Continental J. Medical Research 2: 1 - 5, 2007 © Wilolud Online Journals, 2007.

ANTIBIOTICS COMMONLY USED IN THE TREATMENT OF ACUTE OROFACIAL BACTERIAL INFECTIONS IN GENERAL DENTAL PRACTICE IN DELTA STATE OF NIGERIA. Okagbare T. E. and 2Emudianughe T. S. Department of Preventive Dentistry and 2Department of Pharmacology and Therapeutics, College of Health Sciences, Delta State University, Abraka, Nigeria.


ABSTRACT Information on acute orofacial bacterial infections and the antibiotics commonly used in their management in general dental practice in Delta State, was obtained by reviewing a total of some 300 case records, randomly selected from five hospitals in Delta State. The following bacterial infections: acute dento-alveolar abscess, lateral periodontal abscess, post-extraction infection (dry socket), pericoronitis, acute ulcerative gingivitis (AUG), cellulitis and suppurative sialadenitis were investigated; and the estimates of the number of each type of infection in the five hospitals were found to be similar. Four different antibiotics – ampicillin, penicillin, metronidazole and erythromycin were mostly prescribed, in a variety of regimens for the treatment of orofacial bacterial infections in these hospitals. Majority of patients 138-186(4662%) received a 5-day course of ampicillin (250-500mg, qid) for bacterial conditions other than AUG, for which 3 days of metronidazole (200-400mg tid) was mostly prescribed 22(91.7%). However cellulitis was treated initially or all the way with 300 to 600 mg (0.5 to 1.0 mega units) i.m. or i.v., 6 hourly benzylpenicillin, sometimes in combination with metronidazole.

KEYWORDS: Orofacial bacterial infections, Anitbiotics, General dental practice, Delta State.

INTRODUCTION In the treatment of dental infections phenoxymethylpenicillin has traditionally been regarded as the antibiotics of choice all over the world, with erythromycin as an alternative for patients with known hypersensitivity to penicillins (Chow et al). In Delta State ampicillin is the most commonly prescribed, contrary to the above general impression, with erythromycin also as an alternative for patients with known hypersensitivity to penicillins. Ampicillin injection is sometimes given in a stat. dose of 0.5g followed by oral doses. Where penicillin was prescribed, it was either benzylpenicillin i.m. or i.v. or procaine pencillin i.m. only.


Okagbare T. E. and Emudianughe T. S: Continental J. Medical Research 2: 1 - 5, 2007

The aim of the present study is to obtain information about patterns of acute orofacial infection among patients attending general dental surgeries in Delta State, and to gain information on which antibiotics are mostly prescribed for their treatment.

Table 1 Types / number of acute orofacial infections reviewed per hospital DSC hospital Bacterial infection Acute dento-alveolar abscess Pericoronitis Lateral periodontal abscess Post-extraction infection Acute ulcerative gingivitis Cellulites Salivary gland infection Total 24 14 7 5 5 4 1 60 25 13 5 7 4 4 2 60 25 13 7 6 6 2 1 60 24 15 6 6 4 4 1 60 24 15 7 5 5 3 1 60 122 70 32 29 24 17 6 300 Central hospital Warri Central hospital Sapele Central hospital Agbor Federal Medical Centre Asaba Total

MATERIALS AND METHOD One research assistant was recruited for this study and five hospitals were involved. The hospitals are Delta Steel Company Hospital, Orhuwhorun – Warri; Central Hosptial Warri; Central Hospital Sapele; Central Hospital Agbor and Federal Medical Centre, Asaba all in Delta State of Nigeria. The case records of some 60 randomly selected patients treated with antibiotics for orofacial bacterial infections in each of the hospitals over a period of two to three months were reviewed, adding up to a total of 300. The antibiotics prescribed for the treatment of the following bacterial infections: acute dento-alveolar abscess, lateral periodontal abscess, post-extraction infection (dry socket), pericoronitis, acute ulcerative gingivitis (AUG), supurative sialadenitis (salivary gland infection) and cellulitis were recorded. Also recorded were the prescribed antibiotic regimen (drug, dose and duration).

ANALYSIS The percentage of the number patients administered with each of the antibiotics and the durations prescribed for each antibiotic were generated and compared. RESULTS Four different antibiotics were commonly prescribed as the drug of first choice for the treatment of orofacial bacterial infections-ampicillin, penicillin, metronidazole and erythromycin. A total of 300 cases of bacterial infection were reviewed in this study. The number of cases of infection per hospital is recorded in


Okagbare T. E. and Emudianughe T. S: Continental J. Medical Research 2: 1 - 5, 2007

Table 1 and it shows that the estimates of the number of each type of infection were similar in all the five hospitals. The acute conditions which appeared most frequently were dento-alveolar abscess 122 (40.7%) and pericoronitis 70 (23.3%). Suppurative salivary gland infection was very uncommon 6 (2%). Majority 138-186 (46-62%) of the patients received ampicillin for all conditions other than AUG, for which most 22(91.7%) patients received metronidazole (Table 2). The duration of drug therapy was variable, being either 3, 5 or 7 days (Table 2). A 5-day course was prescribed for all infections, with the exception of AUG, for which 3 days of therapy was prescribed most frequently 11 (45.8%).

