- commonest histological type. In present study
2/neu amplification. (22) we encountered 122 cases of IBC-NST type
The age range and mean age in present which constituted 91%.
study was concordant with study done by In our study maximum cases i.e, 65%
Varughese AA et al (23) where as less similar of cases showed lymphovascular invasion
(24)
to the study done by Engstorm MJ et al in which is similar to the study done by Ch'ng ES
(26)
which mean age noted was much higher et al in which they observed
accounting to 72.5 years and range being 41- lymphovascular invasion is maximum with
102 years. 77.8% of cases. Whereas in study done by
(33)
The observations from the present Schoppmann SF et al lymphovascular
study are concordant with other studies done invasion was seen in less percent of cases i.e.,
(25) (26)
by Ghosh S et al and Ch'ng ES et al 28.1%.
which also shows female preponderance. The tumors were graded using
In the study conducted by Ambroise Modified Bloom Richardson grading system.
M et al (27) and Azizun – Nisa et al (28), the left Most commonly tumors of Grade III
breast was more commonly involved constituting 62% followed by Grade II group
accounting for 59.2% and 57%respectively, of 23% and Grade I were 15% and our results
but right breast was commonly involved in the were concordant with studies done by
present study. Schoppmann SF et al (33) and Hui HU et al. (34)
(29)
The studies of Meena et al and (Table 8)
(30)
Costa M et al show the most common In the present study, positive lymph
quadrant involved was upper outer which was node metastatic deposits were seen in 35.5%
concordant with the present study (40%). of cases. However the studies done by
In study done by Ayadi L et al (31), and Schoppmann SF et al (33)
and Chen S et al (35)
Ghosh S et al (25), observed that the most of the observed maximum cases with metastatic
tumors ranges from 2-5 cm in size which lymph node.

Deoghare S B
Taking into account the cases (41.04%) in the present study which is
(36)
immunohistochemical status, triple negative similar to the studies done by Tiwari et al
cases constitute the highest proportion of 55 and Nikhra et al. (16)
Table 8 - Histological grading and comparison with other studies

Authors Schoppmann Hui HU et al Present study
SF et al
Grade I 14.43% 31% 15%
Grade II 45.18% 44.1% 23%
Grade III 40.37% 24.9% 62%
Table 9 – Luminal Classification and comparison with other studies

Types Tiwari et al Nikhra et al Present study
(Out of 32) (out of 43) (out of 134)
Luminal A 7 14 29 (21.6%)
(ER+/PR+, HER2neu -)
Luminal B 1 4 3 (2.2%)
(ER+/PR+, HER2neu +)
HER2neu positive 6 10 23 (17.2%)
(ER-/PR-, HER2neu +)
Triple negative 18 13 55 (41.04%)
(ER-/PR-, HER2neu -)
Conclusion: risk of the development of breast carcinoma.

The present study was done to Most cases of Grade 1 and ER/PR positivity
highlight the importance of histopathological expression implys a better prognosis. As the
examination in breast carcinoma not only in tumor grade increases, ER/PR expression
establishing diagnosis, but also histologically decreases and HER2-neu expression increases
subtype, predict prognosis based on and Grade 3 tumor and triple negative cases
histological grade and IHC studies. From our indicating for poor prognosis and poor
study, it was concluded that Invasive Breast outcome. Breast carcinoma with HER2-neu
carcinoma, NST was the most common positivity or with triple negativity shows more
histopathological subtype of breast carcinoma. aggressive nature.
Women of 31-50 years are more prone to the

Deoghare S B
Also a previous personal history of 4. Gray GE, Henderson BE, Pike MC.
breast cancer, or a germline BRCA mutation Changing ratio of breast cancer
all appear to be positively associated with incident rates with age of black
Triple negative breast cancer (TNBC). This females compared with white females
finding further supports the revised NCCN in the United States. J Natl Cancer Inst
guidelines that recommend women 60 years of 1980;64:461-3.
age or younger with TNBC to be referred for 5. Massarweh S, Schiff R. Resistance to
consideration of genetic counseling. In endocrine therapy in breast cancer;
addition, there was a lack of association Exploiting estrogen receptor /growth
between TNBC and personal history of factor signalling crosstalk.
Atypical hyperplasia and Lobular carcinoma EndocrRelat Cancer 2006;13:15-24.
in situ. In order to develop more effective 6. Nigam JS, Yadav P, Sood N. A
treatments, better surveillance and improved retrospective study of clinico-
prevention strategies, it is critical to improve pathological spectrum of carcinoma
our understanding of the risk factors that are breast in West Delhi, India. South
associated with the development of triple Asian Journal of Cancer 2014 Jul-
negative breast cancer.37 Sep;3(3): 179-81.
Conflict of interest: None to declare 7. Sun Y, Liang F, Wang K, He J, Wang
Source of funding: Nil H, Wang Y. Prognostic value of
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Chhatriwala M N

Correlation Between Haematological Parameters, Kidney Function Tests and
Liver Function Tests in Plasmodium Falciparum and Vivax Malaria
Mitul Chhatriwala1, Anup Nillawar2, Sandip Patil3 and Dinesh Bure4
Assistant Professor, Department of Biochemistry, Pramukhswami Medical College, Karamsad,
Gujarat1, Professor, Department of Biochemistry, B.K.L Walawalkar Rural Medical College,
Sawarde2, Scientist B, National Aids Research Institute, Pune3 and Assistant Professor,
Department of Biochemistry, BKL Walawalkar Rural Medical College, Sawarde, Maharashtra4
Abstract:
Malaria remains a major cause of morbidity and mortality in India. Plasmodium falciparum
remains the main culprit although cases with vivax malaria are on the rise. Severe malaria as defined
by the WHO criteria has high rate of complications and mortality. In our study we recruited
microscopy positive falciparum and vivax malaria patients. Haematological and biochemical
laboratory investigations were carried out in recruited patients. Both parameters were found to be
significantly derailed in falciparum cases as compared to vivax. A direct correlation has been
observed between kidney function tests (serum creatinine,serum urea) and direct bilirubin levels
across all cases of malaria. Hence these parameters can be used to identify and monitor the progress
of cases of severe malaria as significant proportion of patients fulfilled the criteria of severe malaria
in the cohort.
Keywords:
Severe malaria, parasitaemia, falciparum, vivax
How to cite this article: Mitul Chhatriwala, Anup Nillawar, Sandip Patil and Dinesh Bure. Correlation Between
Haematological Parameters, Kidney Function Tests and Liver Function Tests in Plasmodium Falciparum and Vivax
Malaria. Walawalkar International Medical Journal 2017; 4(2):40-45. http://www.wimjournal.com

Dr. Dinesh Bure, Department of Biochemistry, B.K.L Walawalkar Rural Medical College,
Sawarde-415606, Tal. Chiplun, Dist. Ratnagiri, Maharashtra, India,
E-mail:dinesh2141986@gmail.com, Mobile No.: 9013956796

Chhatriwala M N
Introduction includes severe anaemia, renal failure,

Malaria continues to be a major public hypoglycaemia, DIC, acidosis and
(8)
health issue in India. According to WHO hyperbilirubinemia .
report in 2016 around 1.09 million malaria Though the incidence of severe
cases and 331 deaths were reported at malaria is found more often with
community levels in India(1). Previous P.falciparum,more cases of severe malaria
research suggests that the malaria incidence is with P. vivax are being reported(9). Among the
between 9 and 50 times greater than reported, laboratory indicators for severe malaria
with approximate 13-fold under-estimation of Deranged kidney function tests and
malaria-related mortality(2).Many cases in the hyperbilirubinemia (>3 mg/dl with
past and still being underreported and hence hyperparasitemia) are the laboratory markers
WHO estimated that there were 9-18 million can be easily estimated in peripheral setting
malaria cases responsible for estimated 24000 and can help to pick up the cases of severe
deaths in India in 2016(1). malaria early. Development of severe malaria
The natural course of malaria progresses from increases the probability of complications
asymptomatic parasitaemia, uncomplicated mortality in a patient, hence early
illnessto recovery and in some cases to severe identification of severe malaria and early
malaria and ultimately to death(3).As severe aggressive intervention is likely to decrease
malaria is associated with high the death due to malaria.
mortality,WHO defined the criteria for the With this background, we tried to find
(4)
diagnosis of severe malaria inyear 1990 . out the proportion of deranged lab markers
These criteria’s were revised in year 2000 to and comparison of deranged Kidney function
include laboratory and clinical findings tests and Liver function tests in admitted
associated with poor prognosis in patients with patients of malaria (Both vivax and
(5)
malaria . falciparum).
Progression to severe malaria depends
upon several factors. In individuals infected Material and Methods:
with plasmodium falciparum, young children, This study was carried out at Dhiraj
pregnant women and immunocompromised General hospital, Vadodara. Which a is full-
individuals are particularly vulnerable(6,7).The fledged post- graduate teaching hospital with
laboratory findings indicating severe malaria many super-specialty departments. We