Table 2 Antibiotic of choice and duration of therapy for the treatment of acute orofacial infection Antibiotic Prescribed, % Acute infection Amp Pen Metr Eryth Duration 3 days prescribed, % 7days

5 days

Acute dento-alveolar abscess Lateral periodontal abscess Post-extraction infection Pericoronitis Acute ulcerative gingivitis Salivary gland infection Cellulitis

69 63 63 58 5 41 6

13 11 6 4 1 10 91

9 19 21 32 92 38 2

9 7 10 6 2 11 1

5 8 7 10 46 2 69

91 89 82 81 44 88 26

4 3 6 9 10 10 5

Key: ampicillin (Amp), Penicillin (Pen), metronidazole (Metr), erythromycin (Eryth)

DISCUSSION The infections reviewed in this study have characteristic clinical presentations and diagnosis can therefore usually be made by clinical examination and history. None of the diagnosed infections were proven microbiologically, since it is not a normal practice in general dental situation to make use of diagnostic microbiological laboratories. Therefore, the information reported here should be regarded as reasonable estimates and not taken as actual incidences of each type of infection. Some microbial studies have revealed a predominance of strict anaerobes in acute dento-alveolar abscess (Williams et al 1983, Lewis et al 1986); a majority of which are penicillin-resistant strain of Bacteriodes species (Heimdahl et al 1980). These findings have given rise to recommendations for the use of antibiotics such as metronidazole (Ingham et al 1977), cephalosporins (Cumming et al 1980) or clindamycin (Schuen et al). Clindamycin appears to be more effective against infections involving the bone or fractures,


Okagbare T. E. and Emudianughe T. S: Continental J. Medical Research 2: 1 - 5, 2007

although it is recommended that its usage should be restricted, unless specifically indicated by bacterial culture, due to the possibility of inducing colitis (Mehrohof et al 1976).

Of the drugs prescribed for bacterial infection, three agents (ampicillin, penicillin and metronidazole) accounted for the vast majority (85-97%) of first antibiotics of choice. The popularity of ampicillin here is probably based on the fact that it is easily available, cheap and effective against the majority of bacteria encountered in acute dental infections, and adverse reactions are rare. A high-dose of penicillin regimen was always the treatment of choice for cases of cellulitis like Ludwig’s Angina for which 600 to 1200mg (1 to 2 mega units) benzylpenicillin i.m. or i.v. 6 hourly is commonly prescribed. Metronidazole was the most frequently prescribe agent for AUG and second most frequently prescribed agent for the treatment pericoronitis. This is to be expected since metronidazole, which is only effective against strict anaerobes, has been shown to perform well in the treatment of both these conditions. The low incidence of the use of metronidazole for the treatment of acute dento-alveolar abscess is perhaps surprising, because it has been shown that strict anaerobes predominate and are the most likely pathogens in this infection (Lewis et al 1986, 1988). In addition, metronidazole and a closely related drug ornidazole have been shown to be effective clinically in the treatment of acute dental abscess (Ingham et al 1977, von Konow et al 1983). In this study, the duration of therapy varied from 3 to 7 days, with a 5-day regimen being most popular, apart from the 3-day course of therapy employed (46%) in the management of AUG. It has been recommendation that therapy should be continued for 2 days after resolution of infection. Historically, these duration times may have been adopted due to the fear of encouraging the emergence of resistant bacteria. However, it has been suggested more recently that the use of antibiotics beyond the time of clinical improvement encourages the emergence of resistance bacterial forms rather than reducing it (Lacey et al 1984). The present study has revealed that these four antibiotics, in a variety of regimens, are being used successfully in the management of acute orofacial infections in general dental practice in Delta State of Nigeria. However, it is important that patients who failed to respond to present treatment options or present with unusual clinical signs be recognized, since this may indicate an underlying systemic disease. This is particularly relevant with the prevalence of patients suffering from HIV/AIDS.

ACKNOWLEDGEMENTS We gratefully acknowledge the assistance of the medical record personnel of the five hospitals involved in this study.


Okagbare T. E. and Emudianughe T. S: Continental J. Medical Research 2: 1 - 5, 2007

REFERENCES Chow A W, Roser S M, Brandy F A, (1978). Orofacial odontogenic infections. Ann. Intern. Med; 88:392402. Cumming C E, Ross P W, Smith G F, Lough H, Moyes A, (1980). The use of cefadroxil in the treatment of acute orofacial infections. J. Dent; 127: 247-251 Heimdahl A, von Konow L, Nord C. E, (1980). Isolation of beta –lactamase producing bacteroides strains associated with clinical failures of penicillin treatment of human orofacial infections. Arch. Oral Biol; 25: 689-692. Ingham H R, Hood F J C, Bradburn P, Tharagonnet D, Selkon J B, (1977). Metronidazole compared with penicillin in the treatment of acute dental infections. J. Oral Surg; 14: 264-269. Lacey R W, (1984). Evolution of microorganisms and antibiotic resistance. Lancet; 2: 1022-1025. Lewis M A O, MacFarlane T W, McGowan D A, (1986). Quantitative bacteriology of dentoaveolar abscesses. J. Med. Microbiol; 21: 101-104. Lewis M A O, MacFarlane TW, McGowan D A, MacDonald D G, (1988). Assessment of the Pathogenicity of bacterial species isolated from acute dentoaveolar abscess. J. Med. Microbiol; 27: 109 – 116. Mehrhof A I, (1976). Clindamycin: an evaluation of its role in dental patients. J. Oral Surg; 43: 207-215. Schuen N J, Panzer J D, Atkinson W H, (1974). A comparison of clindamycin and penicillin in the treatment of oral infections. J. Oral Surg; 32: 503 – 505. von Konow L, Nord C E, (1983). Ordnidazole compared to phenoxymethylpenicillin in the treatment of orofacial infection. J. Antimicrob. Chemother, 11: 207 – 215. Williams B L, McCann G F, Schoenknecht F D, (1983). Bacteriology of dental abscess of endodontic origin. J. Clin. Microbiol; 18: 770 - 77

Received for Publication: 07/11/2007 Accepted for Publication: 24/12/2007 Corresponding Author: Dr. T. E. Okagbare Department of Preventive Dentistry, College of Health Sciences, Delta State University, Abraka, Nigeria. E-mail:tuweyire


Continental J. Medical Research 2: 6 - 13, 2008 © Wilolud Online Journals, 2008.

AN OVER VIEW OF THE CLINICAL RELEVANCE OF THE KNOWLEDGE OF THE ORMAL AND ABNORMAL ANATOMY OF THE SELLA TURCICA, USING PLAIN RADIOGRAPHS Zagga AD1 and Saidu SA2 Departments of Anatomy and Radiology. College of Health Sciences. Usmanu Danfodiyo University, Sokoto, Nigeria.
1 2

ABSTRACT Careful examination of the changes within the sella is far more rewarding than measuring the dimensions of the sella. A review was composed via Medline Internet search and literature search. Knowledge of the normal and abnormal anatomy of the sella turcica is significant clinically in the determination of increased intracranial pressure, the determination of direct pressure erosion of the sella from external cases in the immediate vicinity of the sella and the detection of intrasellar expanding lesions. It is concluded that deformity of the sella turcica is often the only clue that abnormality exists within the cranium: hence a familiarity with its anatomy and radiologic appearance is essential. KEY WORDS: Sella turcica, knowledge, normal and abnormal anatomy, clinical relevance.

INTRODUCTION The sella turcica (‘Turkish saddle’) is the superior saddle shaped concavity on the intracranial surface of the body of the sphenoid bone (Chummy and Sinnatamby, 2004). It contains the central hypophyseal or pituitary fossa which lodges the hypophyses cerebri or pituitary gland. It has been shown that about 80% of the sella is occupied by the pituitary gland and that the gland may increase in size during pregnancy (DiChiro and Nelson, 1962). It has also been suggested that the sella increases in size with age (Israel, 1970). The anatomy of the sella turcica is variable in size and shape. It has been classified into three types: round, oval and flat (Jones et al., 2004). It can also be deep or shallow in both children and adults (Isadore, 1976). In profile, the sella at times has a somewhat high concave appearance caused by what appears to be an excavation beneath the anterior clinoids. This is frequently described in children and has no pathological significance. The floor of the sella turcica, which in most cases is concave, may be, flat or even convex (Bruneton et al., 1979). Careful examination of the changes within the sella is far more rewarding than measuring the dimensions of the sella (Jones et al., 2004). This paper aims at looking into the relevance of the familiarity with the normal and abnormal anatomy of the sella turcica in clinical practice, using plain radiographs. Normal anatomy of the sella turcica. The sella turcica (‘Turkish saddle’) is the superior saddle shaped concavity on the intracranial surface of the body of the sphenoid bone (Chummy and Sinnatamby, 2004). It contains the central hypophyseal or pituitary fossa which lodges the hypophyses cerebri or pituitary gland. Anteriorly its bony landmarks include the planum sphenoidale, the limbus sphenoidale, the chiasmatic sulcus, and the tuberculum sellae. Anterolateral landmarks include the optic canal, the anterior clinoid processes, and the optic strut, which forms the floor of the optic canal. The floor of the sella is the roof of the sphenoidal air sinus. Posteriorly,


Zagga AD and Saidu SA: Continental J. Medical Research 2: 6 - 13, 2008

the sella is bounded by the dorsum sellae and the posterior clinoid processes; its lateral margins are the carotid sulci, and its superior boundary is the diaphragma sellae (Newton and Potts, 1971). The planum sphenoidale: - The planum sphenoidale is a thin well-defined plate of bone that extends from the cribriform plate to the limbus sphenoidale. The central portion, which extends forward and articulates with the cribriform plate, has been termed the ethmoidplate. Its lateral extensions form the roofs of the optic canals and blend with the anterior clinoid prosseses. The planum sphenoidale has a smooth upper surface that may be slightly concave. The width of the planum is determined by the degree of separation between the two orbits (Newton and Potts, 1971). The limbus sphenoidale:-The limbus sphenoidale marks the posterior boundary of the planum sphenoidale. The appearance of the limbus varies with the shape of the chiasmatic sulcus. When the chiasmatic sulcus is concave, the limbus sphenoidale is prominent. On the other hand, when the chiasmatic sulcus is convex the limbus is barely discernible (Newton and Potts, 1971). The chiasmatic sulcus: - The chiasmatic sulcus is a depression of variable depth, spanning the distance between the cranial openings of the optic canals. Anteriorly it is bounded by the limbus sphenoidale, and posteriorly the tuberculum sellae. The chiasmatic sulcus is usually horizontal, but it may at times be almost vertical. The width of the chiasmatic sulcus is determined by the width of the planum sphenoidale in an inverse relationship. Thus, a wide planum, leads to a narrow chiasmatic sulcus (Newton and Potts, 1971). The tuberculum sellae: - The tuberculum sellae is a transverse ridge that forms the posterior margin of the chiasmatic sulcus as well as the anterior margin of the pituitary fossa. It spans the distance between the anterior limits of the carotid sulci. This distance is variable and determines the length of the tuberculum sellae. The prominence of the tuberculum sellae is related to the shape of the chiasmatic sulcus (Newton and Potts, 1971). The anterior clinoid processes: - The anterior clinoid processes are formed by the medial prolongation of the free posterior margin of the lesser wing of the sphenoid bone. Between the anterior clinoid processes and the tuberculum sellae is a notch which marks the termination of the carotid groove for passage of the internal carotid artery. Thus, the anterior clinoid processes form the anterior and lateral borders of the carotid sulcus. The appearance, shape, and thickness of the anterior clinoid processes vary considerably. They are frequently asymmetric, and occasionally one may be vestigial or absent. The tips of the anterior clinoid processes are situated slightly lateral to the posterior clinoid processes (Newton and Potts, 1971). The middle clinoid processes: -The middle clinoid processes are in constant elevations on the anterior wall of the pituitary fossa, medial to the carotid artery. At this level the internal carotid arteries pierce the duramater and become intradural. Ossification of the intraclinoid bridge between the anterior and middle clinoid processes leads to the formation of the caroticoclinoid canal (Newton and Potts, 1971). This canal is believed to be a developmental anomaly (Kier, 1968). The floor of the sella: - For purposes of description, the floor of the sella turcica will include portions of the anterior and the posterior walls of the pituitary fossa. The floor of the sella turcica is therefore considered to extend from the tuberculum to the dorsum sellae. In the sagittal plane the floor usually has a rounded appearance, but its horizontal portion may be relatively straight. In the coronal section the horizontal portion of the floor usually has a slightly convex or flat appearance. Occasionally it has a slight downward concavity. The sellar floor may be asymmetric, sloping downward more on one side than on the other. The horizontal portion of the carotid sulcus forms the lateral margin of the floor. The boundary between the floor and the carotid sulcus is normally rounded (Newton and Potts, 1971). The carotid sulcus: - The carotid sulcus is a shallow groove along the superolateral aspect of the sphenoid sinus that is formed by the cavernous portion of the internal carotid artery. The depth of the carotid sulcus varies. The sulcus is usually shallow but may have a prominent inferior border (Newton and Potts, 1971).