Chhatriwala M N
recruited patients of fever diagnosed as 2. Kidney function tests (Creatinine/urea)

malaria on microscopy irrespective of their 3. Hb and differential Blood count.
clinical severity. WHO criteria used to define severe malaria
Inclusion Criterion: 1. Serum creatinine > 3mg/dl
Acute fever diagnosed as Malaria on 2. Serum urea > 120 mg/dl
microscopy (Both P. Vivax and P. 3. Severe anemia (Hb<7gm%)
Falciparum) irrespective of severity of clinical 4. Serum bilirubin > 3mg%
condition. Result and Analysis:
Tests performed on admission: Table 1: Comparative analysis of
1. Liver function tests (bilirubin, ALT, anthropological data and LFT and KFT in P.
AST) vivax and P. falciparum:
P. Vivax (n=29) P. falciparum(n=15)

No. of Patients Male:14 Male:9 p value
Female:15 Female:6
Age 35.31 35.42 0.98
Hb gm% 10.23 10.54 0.69
Platelets 1.68 0.55 0.008
Urea 35.06 46.14 0.31
Creatinine 1.24 1.82 0.002
Sr ALT 46.58 37.85 0.49
Total Bilirubin 2 4.2 0.000018
Direct Bilirubin 0.98 2.17 0.00001
Table 1 shows platelets, serum creatinine and serum bilirubin is affected more in falciparum
infection.
Additionally, female patients affected =0.00001). Rest of the parameters showed no

with P. Vivax show severe anaemia as gender difference. There is moderate
compared to Male patients of P.vivax. correlation between KFT (creatinine and urea)
(MeanHb was lower by 3.3 mg% /p with direct bilirubin across the cohort.

Chhatriwala M N
Table 2:
Sr. Direct bilirubin p value
Sr Creatinine r=0.46 0.001
Sr Urea r=0.35 0.02
In this study, we found following number of patients who fit into the criterion for the definition of
severe Malaria according to WHO.
Table 3:
Criteria Number of patients %
Severe anemia (Hb<7 gm%) 7 16
Total Bilirubin>3 4 9.1
Creatinine>3 2 4.5
Blood urea>120 3 6.8
Discussion: indicating the active hemolysis because of

The aim of the present study is to malaria parasite. Total and direct bilirubin
identify the proportion of patients showing levels were significantly elevated in
derailment in LFT and KFT, differences in lab falciparum malaria. This hepatic dysfunction
manifestations of falciparum and vivax with hyperbilirubinemia is associated with
infection and correlation between laboratory high mortality and complications(12).
parameters in malaria cases. We did not find any significant
Thrombocytopenia was observed in both difference in haemoglobin levels, serum urea
P.falciparum and P.vivaxmalaria as previously and serum ALT in falciparum and vivax cases.
reported(10).The decrease in platelet count was Although the haemoglobin levels in females
significant in P.falciparum as compared to was significantly lower in P.vivax cases. Such
P.vivax. The serum creatinine levels were gender difference has not been reported
higher in patients with falciparum infection previously in vivax malaria.
denoting the derangement in creatinine We observed a moderate correlation
secreting abilities of kidney in falciparum between the kidney function tests (serum
(11)
infection . Hyperbilirubinemia was observed creatinine, serum urea) and direct bilirubin
in both P.falciparum and in P.vivax infection levels. These can be used as an indicator of

Chhatriwala M N
both degree of active hemolysis and degree of Conflict of interest: None to declare
renal function deterioration. Both being Source of funding: Nil
criteria of severe malaria, these two References:
parameters can be used for detection and 1. World health organisation, Regional office
monitoring the cases of severe malaria. of South East Region Health topics: Malaria:
In our study the most common World Malaria report 2014. [Internet]. [cited
observation in severe malaria cases was that of 2017 Dec 14]. Available from:
decreased haemoglobin levels. Around 16% http://www.who.int/malaria/publications/count
patients of severe malaria had severe anemia ry-profiles/profile_ind_en.pdf
(Hb%<7). 9% of patients had 2. Das A, Anvikar AR, Cator LJ, Dhiman
hyperbilirubinemia (Total bilirubin >3mg/dl). RC, Eapen A, Mishra N, et al. Malaria in
Increased serum creatinine and serum urea India: the center for the study of complex
was observed in 4.5% and 6.5% patients malaria in India. Acta Trop. 2012
respectively. This pattern points towards the Mar;121(3):267–73.
pathophysiology of severe malaria. In our 3. Severe malaria. World Health
cohort of patients it is likely that the Organization. Trop Med Int Health 19, Suppl
intravascular hemolysis because of malaria 1, 7–131 (2014)
parasite was responsible for severe anaemia, 4. Severe and complicated malaria.
derailed liver function tests and kidney World Health Organization, Division of
function tests. Control of Tropical Diseases. Trans R Soc
Conclusion: Trop Med Hyg. 1990;84 Suppl 2:1–65.
There is significant difference in 5. Severe falciparum malaria. World
laboratory parameters in cases of falciparum Health Organization, Communicable Diseases
and vivax malaria. Falciparum malaria is more Cluster. Trans R Soc Trop Med Hyg. 2000
likely to cause severe derangement in Apr;94 Suppl1:S1-90.
haemoglobin levels, kidney function tests and 6. Schwartz E, Sadetzki S, Murad H,
liver function tests. There is a moderate Raveh D. Age as a risk factor for severe
correlation between kidney function test and Plasmodium falciparum malaria in
direct bilirubin levels which can be exploited nonimmune patients. Clin Infect Dis Off Publ
for early diagnosis and monitoring of severe Infect Dis Soc Am. 2001 Nov
malaria. 15;33(10):1774–7.

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7. Blumberg L, Lee RP, Lipman J, malaria. J Coll Physicians Surg--Pak JCPSP.

Beards S. Predictors of mortality in severe 2009 Jun;19(6):363–6.
malaria: a two year experience in a non-
endemic area. Anaesth Intensive Care. 1996
Apr;24(2):217–23.
8. Bruneel F, Hocqueloux L, Alberti C,
Wolff M, Chevret S, Bédos J-P, et al. The
clinical spectrum of severe imported
falciparum malaria in the intensive care unit:
report of 188 cases in adults. Am J RespirCrit
Care Med. 2003 Mar 1;167(5):684–9.
9. Singh P, Mehta N, Tada NG.
Comparison of clinical profile and severity of
P. falciparum and P. vivax malaria in a tertiary
care hospital of Surat, India. Int J
ContempPediatr. 2016 Dec 22;3(4):1288–92.
10. Lacerda MVG, Mourão MPG, Coelho
HCC, Santos JB. Thrombocytopenia in
malaria: who cares? Mem Inst Oswaldo Cruz.
2011 Aug;106 Suppl 1:52–63.
11. Koopmans LC, van Wolfswinkel ME,
Hesselink DA, Hoorn EJ, Koelewijn R, van
Hellemond JJ, et al. Acute kidney injury in
imported Plasmodium falciparum malaria.
Malar J [Internet]. 2015 Dec 24 [cited 2017
Dec 20];14. Available from:
https://www.ncbi.nlm.nih.gov/pmc/articles/P
MC4690233/
12. Abro AH, Ustadi AM, Abro HA,
Abdou AS, Younis NJ, Akaila SI. Jaundice
with hepatic dysfunction in P. falciparum

Kargutkar Ajgaonkar S
CASE REPORT
Congenital Hypothyroidism Associated with Maternal Hypothyroidism
and Iodine Deficiency During Pregnancy
Smita Kargutkar-Ajgaonkar
Consultant Endocrinologist, Monmouth Medical Center, Long Branch New Jersey, USA;
Clinical Assistant Professor, Drexel University College of Medicine Philadelphia, PA,
USA
Abstract:
Congenital hypothyroidism is a partial or complete loss of function of the thyroid gland
(hypothyroidism) that affects infants from birth (congenital). The thyroid gland is a butterfly-shaped
tissue in the lower neck. It makes iodine-containing hormones T3 and T4 that play an important role
in regulating growth, brain development, and the rate of chemical reactions in the body (metabolism).
People with congenital hypothyroidism have lower-than-normal levels of these important hormones.
We present a case of a baby born with congenital hypothyroidism whose mother developed iodine
deficiency during pregnancy due to use of non-iodized salt and lack of proper prenatal care.
Key words:
Congenital hypothyroidism, iodine deficiency, maternal iodine deficiency
How to cite this article: Smita Kargutkar-Ajgaonkar. Congenital Hypothyroidism Associated with Maternal
Hypothyroidism and Iodine deficiency during pregnancy. Walawalkar International Medical Journal 2017; 4(2): 46-
50, http://www.wimjournal.com

Smita Kargutkar-Ajgaonkar, Consultant Endocrinologist, Monmouth Medical Center, Long Branch
New Jersey, USA; Clinical Assistant Professor, Drexel University college of medicine Philadelphia,
PA USA, E-mail: AceEndoOffice@gmail.com , Mobile No.: 1-732-413-8000

Case presentation: Discussion:

A baby boy was found to have Congenital hypothyroidism (CH), one
macroglossia, severe constipation and lethargy of the most prevalent endocrine diseases, is
within few days after birth (39 weeks known as a common preventable cause of
gestational age with normal vaginal delivery) mental retardation. (1) The prevalence of CH in
in rural India in Konkan region (Ratnagiri, India is 1 in 2640 based on the study was done
(2)
Maharashtra). About 1 month after birth the by Desai et al. in 1998. The other studies
TSH levels were checked and were very high from India quote a prevalence of 1 in 1985
TSH-150 (0.5-4.5 mIU/L), with low T4 and from Hyderabad(3) and 2.1 in 1000 from
T3. The baby was started on levothyroxine 25 Kochi.(4) A study by Kishore KR, et al
mcg daily and it resolved the constipation, revealed that CHT in India has a high
lethargy and poor growth. On further review it incidence and is an URGENT high priority for
(5)
was evident that the mother (25 years primi- public screening. The first multi-centric
gravida) was not given pre-natal vitamins study screening above 1 lakh neonates born
during the pregnancy. Instead of using iodized throughout India was launched by Indian
salt in cooking she was asked to use saindhav Council of Medical Research (ICMR)
(rock salt) by family due to improper advice National Task Force Team on New Born
by a local natural physician. Baby had a Screening (NBS) at AIIMS New Delhi (2007–
thyroid bed US done which showed absence 2012) and the preliminary results reveal a
of thyroid gland. Family was advised to do a much higher incidence of CH all over India at
radioactive iodine uptake and scan but due to 1 in 1172, particularly in south Indian
(6)
lack of facility in the local area and fear about population (1 in 727) Mass population
the word “Radioactive” family did not do it. screening of newborn infants for CH, first
On work up mother was also found to have introduced in 1974, is today a routine and
hypothyroidism and was also started on effective tool of timely/early diagnosis of CH,
(7)
levothyroxine after delivery. Now baby is used in most of the world . Initiation of
4.5years old and is stable on levothyroxine treatment within the first two to three weeks of
37.5 mcg daily and is showing normal life resulted in both normal IQ and physical
physical and mental development. growth. (7, 8, 9, 10)Many risk factors contribute to
the etiology of CH. In particular, a
multifactorial origin of CH in which genetic

(high frequency of additional malformations) billion individuals have an insufficient iodine

and environmental factors (especially iodine intake. Although goiter is the most visible
deficiency and maternal diabetes) play a role sequelae of iodine deficiency, the major
(11,12)
in the development of the disease. The impact of hypothyroidism due to iodine
signs and symptoms of hypothyroidism deficiency is impaired neurodevelopment,
include lethargy, coarse facial features, poor particularly early in life. In the fetal brain,
feeding or weight gain, jaundice, hoarse cry, inadequate thyroid hormone impairs
macroglossia, large fontanelles, umbilical myelination, cell migration, differentiation and
hernia, cool, dry skin, myxedema, goiter, maturation. Moderate-to-severe iodine
constipation.(13)But the physical finding may deficiency during pregnancy increases rates of
not be present at birth. Elevated TSH levels spontaneous abortion, reduces birth weight,
with low free T4 levels are suggestive of and increases infant mortality. Offspring of
hypothyroidism. In humans, deficient mothers are at high risk for cognitive
untreated congenital hypothyroidism due to disability, with cretinism being the most
thyroid agenesis inevitably leads to cretinism, severe manifestation. It remains unclear if
which comprises irreversible brain development of the offspring is affected by
dysfunction and dwarfism. The mild maternal iodine deficiency. Moderate-to-
appropriateness of the recommended L- severe iodine deficiency during childhood
(15, 16)
thyroxine dose (10-15 µg/kg/day) for the reduces somatic growth. In-spite of that
treatment of congenital hypothyroidism has there are some people who are using non-
been questioned because of the risk of iodized salt in cooking and keeping the
iatrogenic hyperthyroidism. Average range IQ pregnant women away from modern health
scores and positive behavioral adaptation are care and pre-natal care due to ignorance and
observed in congenitally hypothyroid children misguidance.
treated with L-thyroxine doses lower than Conclusion:
currently recommended; the L-thyroxine dose This case stressed the importance of
should be individualized to prevent iatrogenic having high index of suspicion for congenital
hyperthyroidism. TSH normalization should hypothyroidism in babies with lethargy and
not be a primary objective of treatment. (14) failure to thrive. It is important to diagnose
Iodine deficiency is a major public health these babies early in life and treat to prevent
problem; globally, it is estimated that two mental retardation and cretinism. Maternal

pre-natal care using multivitamin containing 2015 Feb 05]. Available

225 mcg of iodine and use of iodized salt in from: http://www.news.chennaionline.com/ch
cooking should be stressed. ennai/ICMR-releasesresults-of-study-on-
Conflict of interest: None to declare Congenital-Hypothyroidism/58cca920-765d-
Source of funding: Nil 492b-8fd3-9b34a8ac2351.col .
References: 7. Aronson R, Ehrlich RM, Bailey JD,
1. Gruters A, Krude H. Detection and Rovet JF. Growth in children with congenital
treatment of congenital hypothyroidism. Nat hypothyroidism detected by neonatal
Rev Endocrinol. 2012; 8(2):104–13. doi: screening. J Pediatr. 1990; 116(1):33–7.
10.1038/nrendo.2011.160. 8. Rovet J, Ehrlich R, Sorbara D.
2. Desai MP, Colaco MP, Ajgaonkar AR, Intellectual outcome in children with fetal
Mahadik CV, Vas FE, Rege C, Shirodkar VV, hypothyroidism. J Pediatr. 1987; 110(5):700–
Bandivdekar A, Sheth AR.Neonatal screening 4.
for congenital hypothyroidism in a developing 9. Glorieux J., Dussault JH, Van Vliet
country: problems and strategies. Indian J G. Intellectual development at age 12 years of
Pediatr. 1987 Jul-Aug; 54(4):571-81. children with congenital hypothyroidism
3. Newborn screening in India, Rama diagnosed by neonatal screening. J
Devi AR, Naushad SM, Indian J Pediatr. 2004 Pediatr. 1992; 121:581-584.
Feb; 71(2):157-60. 10. Kooistra L., Laane C.,Vulsma T., et
4. Sanghvi U, Diwakar KK, Universal al. Motor and cognitive development in
newborn screening for congenital children with congenital hypothyroidism: a
hypothyroidism; Indian Pediatr. 2008 Apr; long-term evaluation of the effects of neonatal
45(4):331-2. treatment . J Pediatr. 1994; 124:903-909.
5. Kishore KR, Ranieri E, Fletcher J 11. Medda E, Olivieri A, Stazi MA, et al.
(2014) Newborn Screening for Congenital Risk factors for congenital hypothyroidism:
Hypothyroidism in India– Is OVERDUE. J results of a population case-control study
Neonatal Biol 3:129. doi:10.4172/2167- (1997-2003). Eur J Endocrinol. 2005 Dec.
0897.1000129 153(6):765-73.
6. ICMR Releases Results of Study on 12. Mane AY, Bhagwat VR, Potey GG
Congenital Hypothyroidism. Chennai online (2007) Assessment of salt iodisation and
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Kronenberg HM. Williams textbook of Mane V (2009) Common salt iodization status
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congenital hypothyroidism. Clin Pediatr
(Phila). 1995; 34(10):521–2.

Nadkarni S M
CASE REPORT
An Unusual Presentation of Bilateral Knee Osteoarthritis– A Case Report
Sunil Nadkarni1 and Shankar Kashyap2
Consultant Orthopedic and Spin Surgeon, Pune1, Consultant Orthopedic and Spin Surgeon,UK2
Abstract:
Introduction:
Tandem spinal stenosis commonly involves the cervical and lumbar spine. The prevalence of
incidentally found cervical stenosis on MRI is 23% to 76%. There is paucity of literature regarding
management of asymptomatic cervical stenosis with predominant or isolated lumbar symptoms and
also the cause of this phenomenon has not been clearly defined.
Case report:
We present a case report of a 62 year Indian male presented to us with predominantly
bilateral knee pains which was so debilitating that he was able to walk only few steps with stick
support. He was considered for total knee replacement initially. He was operated with a cervical
laminectomy and his leg symptoms improved drastically after surgery
Conclusion:
Lower limb symptoms may present with pathology localized in cervical spine. There may or
may not be signs indicating cervical spine involvement. One must have a wider approach and
routinely rule out clinically and radiologically whole spine upto cranio-vertebral junction to avoid
delayed diagnosis due to false localization of sensory symptoms
Key words:
Bilateral Knee, Osteoarthritis, cervical spine, laminectomy
How to cite this article: Sunil Nadkarni and Shankar Kashyap. An Unusual Presentation of Bilateral Knee
Osteoarthritis– A Case Report. Walawalkar International Medical Journal 2017; 4(2):51-61,

Nadkarni S M

Dr. Sunil Nadkarni, Consultant Orthopedic and Spin Surgeon, Pune, Maharashtra, India
E-mail: sunilnadkarni@gmail.com, Mobile No.: 9822096340
Introduction cervical spine stenosis in patients with