Zagga AD and Saidu SA: Continental J. Medical Research 2: 6 - 13, 2008

The dorsum sellae: - The dorsum sellae is the vertical posterior boundary of the sella and is formed by two lateral struts topped by a horizontal strut. It varies greatly in shape and thickness (Newton and Potts, 1971). Mahmoud (1958) found that the thickness of the dorsum ranges from 2 to 7 mm but that only the lateral portions are thick. The central portion is a well-defined hollow between the sturdier lateral pillars and forms a bed for the posterior portion of the pituitary gland. The central portion is often extremely thin. It may even be absent so that a foramen is found within the dorsum sellae (Fry and du Bouley, 1965). The lateral aspect of the dorsum sellae may be grooved by the sixth nerve or by a persistent trigeminal artery. The anterior wall of the dorsum sellae is smooth, whereas the posterior aspect is rough. The roughness of the posterior aspect of the dorsum is due to the dural venous plexus in this location. The posterior clinoid processes are the lateral and superior extensions of the dorsum sellae (Newton and Potts, 1971). The posterior clinoid processes: - The posterior clinoid processes are the lateral and superior extensions of the dorsum sellae. The tips of the posterior clinoid processes are usually rounded, and they project forward and slightly laterally. Occasionally the tips are pointed and may extend forward to join with the anterior clinoid processes (bridged sella) (Newton and Potts, 1971). The diaphragma sellae: - The diaphragma sellae is the dural fold formed by the anterior extension of the tentorium. It is attached anteriorly to the tuberculum, posteriorly to the dorsum, and laterally to the interclinoid ligament, which joins the anterior and posterior clinoid processes. The diaphragma sellae has a central opening that transmits the pituitary stalk (Newton and Potts, 1971). Busch (1951) reported that the thickness of the diaphragma, as well as the size of the opening, varies. He examined 788 sellae turcicae and described three main types of diaphragma sellae: (1) diaphragma forms a complete covering with only a small opening for the pituitary stalk (41.9%); (2) the diaphragma is incomplete, with an opening for the stalk less than 3 mm (37.6%); and (3) the diaphragma is represented by only a rim of tissue less than 2 mm in width (20.5%). In a similar study the opening for the pituitary stalk was noted to be greater than 5 mm in 39% of the cases (Bergland, 1968). In sagittal section the diaphragma sellae usually slopes slightly downward into the sella (Newton and Potts, 1971). Abnormal sella. Small sella There is no constant relationship between the size of the sella and the size of the hypophysis. It is very unusual for the sella to be abnormally small. The sella that appears small in the lateral projection may nevertheless be normal because of its greater than average width (Fisher and DiChiro, 1964). A small sella may be found in pituitary hypopituitarism (Riach, 1966), and growth hormone deficiency (Fisher and DiChiro, 1964) if the onset of the disease is before the age of six years. Fisher & DiChiro (1964) found the sella to be small in 56.8% of forty-four subjects with hypopituitarism. Fisher and DiChiro (1964) also found a small sella in 13.5% of subjects with genetic dwarfism. The sella turcica was also reported to be small in a 13½ year old boy with Cushing’s syndrome due to an adrenocortical adenoma (Steinbach et al., 1963). A small sella was also reported in Sheehan’s syndrome (Meador and Worrel, 1959). A small sella in lateral profile may also be found in dystrophia myotica but is not diagnostic of this condition (Caughey, 1952). The sella may be vestigial. This entity has been termed dysplasia of the sella (Lundberg and Gemzell, 1966). Large sella without local bone destruction Intrasellar masses may cause enlargement of the sella with preservation of cortical bone. In these instances there is uniform enlargement with a deepening of the floor, and thinning, as well as posterior displacement of the dorsum. Uniform enlargement of the sella is most commonly seen in pituitary tumors, which include chromophobe adenoma, easinophilic adenomas, basophilic adenoma, Nelson’s Syndrome, polyadenomatosis, and carcinoma of pituitary. Others are empty sella syndrome, craniopharyngioma, intrasellar aneurysm, hypothyroidism, hypogonadism, neurofibromatosis and oxycephaly (Bergland et al., 1968). Large sella with local bone destruction or erosion


Zagga AD and Saidu SA: Continental J. Medical Research 2: 6 - 13, 2008

Erosion of undersurface of anterior clinoid processes and chiasmatic sulcus Erosion of undersurface of anterior clinoid and chiasmatic sulcus can result from glioma of optic chiasm, optic nerve glioma, J sella, optic nerve sheath tumor, pituitary adenoma, aneurysm, dilated third ventricle, craniopharyngioma, frontal lobe tumour, Hunter’s syndrome/mucopolysaccharidoses type 11/gargoylism, neurofibromatosis and carotid cavernous fistula (Newton and Potts, 1971). Erosion of upper surface of anterior clinoid processes This condition may result from supra-sellar meningioma, increased intracranial pressure due to dilated third ventricle, aneurysm, frontal lobe tumour, suprasellar arachnoid cysts in gargoylism (Newton and Potts, 1971). Localized erosion of floor Localized erosion of the sella turcica floor may be due to nasopharyngeal tumor, sphenoid sinus mucocoele, metastases e.g. from carcinoma of the prostate, basal encephalocoele, giant cell tumor, leiomyoma, juvenile nasopharyngeal angiofibroma and postoperative sella (Newton and Potts, 1971). Erosion of dorsum and posterior clinoid processes Lateral surface: - This may be affected by parasellar meningioma, neurofibroma, chordoma, aneurysm of internal carotid artery, anomalous vessels, and miscellaneous conditions; e.g. epidermoid and subarachnoid cysts (Newton and Potts, 1971). Anterior surface of dorsum: - This may be eroded by intrasellar masses, including pituitary tumors (Newton and Potts, 1971). Upper surface of dorsum and posterior clinoid processes: - These may be eroded by the supra-sellar masses such as craniopharyngioma, optic chiasm glioma, hypothalamic tumor, meningioma, subarachnoid cyst, aneurysm, histiocytosis X, atypical teratoma (ectopic pinealoma), lipoma, dilated third ventricle, frontal glioma and dermoid cyst (Newton and Potts, 1971). Posterior surface: - The posterior surface of the dorsum sellae may be eroded by posterior fossa tumours (e.g. astrocytoma in children), metastasis (e.g. from colloid carcinoma), arachnoid cyst and basilar artery aneurysm (Newton and Potts, 1971). Local bony sclerosis and change in texture This may be brought about by disease conditions like fibrous dysplasia, ossifying fibroma, meningioma, metastatic tumours to the skull, suprasellar tumors (such as craniopharyngioma, atypical teratoma), osteochondroma, osteoma, chondroma of the skull, the clivus, the cerebello pontine angle, and the planum (Minagi and Newton, 1969), soft tissue masses, miscellaneous conditions, such as infections (e.g. tuberculosis, coccidioidomycosis, or pyogenic abscess), trauma (e.g. fracture of the dorsum sellae, floor of the sella and clivus) (Engels, 1961). Changes in sella in increased intracranial pressure Erosion of sellar cortex: Erosion of the cortical bone that lines the pituitary fossa is usually seen earliest at the anterior part of the base of the dorsum. The erosion often spreads to involve most of the sellar floor but occasionally is first recognized more anteriorly (Newton and Potts, 1971). Mahmoud (1958) showed that the process is truly an erosion caused by osteoclasts and that the pits produced in the lamina dura tend to coalesce. In the earlier stages optimal roentgenograms may reveal pinpoint interruptions of the white line of the lamina dura. As erosion progresses, the roentgenographic appearance becomes more obviously abnormal. The outlines of the sella (i.e. lamina dura) are described as rubbed out or osteoporotic (Newton and Potts, 1971). Erosion of top of dorsum sellae:


Zagga AD and Saidu SA: Continental J. Medical Research 2: 6 - 13, 2008

Destruction of top of dorsum may include loss of those rough elements of bone that are the site of attachment of the petroclinoid ligaments. As a result of erosion of the posterior clinoid processes, the dorsum in the lateral view may appear as a truncated cone with a flattened top or as a thin spike. In both cases the upper margins are poorly demarcated unless all that remains is a single flake of bone (Newton and Potts, 1971). Changes in anterior clinoid processes: The anterior clinoid processes are affected late and in ways different from those of the posterior. In long standing hydrocephalus, the entire base of the skull may be thin. The anterior clinoid processes become thinner and sharper, and in lateral views they may be difficult to recognize. In the posteroanterior inclined projection the anterior clinoid processes and the lesser wings of the sphenoid form frail and indistinct lines (Newton and Potts, 1971). Enlargement of sella When the sella enlarges as a result of raised intracranial pressure or hydrocephalus, invariably some erosion or alteration of shape occurs. In raised intracranial pressure the sella may become enlarged in one of three ways: (1) the lamina dura may be destroyed so completely that it no longer has the strength to withstand intracranial pressure as a result the sellar floor herniates downward into the sphenoid sinus; (2) coalescence of erosions in cancellous bone, particularly at the base of the dorsum sellae, may cause the cavity of the sella to extend downward into the clivus, this extension may be appreciated in histologic sections but the cavity does not reach sufficient size to be recognised easily on roentgenograms; (3) enlargement may take place by less dramatic changes in long standing conditions. Erosion is not a feature; but growth under abnormal stimuli causes a peculiar shape of sella. The commonest of these peculiarities is seen sufficiently often to be considered characteristic of chronic obstructive (non-communicating) hydrocephalus. It is not a true enlargement of the sellar cavity itself. The dorsum is short, indeed sometimes extremely so. The longest axis of the sella turcica in the lateral view is more or less in line with clivus. The reason for this appearance is that the anterior sellar wall is elongated upward into the chiasmatic sulcus, which itself is enlarged. Commonly the anterior clinoid processes, presumably because of unusual torsion on their ligaments, are blunt and massive. The upper cavity, limited anteriorly by the chiasmatic sulcus, is occupied by the dilated third ventricle. The cortex is often well formed and without erosions (Newton and Potts, 1971). Pressure changes of some sort may be noted in about one third of patients with tumors distant from the sella. Of these, 20% do not have papilledema, and amongst them are many who, despite short clinical histories and the absence of other signs of raised intracranial pressure, have longstanding and operable tumors. The earliest detectable abnormality is usually a loss of the lamina dura. Under ideal circumstances this loss is occasionally detected within a few weeks after onset of raised pressure (Tonnis et al., 1954). Erosion of lamina dura As an isolated sign, without any other abnormality of the sella turcica, erosion of the lamina dura was found in about 12% of intracranial tumours (Category I erosion) (du Bouley and El Gammal, 1966). In about twice this number of patients with either infra- or supratentorial tumours, erosion of the lamina dura and some additional sellar abnormality were seen. Such erosion occurs in many cases of aqueduct stenosis, but virtually never in communicating hydrocephalus (Newton and Potts, 1971). Erosion of top and back of dorsum sellae Tumours of the posterior fossa cause erosion of the top and back of the dorsum sellae (category II erosion) (du Boulay and El Gammal, 1966), about twice as often as do supratentorial tumours. Even so, however, only 10% of posterior fossa tumours are associated with such erosion. In patients with supratentorial tumours, category II change is usually associated with other sellar abnormalities, particularly an extensive erosion of the lamina dura. With hydrocephalus resulting from infratentorial masses, it may be seen alone, however. Still more commonly this type of erosion results from a suprasellar tumour (Newton and Potts, 1971).