Tandem spinal stenosis(TSS) is symptomatic lumbar spine spondylosis has
defined as concomitant stenosis at two or been described with incidence being 23% to
(2,4,5)
more regions of spine usually involving 76% in previous studies. In these
cervical and lumbar level which has been scenarios, indications for surgery of cervical
described since the 1960’s. (1,2) TSS manifests spine have not yet been completely established
(6)
as a mixed picture involving upper and lower in literature. Recently a case series
motor neuron symptoms and signs – describes relief of lumbar symptoms of all 6
intermittent neurogenic claudication, gait patients after operating over asymptomatic
disturbances, paraesthesias with varied cervical spine but with positive clinical signs
involvement of upper and lower limbs. of cervical myelopathy. (7)
Cervical spine stenosis is traditionally We present a case report of a 62 year
described as sagittal diameter being less than male who presented to us with predominantly
10mm.(3) leg symptoms with knee bilateral knee pains
In a case of concomitant lumbar and who was operated with a cervical
cervical symptoms, surgery for cervical spine laminectomy. His leg symptoms drastically
halts the progress of clinical worsening of improved after surgery
cervical myelopathy. Dilemma arises when
patient presents with predominant or isolated Case report:
lumbar symptoms without cervical symptoms A 62 year old male retired gentlemen
but with signs of cervical myelopathy. community ambulatory still actively involved
Dilemma also arises when these patients have in social service in the local area presented to
no cervical signs but radiographic evidence of us with bilateral knee pains and difficulty in
cervical spine stenosis with or without MRI walking 5 1/2 years ago. X rays showed mild
cord signal changes. Incidental asymptomatic

WIMJOURNAL,
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Nadkarni S M
to moderate degenerative changes in both knee

joints (Fig. 1).
Fig. 2 Pre-operative
operative standing xrays prior to
lumbar spine surgery Dec 2012 showing grade
1 anterolisthesis at L34 and L45 levels
He was operated with L2 to L5

decompression with L34 and L45
transforaminal lumbar interbody fusion and
L23 posterolateral fixation fusion (Fig. 3).
Fig. 1 bilateral knee standing Xrays showing
mild to moderate osteoarthritis
The distribution of pain, claudication

symptoms and pain in knees were
disproportionate to the degenerative changes
seen on Xrays which led us to investigate the
lumbar spine. This revealed a degenerative Fig. 3 Immediate post--operative Xrays
lumbar spondylosis with lumbar stenosis and showing L2 to L5 decompression with L34
lysthesis at L34 L45 levels (Fig 2). and L45 transforaminal lumbar interbody
fusion
on and L23 posterolateral fixation fusion
He was symptom free in the interim

period. There was no neurological deficit
before or after his lumbar surgery. The patient

WIMJOURNAL,
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Nadkarni S M
made a good recovery with reduction in pain involvement and no neurological involvement
and improvement in walking distance
distance. He was of upper and lower arms. Deep tendon reflexes
walking well for almost 5 years. were normal and Babinski’s sign was normal.
After 5 years once again he developed a X rays revealed medial compartment
recurrence of bilateral knee pain of 6 months osteoarthritis (Fig. 5).
which failed to respond to conservative
treatment. He was barely able to walk few
steps with a walking stick support (Fig. 4).
Fig.5 severe medial compartment

osteoarthritis in both knees
Fig. 4 Preoperative stooped walking posture
He was being considered initially for

He had a pronounced limp and varus
bilateral unicondylar knee replacement.
in both knees. Bilateral knee joints were
However in view of the distribution and nature
mildly tender, with crepitus of knee joint
of symptoms and lumbar spine being already
movement. There was no flexion deformity.
decompressed it was felt prudent to investigate
No ligament laxity in any plane. His VAS
the spine. This showed a cervical stenosis with
score for both leg pains was 10. We decided to
hyperintensity cord changes on T2 weighted
evaluate him neurologically for the whole
images (Fig. 6 to Fig. 11).
spine because the severity of his symptoms
was not corroborating clinically and
radiologically. There was no sphincter

WIMJOURNAL,
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Nadkarni S M
Fig. 7 Lateral- flexion and extension image of

Fig. 6 AP xray image of cervical spine
cervical spine showing no instability
Fig. 8 Sagittal MRI T2 weighted sections showing cervical stenosis from C4 to C7 with cord
hyperintensity at C67 level
Fig. 9 Sagittal MRI T1 weighted sections

WIMJOURNAL,
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Nadkarni S M
Fig. 10 Axial MRI T2 weighted sections till C56 levels showing maximum stenosis at C56 level
Fig. 11 Axial MRI T2 weighted sections through - C6 lower end plate, C67 disc space, C7 upper end
plate from left to right (level with most stenosis of all levels)
His preoperative ODI score was 100 Table 1- Preoperative JOA cervical
and JOA cervical myelopathy evaluation myelopathy evaluation questionnaire
questionnaire was as given below (Table 1). To avoid damage to the cord during
intubation a cervical decompression was
Characteristic Score offered to him before the planned unicondylar
Cervical spine function 80 knee replacements for the degenerative knee
Upper extremity function 78.94
Lower extremity function 27.27 pain and deformity. A cervical laminectomy
Bladder function 93.75 was undertaken on. Post operative day he
Quality of Life 77.08
resumed his walking rapidly. On VAS scale
his knee pain reduced from 10 before cervical

WIMJOURNAL,
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Nadkarni S M
spine surgery to 1 at from first follow up till He was ambulated next day with
final follow up. He walked without assistance. walker support initially and was walking
His symptom relief was assessed without any support at discharge on
independently by 2 joint replacement postoperative day 3. His VAS score at 1
surgeons. They felt it was not necessary to month, 2 month and 4 month followup was 1.
proceed with knee replacements. He was His ODI score at 2 month and 4 month
therefore discharged home. At last follow up followup was 10 and respectively. His JOA
at 6 months he is walking a distance of 3-4 cervical
vical myelopathy evaluation questionnaire
kms. He does not use any walking aid. His were as below (Table 2)
posture has improved considerably. His wife
commented that he is now walking straight Characteristics 2 month 4 month
without a stoop. (Fig. 12) followup followup
score score
Cervical spine 100
function
Upper extremity 100
function
Lower extremity 86.36
function
Bladder function 93.75
Quality of Life 81.25
Table 2 - post operative JOA cervical

myelopathy evaluation questionnaire
Discussion:
Tandem spine stenosis typically involves
cervical and lumbar spine with radiological
Fig.12 walking and standing posture at final
prevalence from 23% to 76% and Molinari et
followup
al have mentioned the prevalence of
symptomatic patients being from 0.09% to

Nadkarni S M
(8)
25%. Furthermore,this high occurrence of Some authors have tried to establish clinical
TSS can be compounded by 5% per year of symptoms associated with this phenomenon
(11,12,17)
development of cervical myelopathy from but have failed to give a definitive
asymptomatic cervical stenosis. (9) diagnostic test for it. Sung RD et al have
False localization signs of spinal cord have shown that patients with radiculopathy and
(10-18)
been described previously. False electrophysiological abnormalities of the
localization leads to delay in diagnosis and a cervical cord have a 90% chance of
timely diagnosis of cervical myelopathy has developing symptomatic myelopathy.(19)
been shown to halt the disease progression. However, usefulness of electrophysiological
(10)
Ross et al had presented a report with studies in detecting cervical myelopathy in
cervical compressive myelopathy with patients without signs and symptoms has not
(11) (6) (20)
predominantly knee pain. Neo et al been described. Aebli et al in a recent
described ipsilateral popliteal pain caused by imaging study of trauma patients have shown
(12)
cervical disc herniation. Langfitt TW et al that a Torg-pavlov ratio of <0.7 was a possible
described pain in the back and legs caused by predictor of symptomatic spinal cord injury
cervical spinal cord compression. Various following minor trauma.
(14, 17)
explanation have be given, like crossing In our case the patient had come with a
of spinothalamic tracts obliquely 2 or 3 levels stooping posture and a waddling gait with
above the affected segment, venous stasis symptoms and signs indicating osteoarthritis
causing hypoxic damage of anterior horn cells, of both knees. His symptoms were relieved
lamination of sensory tracts placing the with cervical spine decompression. Along
cervical tracts more centrally. None of these with these evidences and our previous
theories have been able to give an exact experience of relief of lumbar symptoms in a
explanation for this phenomenon. Whatever patient with cervical and lumbar stenosis with
the explanation, irritation of spinothalamic symptoms we had an approach towards the
tract tracts or disinhibition of the pain thinking to evaluate the whole spine
pathways leads to a mis-interpretation of non- pathology. We routinely screen whole spine
nociceptive signals in the ascending tracts with MRI to rule out any proximal pathology.
even in the absence of any sensory stimuli We had not done an NCV study because given
which leads to false localization. the fact that his lumbar spine was already
decompressed 4yrs ago with associated

Nadkarni S M
occasional upper limb symptoms it was easier upper levels of spine clinically and
for us to clinically pinpoint the pathology at radiologically before concluding the present
cervical level. It was further proven with the symptoms to from lumbar spine because it the
MRI picture of cervical stenosis and cervical cord which connects the brain to the
myelopathy. rest of the body neurologically. So it is worth
(7)
Daniel Felbaum et al in their study having a thought that pain symptoms in rest of
had 6 patients who presented with solely leg the body can be related to cervical spine or
symptoms. Some patients radiographic higher. It is also worth contemplating whether
findings did not match clinically and some had having a abnormal flexed posture of the neck
myelopathic signs without symptoms. All 6 in today’s world of continuous use of hand
patients had significant postoperative pain held devices and social networking can lead to
relief with mean pre-operative VAS of 6.7 vs. increase in cervical degenerative process and
3.7 postoperative. Our patient did not have myelopathy. It is just a conjecture and further
any myelopathic signs or symptoms only studies are needed to establish it.
paraesthesias and pain along C8 distribution
albeit C78 region showing no compression on Conclusion:
MRI. So clinical picture was corroborating We must have a broader perspective to
with cervical stenosis seen on MRI which was accommodate the idea of screening the upper
further justified by visualization of cord levels of spine clinically and radiologically
hyperintensity seen on T2 weighted MRI with any patient with predominant or isolated
images at C67 level. Postoperatively his leg lumbar symptoms. There may or may not be
and arm symptoms improved drastically so clinical signs of cervical spine involvement.
much that he doesn’t feel the need for knee This case report does not establish a definite
replacement surgery. His walking distance cause and effect relationship but it gives an
improved. He was walking with a straight impetus to reconsider the classical teaching of
posture without support. evaluating upper levels of spine up to the
This case doesn’t necessarily establish cranio-vertebral junction.
a cause and effect relationship however it
gives an impetus to have a wider approach Conflict of interest: None to declare
when we see a patient with leg symptoms. We Source of funding: Nil
need to be careful in ruling out involvement of

Nadkarni S M
References: Neurol Neurosurg. 2014, 124:114–

1. Teng P, Papatheodorou C: Combined 118.
cervical and lumbar spondylosis. Arch 7. Felbaum DR , Fayed I, Stewart JJ
Neurol. 1964, 10:298-308. , Sandhu FA.
2. Hitselberger WE, Witten RM. Relief of Lumbar Symptoms After Cer
Abnormal myelograms in vical Decompression in Patients with
asymptomatic patients. J Neurosurg Tandem Spinal
1968;28:204–6. Stenosis Presenting with Primarily Lu
3. Torg JS, Pavlov H, Genuario SE et-al. mbar Pain.Cureus. 2016 Dec
Neurapraxia of the cervical spinal cord 24;8(12):e940. doi:
with transient quadriplegia. J Bone 10.7759/cureus.940.
Joint Surg Am. 1987;68 (9): 1354-70. 8. Molinari RW, Gruhn WL, Molinari C
4. Lee SH, Kim KT, Suk KS, Lee JH, (2014) Tandem Spinal Stenosis (TSS):
Shin JH, So DH, et al. Asymptomatic Literature Review and Report of
cervical cord compression in lumbar Patients Treated with Simultaneous
spinal stenosis patients: a whole spine Decompression. J Spine 4: 200.
magnetic resonance imaging study. doi:10.4172/2165-7939.1000200
Spine (Phila Pa 1976) 2010;35:2057– 9. Lee SH, Kim KT, Suk KS, Lee JH,
63. Shin JH, So DH, et al. Asymptomatic
5. Kim BS, Kim J, Koh HS, Han SY, Lee cervical cord compression in lumbar
DY, Kim KH. Asymptomatic cervical spinal stenosis patients: a whole spine
or thoracic lesions in elderly patients magnetic resonance imaging study.
who have undergone decompressive Spine (Phila Pa 1976) 2010;35:2057–
lumbar surgery for stenosis. Asian 63.
Spine J 2010;4:65–70. 10. Michael D. Ross, PT, DHSc1; Ryan
6. Ghobrial GM, Oppenlander ME, Elliott, PT . Cervical Cord
Maulucci CM, Viereck M, Prasad S, Compressive Myelopathy in a Man
Sharan AD, Harrop JS: Management With a Primary Complaint of Knee
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11. Neo M, Ido K, Sakamoto T, herniation. Hawaii Med J. 1974;

Matsushita M, Nakamura T. Cervical 33(10):376–381.
disc herniation causing localized 19. Sung RD, Wang JC. Correlation
ipsilateral popliteal pain. J Orthop Sci. between a positive Hoffmann’s reflex
2002;7(1):147–150. and cervical pathology in
12. Langfitt TW, Elliott FA. Pain in the asymptomatic individuals. Spine
back and legs caused by cervical (Phila Pa 1976) 2001;26:67–70.
spinal cord compression. JAMA. 20. Aebli N, Wicki AG, Ruegg TB, Petrou
1967;200(5):382– 385. N, Eisenlohr H, Krebs J. The Torg-
13. Scott M. Lower extremity pain Pavlov ratio for the prediction of acute
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JAMA. 1956;160(7):528–534. 2013;13:605
14. D R S Jameison, E Teasdale, H J
Willison. False localizing signs in
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associated with chronic cervical disc

Kawade V Y
CASE REPORT
Secondary Repair of Third Degree Perineal Tear Leading to Fecal
Incontinence in 2 Cases
Vasant Kawade1 and Abhijit Ambike2
Professor and Head, Department of OBGY, B.K.L.Walawakarl Rural Medical College
and Hospital, Sawarde1,Assistant Professor, Department of OBGY, B.K.L.Walawakar
Rural Medical College and Hospital, Sawarde 2
Abstract:
Obstetric injury is the commonest cause of anal incontinence. According to Mr. Abdul H
Sultan and Miss RaneeThakar, UK, who have done extensive work in this field, ‘Every woman who
has a vaginal delivery has a 3rd or 4th degree tear until proved otherwise and a 3rd or 4th degree tear
cannot be excluded without a rectal examination’. We report two cases of anal incontinence as a
result of third degree perineal tear and complete disruption of the perineum secondary to childbirth.
Secondary repair of anal sphincter and perineal reconstruction in a rural tertiary care hospital
rendered excellent immediate clinical result.
Key words:
Obstetric injury, Perineal Tear, vaginal delivery
How to cite this article: Vasant Kawade and Abhijit Ambike. Secondary Repair of Third Degree Perineal Tear
Leading to Fecal Incontinence in 2 Cases. Walawalkar International Medical Journal 2017; 4(2): 62-
69,http://www.wimjournal.com

Dr.Vasant Kawade, Professor and Head, Department of OBGY, B.K.L.Walawalkar Rural Medical
College and Hospital, Sawarde-415606, Ratnagiri, Maharashtra.
E-mail: drvkawade1986@gmail.com, Mobile No.: 9422252904
Introduction: resulting in lack of bowel control. 4 to 6% of

Obstetric injury is the commonest women who have vaginal deliveries will suffer
(1)
cause of perineal and anal sphincter injury from faecal incontinence .However there is

Kawade V Y
a wide variation in the reported incidence of delivery 2yrs ago. Her first delivery was a full
anal sphincter muscle injury from childbirth, term normal delivery, seven years back. Left
with the true incidence likely to be mediolateralepisiotomy was given then and
approximately 11% of postpartum women she had anuneventfull postnatal period. Two
(2)
.The damage may be overt or occult. Faecal years back she had second childbirth. It was a
and or flatalincontinence resulting from this full term outlet forceps delivery for prolonged
damage is a debilitating problem with II stage of labour. The baby weight was
significant medical,psychological, social and 3000gms. She had a third degree perineal tear
economic implications. Treatment options then, which was sutured by the attending
include conservative, non-operative obstetrician in the delivery room under local
interventions (for example pelvic floor muscle anesthesia. On the seventh postnatal day she
training, biofeedback, drugs) and surgical developed incontinence for gas followed by
procedures. A surgical procedure may be incontinence for stools. This incontinence
aimed at correcting an obvious mechanical worsened over time and since then she has
defect, or augmenting a functionally deficient flatal and faecal incontinence.
but structurally intact sphincter complex. Her general and systemic
Sometimes the tear is missed and the repair is examinations were normal. On local
performed months or years after the injury, examination the perineum was absent. The
usually by a specially trained surgeon posterior vaginal wall and the anterior wall of
(secondary repair). A secondary repair may anal canal were fused. The anal opening was
also be performed when a primary repair has patulous with stains of fecal material on the
been unsuccessful.Secondary repair is usually perianal skin. Pervaginal examination revealed
offered to patients with gross faecal a wide patulous vagina. On per rectal
(3)
incontinence . The outcome depends on the examination the tissue between the anus and
extent of the anal sphincter damage and vagina was thinned out and she could not
(3)
associated neurological injury . tighten her spincters over the examining
finger.
Case I: Subsequently the
28yrs old, mother of two presented in patientunderwentsecondary perineal repair
the outpatient department with complaints of under regional anaesthesia. It was a 3b degree
incontinence for gas and stools since her last tear. Layered repair was done after