Zagga AD and Saidu SA: Continental J. Medical Research 2: 6 - 13, 2008

Erosion of planum sphenoidale: After many months of raised intracranial pressure, erosion of the lamina dura may have extended to the planum sphenoidale. The usually crisp white line of that structure blurs or disappears. Nearly always before this disappearance, the top of the dorsum has also been damaged. The combination of erosion of the top of the dorsum sellae, of the lamina dura, and of the planum sphenoidale (category III sellar change) (du Bouley and El Gammal, 1966) is nearly always caused by a slow growing frontal or posterior frontal tumor. Often this tumour is glioma, sometimes a meningioma. Differentiation between the effects of raised intracranial pressure and the effects of local tumours. Destruction of the cortical lining of the pituitary fossa may also accompany the growth of tumours, particularly pituitary tumours, within the sella. After thorough examination of the plain roentgenograms of the skull, only about 3% of all pituitary tumours cause confusion regarding diagnosis. The majority of the plain roentgenograms present fairly obvious evidence of the true nature of tumour (Newton and Potts, 1971). Ballooning of the pituitary fossa is the most common of the additional and specific signs in pituitary adenoma. Sclerosis of bone betrays a meningioma or occasionally a chordoma. Rarely, gliomas of the optic chiasm cause a characteristic excavation in the anterior part of the sellar region. Craniopharyngioma is usually suprasellar and retrosellar. Although a fair number of these tumours protrude into the cavity of the pituitary fossa as well, half of all craniopharyngiomas cause a shortened and extremely flat dorsum. The cortical top of the dorsum in these cases is usually preserved. The abnormality may therefore be distinguished from that caused by frontal tumours and from those producing hydrocephalus (Newton and Potts, 1971). Differentiation between the changes of pressure in adults and the effect of local tumour and disease is more difficult in the following circumstances: (1) when there is apparently complete destruction of the dorsum sellae; in these situations one should search for displacement of fragments, away from the cavity of the sella (intrasellar tumor), or toward it (hydrocephalus and craniopharyngioma); (2) when, occasionally, erosion of the lamina dura by pituitary adenoma is accompanied by enlargement of the sella, which nevertheless is not characteristically ballooned in shape; (3) rarely, when metastatic carcinoma has spread from the pituitary fossa or the suprasellar region; destruction, or at least an obvious change in texture, extends more deeply into the bone than is the case with raised intracranial pressure (4) when the lesion, usually an aneurysm of the internal carotid, is truly parasellar; in these situations the lateral roentgenogram may suggest at first glance an enlargement and osteoporosis. Careful examination of all views reveals the true state. A faint but sharply outlined dorsum (of which as much as one lateral half may be missing), destruction of one lateral half of the sellar floor, and destruction usually of an anterior clinoid process are all visible (Newton and Potts, 1971). Changes in sella in childhood. Similar to adults, the lamina dura in children is eroded in similar situations and after a similar length of time. Changes in sella in childhood may be over looked because diastasis of the sutures attracts the attention of the radiologists. Destruction of the top of the dorsum results particularly from tumours of the posterior fossa that cause hydrocephalus. Rarely destruction may be seen as a result of long-standing frontal and fronto-parietal masses that push the base of the brain against the base of the skull (Newton and Potts, 1971). In children, however, opportunities for the more chronic sellar changes are fewer. Moreover, slow-growing frontal tumours, which in adults cause many of the most severely damaged sellae, are exceptional before the age of 30. Consequently chronic sellar changes in children tend to be restricted to those suffering from developmental abnormalities, especially aqueduct stenosis. In infancy, changes resulting from communicating hydrocephalus are confined to a simple elongation of the sella, which may accompany a general expansion of the head (Newton and Potts, 1971).


Zagga AD and Saidu SA: Continental J. Medical Research 2: 6 - 13, 2008

Changes in sella with relief of raised intracranial pressure. Roentgenograms obtained after excision of cerebral tumors and after operative procedures for the relief of hydrocephalus have been studied. These indicated that osteoclastic resorption ceases rapidly and is replaced by increased new bone formation. Within a few weeks the lamina dura reappeared and some evidence of repair of the dorsum sellae and posterior clinoid processes was seen. The fact that bone (e.g. the posterior clinoid processes) should reappear, must mean that some periosteal or osteoid tissue had not been destroyed entirely. Total destruction and displacement, however, cannot be corrected, so the reformed bone in advanced cases is abnormal in shape. The dorsum may be short, or the cavity of the sella enlarged (Newton and Potts, 1971). From observation of patients with recurrent symptoms, the susceptibility to erosion of the reformed lamina dura appears to be much less than that of the original bone lining. A second episode of raised intracranial pressure rarely causes erosion (Newton and Potts, 1971). CONCLUSION It is concluded that deformity of the sella turcica is often the only clue that abnormality exists within the cranium: hence a familiarity with its anatomy and radiologic appearance is essential. REFERENCES Bergland, R.M., Ray B.S., Torack, R.M. 1968. Anatomical variations in the pituitary gland and adjacent structures in 225 human autopsy cases. J. Neurosurg.; 28:93-99. Bruneton, J. N., Drouilard, J.P., Sabatier, J.c., Elie, G.P and Travenir, J.F, 1979. Normal variants of the sella turcica. Comparison of Plain radiographs and tomograms in 200 cases. Radiology;131:99104. Busch, W. 1951. Die Morphologic der sella turcica und ihre Bexiehungen zur Hypophyse, Arch. Path. Anat.; 320: 437-458. Caughey, J. E. 1952. Bone changes in the skull in dystrophia myotonica, J. Bone Joint Surgery.; 34B, 343359. Chummy S. and Sinnatamby (2004). (Editors) Last’s Anatomy: Regional and Applied; 10th edition. Churchill Livingstone; Edinburgh, London,NewYork, Philadelphia, Sydney, Toronto.pp501-504. DiChiro, G. and Nelson, K. B., 1962. The volume of the sella turcica. AJR Am. J. Roentgenol.; 87: 9891008. du Boulay, G. H., and El Gammal, T. 1966. Classification, clinical value and mechanism of sella turcica changes in raised intracranial pressure, Brit. J. Radiol.; 39: 422-442. Engels, E. 1958. The roentgen appearance of the carotid sulcus of the sphenoid bone, Acta Radiol.; 49: 113-116. Engels, E. 1961. Basal skull fractures involving the sella turcica. Clin. Radiol.; 12: 177-178. Fisher, R. L. and DiChiro, G. 1964: The small sella turcica. Amer.Roentgenol.; 91: 996-1005. Fry, K. I., and du Boulay, G. H. 1965. Some observations on the sella in old age and arterial hypertension, Brit. J. Radiol.; 38: 16-22. Isadore Meschan M.A. M.D, 1976. An Atlas of Anatomy Basic to Radiology. 1st Edition. W. B. Saunders Company; Philadelphia, London, Toronto. pp343-349.