Kawade V Y
identification of the external sphincter ends by now she developed urgency for stools as well.
overlapping method with 1-0 polyglactin Her third delivery thirteen years ago was again
(Vicryl). Redunadantposterior vaginal mucosa a precipitate full term vaginal delivery at
was cut, perineum reconstructed and perianal home. Now immediately after this delivery
skin was sutured longitudinally resulting in faecal incontinence worsened. After her
lengthening of the distance between posterior second delivery she could hold her stools for
four cheet and anal opening. Postoperatively sometime, but now she could not after the last
perineal care was instituted, oral feedings childbirth.
were started after 48 hours. She was put on On local examination there was
broad spectrum antibiotics, analgesics and deficient perineum, anterior anal wall was
laxatives. Postoperative recovery was good fused with posterior vaginal wall and the
and one month after repair she had developed anterior margin of anal opening was
good continence for flatus, liquids and solids. withdrawn under the vaginal mucosa. Her anal
sphincter had no tone. Secondary perineal
Case II: repair was done under regional anesthesia. It
The second patient, was a 40 yr old was a 3c degree tear. Repair was done by
lady complaining of incontinenc for gas, Noble Mengert’s pull through procedure.
liquid and solid stools. Seventeen years ago External anal sphincter was plicated by
she had a full term vaginal delivery at home overlapping method. The internal sphincter
conducted by a traditional birth attended. In was sutured separately. After cutting the
this delivery there was abig perineal tear with excess vaginal wall and perineal
lots of bleeding. Surprisingly she did not seek reconstruction, the mucosa and skin was
any medical care and the wound healed closed Anal mucosa was sutured to the
gradually but she developed incontinence for perineal skin.
flatus. Her second pregnancy fifteen years Postoperative care for both the patients
back terminated in a full term precipitates was same and she made a good recovery. She
vaginal delivery at home. It was after this has developed good continence for solid and
puerperal period she realised that there was no semisolid stools till date and we expect she
skin between the vagina and the anal opening. develops total flatal and faecal continence
She could feel only a small thin filmy layer in over a period of time.
between. Flatal incontinence continued but

WIMJOURNAL,
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Kawade V Y
After repair & Perineum reconstruction
(2)
Discussion: reporting, awareness . Majority of the
In obstetric practice, the anal sphincters may sphincter tears can be identified clinically by a
be injured at the time of vaginal delivery. suitably trained clinician. In those with
These injuries are classified as third degree recognized tears at the time of delivery repair
lacerations when the external anal sphincters should be performed using long term
(EAS) are lacerated and fourth degree when absorbable sutures. Patients presenting later
the ano-rectal mucosa is breached.
hed. Obstetric who fail either conservative treatment,
trauma is a major cause of anal incontinence primary repair or are missed and who have a
but it is only recently that attention has been substantial sphincter disruption, elective
1, 4,5) (2)
focused on this subject ( . Occiptoposterior repair, may be attempted . There is a
position during delivery.primigravida, high significant relationship between a sphincter
birth weight, prolonged II stage are the risk tear that was symptomatic
mptomatic after delivery and
factors for anal sphincter tear. Forceps continence deterioration (28%) sustained at 5
delivery and nulliparity are also risk factors and 10 years. However, no relationship was
for recognized anal sphincter injury at the time found over 10 years for those women who
of vaginal delivery. sustained a sphincter tear but whose
A trend towards an increasing continence did not deteriorate postpartum (6).
incidence of third or fourth-degree
degree perineal On immediate diagnosis
iagnosis after delivery
tears by 2 to7 fold indicates better detection, the surgical strategy should be identification

Kawade V Y
of additional birth injuries and exact management of cervical and high vaginal tears
classification (Table 1) of the perineal tear by should be undertaken and then management of
means of speculum inspection and digital the perineal tear.
(1)
rectal examination . If neccessary first
Table 1 Classification of Perineal tear
First degree Injury to perineal skin

Second degree Injury to perineum involving perineal muscles but not involving the anal
sphincters
Third degree Injury to perineum involving the anal sphincter complex.
3a: <50% of ext anal sphincter thickness involved

3b: >50% EAS thickness involved
3c: both EAS and IAS involved
Fourth degree Involves anal sphincter complex (EAS and IAS) and anorectal mucosa
pullthrough procedure. The layered method
Delaying the repair should not be provides
recommended routinely, but can be an
alternative under special circumstances when optimal surgical approach in majority of the
appropriate surgical expertise is not readily patients.Reconstructive surgery should restore
available. If missed or tear in cases of the right angle configuration of the rectal neck
domicillary delivery,many do not seek by appropriate plication of the puborectalis
(8)
medical attention because of embarrassment. muscle . The important base and
In these secondary repair should be done after intermediate loops of the external anal
a proper diagnosis by a well trained surgeon in sphincter (EAS) should be identified and
an appropriate setting (7). repaired to ensure anatomical control of gas
Old third and fourth degree perineal and liquid stool. The two recognised methods
tears with partial or complete loss of anal of repair of damaged external anal sphincter
sphincter and perineum can be repaired either (EAS): are end-to-end (approximation) repair
by the layered method of repair or the Warren and overlap repair by absorbable suture
flap procedure or the Noble-Mengert anal material (7).

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Kawade V Y
Figure 1. Old III degree perineal tear Figure 2.Anal Canal- diagrammatic illustration
The limited data available shows that The prognosis following external anal
compared to immediate primary end
end-to-end sphincter repair is good with 60–80%
60
(1,7)
repair, early primary overlap repair appears to asymptomatic at 12 months .Women with
be associated with lower risks for faecal injuries
uries to the internal anal sphincter or rectal
urgency and anal incontinence symptoms. mucosa have a worse prognosis for future
However it would be inappropriate to continence problems. Preoperative counseling
recommend one type of repair in favour of should emphasise that although most patients
another (7). Anal sphincter repair carried out by will improve after the procedure, continence is
appropriately trained staff is associated with rarely perfect, many have residual
resi symptoms,
low morbidity, irrespective of the suture and some may develop new evacuation
material and repair method used. A surgeon disorders (9).
should use the technique with which he or she In conclusion, obstetric anal sphincter
(7,9)
is most familiar .Efforts to identify occult damage, and related fecal in continence are
Internal anal sphincter (IAS) injury and repair not uncommon. Risk factors for such trauma
this separately as well as the EAS may are well recognized, and should allow for
improve patient outcome. Improvement in the reduction of injury by proactive management.
functional length of the sphincter Improved classification, recognition, and
(3,7)
corresponded to a successful outcom
outcome . At follow-up of at-risk
risk patients should facilitate
the end of 36 months there appears to be no improved outcome. Secondary repair is
difference in flatus or faecal incontinence usually offered to patients with gross faecal
between the two techniques (10). incontinence, The outcome depends on the

Kawade V Y
extent of the anal sphincter damage and 3. National institute of Clinical

(3,7)
associated neurological injury . In remote, Excellence (NICE) 2013. Faecal
rural, poor resourced areas and poor reporting incontinence: the management of
we will see more and more patients needing faecal incontinence in adults. Clinical
secondary repair. guidelines CG :49, National Institute
for Health and care Excellence
Conflict of interest: None to declare (NICE).
Source of funding: Nil 4. SultanAH1, ThakerR. Lower genital
Acknowledgements: tract and anal sphincter trauma. Best
We thank the management and Pract Res ClinObstetGynaecol. 2002
administration of B.K.L Walwalkar Rural Feb;16(1):99-115.
Mecical College and hospital for providing the 5. Leeman L, Spearman M, Rogers R.
facilities for the management of these patients. Repair of Obstetric Perineal
We also thank the staff and residents of obgy, Lacerations. AmFam Physician 2003;
anesthesia department, nursing staff of the 68: 1585–90.
wards and operation theatre for their 6. Frudinger A1, Ballon M, Taylor SA,
preoperative and postoperative care. Halligan S. The natural history of
clinically unrecognized anal sphincter
References: tears over 10 years after first vaginal
1. Fernando RJ, Sultan AH, Freeman delivery. Obstet Gynecol. 2008
RM, Williams AA, Adams EJ. May;111(5):1058-64.
Third- and Fourth-degree Perineal 7. Fernando R1, Sultan AH, Kettle C,
Tears, Management (Green-top Thakar R, Radley S. Methods of repair
Guideline No. 29) for obstetric anal sphincter injury.
Published: 12/06/2015 Cochrane Database Syst Rev. 2006 Jul
2. Dudding TC1, Vaizey CJ, KammMA . 19;(3):CD002866.
. Obstetric anal sphincter injury: 8. Howard W Jones III, John A Rock,
incidence, risk factors, and TeLinde’s OperativeGynecology ,11th
management. Ann Surg. 2008 edition. Anal Incontinence and
Feb;247(2):224-37. Rectovaginal Fistulas.

Kawade V Y
9. Williams A1, Adams EJ, Tincello DG,

Alfirevic Z, Walkinshaw SA,
Richmond DH. How to repair an anal
sphincter injury after vaginal delivery:
results of a randomised controlled
trial. BJOG. 2006 Feb;113(2):201-7.
10. Fernando RJ1, Sultan AH, Kettle C,
Thakar R. Methods of repair for
obstetric anal sphincter injury
Cochrane Database Syst Rev. 2013
Dec 8;(12):CD002866.
.