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Israel, J. H, 1970. Continuing growth in sella turcica with age, AJR Am. J. Roentgenol.; 108: 516-527. Jones, R.M., Faqir, A., Millet, D.T., Mous, K.F., McHugh, S, 2004. Bridging and Dimensions of Sella Turcica in Subjects Treated by Surgical Orthodontics Means or Orthodontics only. The Angle Orthodontist; 75(5): 714-718. Kier, E.L. 1968. The infantile sella turcica. New roentgenologic and anatomic concepts based on a developmental study of the sphenoid bone. AJR Am. J. Roentgenol.; 102:747-767. Laschi, G. 1931. Un caso di foramen dorsi sellae, Radiol. Med.; 18: 707-712. Lundberg, P. O. and Gemzell, C. 1966. Dysplasia of the sella turcica: Clinical and laboratory investigations in three cases, Acta Endocrinol.; 52:478-488. Mahmoud, M.S. 1958. The sella in health and disease: value of the radiographic study of the sella turcica in morbid anatomical and topographic diagnosis of intracranial tumours, Brit. J. Radiol.; Supp. 8, 1-100. Meador, C. K. and Worrel, J.L. 1959. The sella turcica in post- partum pituitary necrosis (Sheehan’s Syndrome). Ann. Intern. Med.;65: 252-264. Minagi, H., and Newton, T. H. 1969. Cartilaginous tumours of the base of the skull, AJR Am. J. Roentgenol.; 105: 308-313. Newton, T.H. and Potts, D.G. 1971. (Editors) Radiology of the skull and brain, The Skull: Volume 1, Book 1; The CV Mosby Company; Saint Louis; pp359-405. Riach, I.C.F. 1966. The pituitary fossa in childhood with particular reference to hypopituitarism, Brit. J. Radiol.; 39: 241-243. Steinbach, H. L., Noetzei, M., and Ozoof, M. B. 1963. Small pituitary fossa in Cushing’s syndrome due to adrenal neoplasm, Neuro Eng. J. Med.; 269: 1286-1289. Tonnis, W., Schiefer, W., and Rausch, F. J. 1954. Sella veranderungen bei gesteigerten schadelinnendruck, Deutsch Z. Nervenheilk., 171: 351-369. Received for Publication: 07/11/2007 Accepted for Publication: 24/12/2007 Corresponding Author: Dr. A.D. Zagga, Department of Anatomy, College of Health Sciences, Usmanu Danfodiyo University, PMB 2346, Sokoto, Nigeria. E Fax: +234-80-231514.


Continental J. Medical Research 2: 14 - 19, 2008 © Wilolud Online Journals, 2008.

POST PRANDIAL BLOOD PRESSURE CHANGES IN PATIENTS WITH CHRONIC RENAL FAILURE DURING HEMODIALYSIS. Onyemekeihia UR1, Esume CO 2, Bamgboye LE,3 Anyanwu BE4 Department of Medicine, Nephrology Unit, Central Hospital, Warri. 2 Department of Pharmacology and Therapeutics, Delta State University, Abraka. 3Nephrology Unit, St. Nicholas Hospital, Lagos. 4 Department of Family Medicine, Delta State University, Abraka.

ABTRACT: Hypotension is a recognized complication of hemodialysis (HD), and many factors had been implicated one of which is eating before or during hemodialysis. Postprandial hypotension (PPH) was first recognized in 1977 by Seyer Hanseen. PPH is defined as decrease in systolic blood pressure or diastolic blood pressure of 20mmhg or more and 10mmhg or more respectively. The mechanisms of PPH are not fully understood but factors such as Impairment of baroreflex function, Inadequate postprandial increase in cardiac output, Impaired peripheral vasoconstriction, Insulin induced vasodilatation and Release of vasodilatory gastrointestinal peptides with attendant splanchnic blood pooling have been implicated. This study investigates the effect of food on blood pressure of patients during hemodialysis, with the view of proffering advice about meals during HD. The study was carried out over a six weeks period in St. Nicholas hospitals, Lagos, a privately owned 50-bedded hospital with a well developed renal transplant unit and a state of the art dialysis centre. There is also an efficient catering unit. Sixty one subjects were studied, 31 sessions being test session and 30 being controls. Of the 31 test sessions, 18 (58%) were males; and 13 (42%) were females while 18 (60%) of the controls were males and 12(40%) females, with age ranging from 15-79 years. The nature of the study was explained to the patients and consent obtained. Those who wished to eat were given a standard meal of their choice. Before the start of HD or eating, initial BP was taken. Freizinus(R) 4008 HD machines and bicarbonate dialysate fluid were used for all patients. Blood pressure was monitored hourly for 4 hours. The patients who took antihypertensives before hemodialysis or had cause to take them during HD were excluded from the study. Those who did not eat were used as controls. There was Postprandial hypotension in 7 (23%); 6(86%) Diastolic Blood Pressure only, 1 (14%) both Systolic blood pressure and Diastolic Blood Pressure. All the patients were monitored for symptoms of weakness, dizziness, and chest pain. KEYWORDS: Postprandial, blood pressure, changes, patients, chronic renal failure, hemodialysis.