Jadhav A A

Pleural Fluid Glucose – Routine but Vital Biochemical Parameter for
Differential Diagnosis of Effusions
Ashish Jadhav 1, Anuradha Jain2, ArvindYadav3 and Poonam Kamble4
Professor and Head, Department of Biochemistry, Ananta Institute of Medical Sciences
and Research Centre, Rajsamand1, Assistant Professor, Department of Biochemistry,
Gandhi Medical College, Bhopal2, Professor, Department of Biochemistry, B.K.L
Walawalkar Rural Medical College and Hospital, Sawarde3, Tutor, Department of
Biochemistry, B.K.L Walawalkar Rural Medical College and Hospital, Sawarde,
Maharashtra, India4
Abstract
Biochemical parameters in pleural fluid are usually done to identify the cause of pleural
effusion. Differentiating the effusion into either transudative or exudative is a logical first step, with
further investigations dictated by the clinical features and these results. Light’s criteria and other
biochemical parameters help to obtain a result for differentiating the effusion. Not a single laboratory
value will draw a conclusion of being the effusion as transudative or exudative, hence combining
number of biochemical test will help to obtain a definitive result.
Pleural glucose measurement is routine and age old parameter used to identify cause of
pleural effusion. In this review we tried to evaluate the usefulness of pleural glucose in effusion. In
country like India, where all routine and specialized biochemical parameters may not be available for
identifying the specific cause of effusion, the estimation of pleural glucose may help to draw an
initial approach for classifying an effusion.
Key Words:
Pleural effusion, glucose, Light’s criteria, Exudate, Transudate
How to cite this article: Ashish Jadhav , Anuradha Jain, ArvindYadav and Poonam Kamble. “Pleural Fluid
Glucose” – Routine but vital biochemical parameter for differential diagnosis of effusions. Walawalkar
International Medical Journal 2017; 4(2): 70-79. http://www.wimjournal.com

Jadhav A A

Dr.Ashish Anantrao Jadhav, Professor and Head, Department of Biochemistry, Ananta Institute of
Medical Sciences and Research Centre, Rajsamand-313202 , Rajasthan, India,
Email ID: drjadhavaa@yahoo.co.in, Mobile No.: 8529886830
Introduction: ultimately drains into the mediastinal lymph

The pleura comprise two thin layers of nodes. This lymphatic drainage is capable to
a tissue that protects and cushions the lungs. drain up to several hundred millilitres of
The inner layer (visceral pleura) wraps around additional fluid per day without the
the lungs. The outer layer (parietal pleura) development of an effusion.
lines the inside of the chest wall and
diaphragm. A liquid, called pleural fluid, Normal pleural fluid has the following
lubricates the pleural cavity so that the two characteristic:
layers of pleural tissue can slide against each • Clear ultra-filtrate of plasma that
other. Pleural fluid is an ultra-filtrate of originates from the parietal pleura
plasma. Usually there is less than 10 ml of • A pH of 7.60 – 7.64
(1)
fluid in each pleural cavity. (Approximately • Glucose content similar to that of
1 ml of fluid). Pleural fluid is filtered from the plasma
systemic capillaries in the parietal pleural • Protein content of less than 2 %
compartment through pressure gradient into (1-2 g/dL)
the pleural space. • Lactate dehydrogenase (LDH)
Pleural fluid is secreted into the less than 50 % of plasma
pleural space and is greatest at the apex while • Fewer than 1000 white blood cells
absorption is maximum towards the (WBCs) per cubic millimetre
diaphragm and mediastinum, where more Pleural effusion, also called “water on
lymphatic are located. The fluid is drained out the lungs”, is an excessive build-up of fluid in
predominantly through the stomata of the the pleural space resulting from excess fluid
parietal lymphatic present between the parietal production and/or decreased absorption.
mesothelial cells. These small lymphatic

Jadhav A A
Fluid production is increased if there is: caused by a disturbance of hydrostatic or

i. Elevation of the hydrostatic pressure colloid osmotic pressure with no pleural
gradient (e.g. in congestive cardiac disease involvement. In contrast, an exudate
failure, portal hypertension) signifies involvement of the pleura by an
ii. A decreased in colloid osmotic inflammatory or malignant process causing
pressure (e.g. in hypoproteinemia) increased capillary permeability.
iii. Increased permeability of the capillary The initial diagnostic consideration
vessels (e.g. in infection, malignancy, while dealing with a pleural effusion is to
inflammation) distinguish it into either transudates or
exudates. Looking back into the history of
Fluid removal is decreased if there is: biochemical analysis of pleural fluid, glucose
i. Impaired lymphatic drainage (e.g. in was one of the important biochemical
some neoplasm) parameter to be analysed. To our knowledge,
ii. Decreased pressure in the pleural the first documented research article on
space (e.g. in bronchial obstruction, estimation of sugar in pleural fluid was
(2)
atelectasis) published in 1929. Subsequently numerous
(3 – 11)
Pleural fluid is one of the common authors has determined the diagnostic
body fluid that is submitted for biochemical value of sugar in pleural effusions. Hence,
analysis. Thoracentesis are always performed sugar was the first biochemical parameter to
for new and unexplained pleural effusions be analysed in evaluation of pleural fluid,
when sufficient fluid is present to allow a safe which was the followed by estimation of
(12)
procedure. When pleural fluid is sent for protein. However, these initial parameters
examination, the laboratory is often asked to fails to clearly distinguish the effusion into
determine whether it is a transudate or an transudate and exudate.
exudate. Transudate, which is formed from Although a number of biochemical tests
ultrafiltration across a membrane, haslow have been proposed to distinguish transudate
protein content, whereas exudates are formed from exudate, the criteria proposed by Light et
by active secretion or leakage and hashigh al (13) have become the standard criteria (Table
protein content. The presence of a transudate 1).
effusion signifies a non-inflammatory process

Jadhav A A
Table 1:
Pleural fluid is classified as exudate if any of the following criteria are met:
Light’s Criteria
1. Pleural fluid to serum protein ratio greater than 0.5
2. Pleural fluid to serum LDH ratio greater than 0.6
3. Pleural fluid LDH level greater than two thirds normal serum value
Light’s criteria requires measurement of both minus pleural protein concentration level of
pleural and serum protein and LDH. However, less than 3.1 g/dL will more correctly
a meta-analysis of 8 studies with 1448 patients identifies exudates in these patients. Although
suggest that the following combined pleural pleural fluid albumin is not typically
fluid measurements may have sensitivity and measured, a gradient of serum albumin to
specificity comparable to the criteria proposed pleural fluid albumin of less than 1.2 g/dL will
(14)
Light’s et al for identifying exudates. also identify exudates in these patients. (16)
(17)
• Pleural fluid LDH value greater than In 2006, Muller T and Haltmayer I
0.45 of the upper limit of normal found that serum and pleural fluid N-terminal
serum values pro-brain natriuretic peptide (NT-proBNP)
• Pleural fluid cholesterol level greater was increased in pleural fluid of patients with
than 45 mg/dL congestive cardiac failure. The value above
• Pleural fluid protein level greater than 4000 ng/L was found to have sensitivity and
2.9 g/dL specificity of 90 and 93% respectively, and
The criteria proposed by Light et al hence may help to confirm heart failure as the
and these alternative criteria distinguish nearly cause of an otherwise idiopathic chronic
all exudates from transudates correctly, but effusion.
they misclassify approximately 20 – 25 % of Pleural Fluid Glucose:
transudates as exudates, usually in the patients Glucose measurement is commonly
of long – term diuretic therapy for congestive requested on pleural fluid samples. Many
cardiac failure (because of the concentration times the sample is often sent without fluoride
of protein and LDH within the pleural space oxalate preservative and simultaneous serum
due to diuresis).(15) Using the criteria of serum glucose is rarely measured. In addition to
previously discussed tests, glucose should be

Jadhav A A
measured during the initial thoracentesis. A glucose molecule with a molecular weight of
glucose concentration greater than 95 mg/dL 180 should easily pass between the pleural
is nearly always associated with a transudate. fluid and plasma. If there were no block in the
Lower concentrations are reported in exudates transport of glucose from the blood to the
with infections and in malignancy but the pleural cavity, the pleural fluid glucose
glucose concentration is extremely variable in concentration should remain at the same level
exudates overlapping many diseases. (18, 19) as that in plasma. Hence the pleural glucose
At the initial stages for the diagnostic level in transudate is same as that of plasma.
(25)
value of glucose in pleural effusions, these
authors (2-11) have used either Folin – Wu (20,21) The documented causes of decreased
(22)
or Hagedorn – Jensen method or the glucose levels in pleural effusions are due to
method is not mentioned. These methods are inflammatory disorders like tuberculosis,
not specific for estimation for glucose and malignancy, parapneumonic effusion,
they calculate total reducing sugars and rheumatoid pleurisy, esophageal rupture and
reducing substances present in the given body empyema.(18, 19, 26 – 32)
Other rare causes are
fluid. Hence they give apparent glucose value paragonimiasis, haemothorax, the Churg –
rather than true glucose value. With the Strauss syndrome and occasionally lupus
establishment of other specific methods like pleuritis. (32)
glucose oxidase and peroxidase, (23) the results Tuberculous and malignant effusion
obtained were of true glucose. has pleural glucose level below than 60
(32)
Although numerous biochemical mg/dL. There are two reasons suggested
parameters are studied for differential for this. These are over-utilization of glucose
diagnosis of exudates, only few are measured by pleural fluid and pleural thickening causing
for transudates. As stated earlier, pleural transport defect of glucose. There occurs
glucose concentration in transudate is same as acidosis of pleural fluid in tuberculous and
that of blood glucose level; however, uric acid malignant effusion and the cause of this
(24)
concentration is increased in transudates as acidosis is the accumulation of lactic acid and
compared to exudates. The capillary bed of the dissolved carbon dioxide as the end product of
(33)
lungs is comprised of non-specific tissues, glucose metabolism. Acidic effusions have
(26, 27, 34)
which have small pores that admit molecules low glucose and pH and high lactate.
(25)
upto a molecular weight of 1000. Thus, Sources of metabolic end product are

Jadhav A A
leucocytes, pleural cells, bacterial and below 1000 IU/L, the the parapneumonic
(26, 33, 35, 36)
malignant cells. effusion is uncomplicated and surgical
(37)
Further Sakchai Limthongkulet al drainage is not necessary.
stated that in tuberculous and malignant A low level of pleural glucose is
effusion, there is overproduction of lactic acid always seen in empyema with very low level
(41, 42)
and carbon dioxide due to over-utilization of occurs with some frequency. The
glucose and oxygen. The decreasing pleural predominant mechanism for this is increased
fluid pH and increasing pleural fluid carbon utilization of glucose by the constituent of the
dioxide has a significant linear relationship pleural fluid, namely, multiplying bacteria and
(41)
with decreasing PO2, increasing protein and phagocytosing leukocyte. A relative block
decreasing glucose in pleural fluid. These to the influx of glucose into the pleural
indicated a leakage of serum protein into the membrane may also play a role. (28)
pleural cavity and the over-utilization of Very low level of pleural glucose i.e.
glucose relative to transport defect of low less than 10 mg/dL is almost seen in
(43)
pleural fluid glucose concentration in the rheumatoid effusion. This is because the
acidotic fluid of tuberculous and malignant pleural fluid glucose concentration in acidotic
(38) (39)
effusion. A de Pablo et al stated that pleural fluid correlates with the degree of
patient with residual pleural thickening more pleural fluid acidosis rather than the disease
(44) (45)
or equal to 10 in tuberculosis had a state itself. While Light RW have
significantly low glucose level. suggested that accumulation of glucose end
(27)
Light RW et al stated that patients product resulting from pleural metabolism
with complicated parapneumonic effusion probably contributes to the low pH of
have low glucose and pH and high LDH. rheumatoid effusion, it appears that the efflux
Patients with pleural fluid glucose 40 mg/dL block to H+ by the rheumatoid pleura is a more
and pH below 7.0 had complicated important factor for the low level of glucose.
parapneumonic effusion and immediate tube Some authors have suggested that
thoracotomy should be done. Pleural glucose pleural glucose level also indicate the outcome
above 40 mg/dL either had a complicated or of pleurodesis in malignant pleural effusion.
(46)
uncomplicated parapneumonic effusion. Sahn The pleural level of glucose below 60
and Light (40) proposed that if the pleural pH is mg/dL is associated with pleurodesis failure.
(47)
above 7.30, glucose 60 mg/dL and LDH value

Jadhav A A
Conclusion: 4. Nassau E. Sugar content of pleural

A vast range of biochemical tests has fluid. Diagnostic and prognostic value
been put forward as being useful in the of estimations of the free sugar in
investigation of pleural fluid collections, with pleural effusions. Tubercle. 1941; 22:
the dual aim of differentiating transudates 249
from exudates and knowing the cause of 5. Gelenger SM and Wiggers RF.
effusion. In country like India, where all Relationship of the pleural fluid sugar
biochemical tests required for definitive to pulmonary tuberculosis. Dis Chest.
diagnosis of effusions at a health institute may 1949; 15: 325 – 328
be not available, routine biochemical test 6. Calnan WL et al. Diagnostic value of
including glucose may give a direction to the glucose content of serous pleural
approach the definitive diagnosis and to effusions. Brit M J. 1951; 1: 1239 - 40
initiate a treatment in pleural effusions. 7. Engeset A and Lygren T. “Sugar
Pleural glucose concentration below estimations in effusions: The
30 mg/dL indicates rheumatoid pleuritis or diagnostic value in tuberculous
empyema and between 30 – 60 mg/dL pleurisy.” Nord Med. 1953; 49: 290
indicates tuberculous, malignant or lupus 8. Barber LM et al. Glucose level in
effusion, or esophageal rupture. pleural fluid as a diagnostic aid.Dis
Chest. 1957; 31: 680– 687
Conflict of interest: None to declare 9. Politzer WM. An investigation into the
Source of funding: Nil diagnostic value of pleural fluid sugar
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cytology of chemistry fluids. J Lab 293
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22: 121

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with effusion. Dis Chest. 1960; 321 – 18. Light RW and Ball WC. Glucose and
324 amylase in pleural effusions. JAMA.
12. Wolanska A and Osinska K. Studies 1973; 225: 257 – 60
on levels of lipids and proteins in 19. Berger HW and Maher G. Decreased
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13. Light RW et al. Pleural effusions: the 1971; 103: 427 – 9
diagnostic separation of transudates 20. Folin O and Wu H. A system of blood
and exudates. Ann Intern Med. 1972; analysis. J Biol Chem. 1919; 38: 81 -
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14. Heffner JE et al. Diagnostic value of 21. Folin O and Wu H. A system of blood
tests that discriminate between analysis. Supplement I. A simplified
exudative and transudative pleural and improved method for
effusions. Primary Study Investigators. determination of sugar. J Biol Chem.
Chest. 1997; 111 (4): 970 – 80 1920; 41: 367– 374
15. Romero-Candeira S et al. Influence of 22. Hagedorn HC and Jensen BN. The
diuretics on the concentration of ferricyanide method for blood sugar.
proteins and other components of BiochemischeZeitschrift. 1923; 137;
pleural transudates in patients with 92 – 95
heart failure. Am J Med. 2001; 110 (9): 23. Trinder P. Determination of glucose in
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malignant effusions. Am Rev Resp Dis. 118: 893-900
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26. Potts DE et al. The glucose-pH pH in malignant effusions. Arch Intern
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WIMJOURNAL, Volume No. 4, Issue No.

2, 2017 pISSN 2349-2910, eISSN 2395-0684

ORIGINAL RESEARCH ARTICLE

© Walawalkar International Medical Journal 1

Address for correspondence:

Introduction: mellitus since it represent majority of cases.

© Walawalkar International Medical Journal 2

Insulin resistance: off springs of diabetics and non diabetic

© Walawalkar International Medical Journal 3

committee of our tertiary care hospital Method:

© Walawalkar International Medical Journal 4

Discussion: the KCNQ1 gene related to insulin secretion

© Walawalkar International Medical Journal 5

© Walawalkar International Medical Journal 6

ORIGINAL RESEARCH ARTICLE

© Walawalkar International Medical Journal 7

Address for correspondence:

Introduction: been fully screened & is not contaminated by

© Walawalkar International Medical Journal 8

level of dependency, loss of productive labour Study population:

© Walawalkar International Medical Journal 9

Table 2. The age and sex wise contribution of donors

© Walawalkar International Medical Journal 10

Table 3. Distribution of reactive/ positive and safe blood bags.

Table 4. The age wise seroprevalence of TTI’s

21 - 30 4349 2[0.02%] 29[0.36%] 3[0.03%] 2 [0.02%] 1[0.01%]

© Walawalkar International Medical Journal 11

Table 5. Taluka wise distribution of donors

Sr. Region Total blood HIV HBsAg HCV VDRL MP

Discussion: recipient. In developing countries the

© Walawalkar International Medical Journal 12

Table 6. Comparison of our study with others.

© Walawalkar International Medical Journal 13

Table No.7: Comparison of transfusion transmitted infections: Prevalence rate in different

Conclusion: Conflict of interest: None to declare

© Walawalkar International Medical Journal 14

5. Rangrao H. Deshpande et al. Blood J Blood disorder Transf 2015 6 : 2 vol.

© Walawalkar International Medical Journal 15

Peoples Journal Of Scientific Research,

© Walawalkar International Medical Journal 16

ORIGINAL RESEARCH ARTICLE

Material and methods:

© Walawalkar International Medical Journal 17

Introduction: health, integrated management of childhood

© Walawalkar International Medical Journal 18

g/dl or a haematocrit less than 33% (WHO, Study area:

Aim: Sample size:

© Walawalkar International Medical Journal 19

offered. Thus, pregnant women were Ethical approval:

© Walawalkar International Medical Journal 20

Table 1: Association between

Maternal Age 21.92+2.3 21.86+ n.s

spacing 2 or <2 18 16 n.s

Family size (>3) 39 27 p=0.0056

Diet (non veg) 15 5 p=0.0062

Figure 2: Knowledge abo

© Walawalkar International Medical Journal 21

Figure 3: Family Size and anemia among the study population

Figure 4: Diet and Anemia among the study population

© Walawalkar International Medical Journal 22

Table 2: Assessment of knowledge among the study population

Assessment Cases Controls Significance

Discussion: gestational age, gravida and parity are also