INTRODUCTION Hypotension is a recognized and preventable complication of HD and our current understanding of postprandial hypotension is limited by the lack of a standardized, clinically meaningful definition (Jansen,1995). Analogous to orthostatic hypotension, postprandial hypotension is commonly defined in the literature as a decrease in systolic blood pressure of 20mmhg or more within 2 hours of the start of a meal (Jansen, 1995). Postprandial hypotension also develops when the absolute level of systolic blood pressure after a meal decreases to less than 90mmhg and when the systolic


Onyemekeihia UR et al: Continental J. Medical Research 2: 14 - 19, 2008

blood pressure before a meal was greater than 100mmHg (Jansen 1995). After a meal, supine heart rate and cardiac output increase, while supine diastolic blood pressure and total systemic resistance decreases in normal healthy individuals. Food ingestion increases splanchnic and hepatic blood flow. Redistribution of volume compromises cardiac filling, decreases cardiac output, and leads to a decrease in mean arterial pressure. TABLE 1: MEAN BP AT VARIOUS TIMES DURING HD





171 ----94


23 ----14

169 23 ----- ± ----92 18


168 -----92 169 -----94

23 ± -----15 31 ± -----19

168 ---- ± 91

22 -----12


176 27 ----- ± -----95 16


169 ------93

28 ± -----18

176 26 ----- ± -----93 17


169 -----92

24 ± -----19

182 27 ----- ± ----97 15

During hemodialysis and hypovolemia, the body tries to conserve blood flow to vital organs by vasoconstriction. Food ingestion during dialysis results in an obligatory increase in splanchnic blood flow with sequestration of blood in the splanchnic pool and decreases venous return. Though eating during hemodialysis sessions is a widespread practice, it may lower blood pressure, probably due to a reduction in peripheral vascular resistance from food’s effect on alimentary tract blood flow (Barakat et al 1993). Other factors responsible are, Impairment of baroreflex function, Inadequate postprandial increase in cardiac output, Impaired peripheral vasoconstriction, Insulin induced vasodilatation and Release of vasodilatory gastrointestinal peptides (Jansen 1989). Postprandial hypotension (PPH) was first


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recognized in 1977 by Seyer-Hanseen in a patient with Parkinson’s disease (Seyer-Hanseen 1977). Sherman et al in 1988 studied postprandial blood pressure changes during hemodialysis. In this study of 9 patients who had end stage renal disease (ESRD), but not diabetes, a standard meal was given during 62 of 125 dialysis treatments. Meals consisted of two slices of white bread, 2 ounces of turkey breast, pound cake, and 4 ounces of cranberry juice. During dialysis, blood pressures were measured by sphygmomanometry at 30-minute intervals prior to meals and every 15 minutes following meals. Hypotension was defined as a 25% or greater fall in mean arterial pressure from the blood pressure recorded immediately prior to feeding time. The investigators found that there were 13 episodes of symptomatic hypotension in the 45-minute postprandial intradialytic period compared with two episodes during the corresponding fasting period.

TABLE 2: BP WITH RESPECT TO SEX AT VARIOUS TIMES 0 hr TEST Males Females 1 hr 2 hrs 3hrs 4hrs

167 ± 96 173 ± 90

25 14 22 15

165 ± 92 172 ± 91

24 17 23 14

163 31 ± 94 20 175 31 ± 94 19 167 25 ± 93 17
186 29 ± 95 16

166 ± 94 172 ± 93

25 19 31 16

167 ± 91 172 ± 93

22 16 25 16


166 23 ± 94 12
173 23 ± 90 16

164 25 ± 92 15
172 29 ± 91 19

169 22 ± 93 15
184 30 ± 94 19

176 26 ± 98 13
188 28 ± 97 17

females CONTROL

Barakat et al in 1993 reported that food ingestion during dialysis causes hypotension primarily because of decrease in systemic vascular resistance. Other workers have demonstrated postprandial hypotension during Haemodialysis ( Shibagaki 1998, Zocalli 1989 and Hirakata 1987). It May result in syncope, fall, dizziness, weakness, angina pectoris and stroke. Postprandial hypotension is distinct from and probably more common than orthostatic hypotension (Jansen and Lipsitz 1995). AIMS AND OBJECTIVES To determine the effect of food on blood pressure of patients during haemodialysis, with the view of proffering advice about feeding during haemodialysis. MATERIALS AND METHOD The study was carried out over a 6-weeks period in ST. Nicholas hospital, Lagos (SNH).SNH is a privately owned 50 bedded hospital with a well developed renal transplant unit and a state of the art dialysis centre with 7 functional dialysis machines. It also has standard and efficient catering unit. Freizinus 4008 HD machines and bicarbonate dialysate fluid was used for all patients. There were a total of 61 subjects all of whom were hypertensive but not diabetic with age ranging between 15-79 years. Thirty one of them wished to eat and were given a standard meal of their choice and used as test subjects. Thirty of them who did not eat were used as controls.


Onyemekeihia UR et al: Continental J. Medical Research 2: 14 - 19, 2008

Patients who took antihypertensive before HD or had cause to take them while on HD were excluded. The nature of the study was explained to patients, and consent obtained. Before the start of HD or eating, initial BP (O HR) was taken. Blood Pressure was monitored hourly for 4 hours by Sphygmomanometry and recorded. All the patients were monitored for symptoms of weakness, dizziness, and chest pain. The Data was analyzed using the SPSS+PC statistical package and test of significance was done using ttest.

RESULTS: Sixty one sessions were studied: 31 test sessions and 30 controls and their blood pressures are as presented in table 1. Of the 31 test sessions, 18 (58%) were males and 13 (42%) were females. Of the 30 control, 18 (60%) were males and 12 (40%) were females. The Patients ages ranged between 15 and 79 years. All patients in the sessions had hypertension. The

172 26 MMHG, with the males having a mean blood ± 99 17 167 26 177 27 pressure of MMHG and the Females MMHG. The Mean BP in the test and ± ± 94 16 93 18 169 27 174 25 MMHG and MMHG respectively. control for both sexes was ± ± 93 17 93 17
Mean Blood Pressure for all patients was There was Postprandial hypotension in a total of 7 (23%) patients; 6 (86%)of whom had Diastolic Blood Pressure reduction only and 1 (14%) had Systolic blood pressure and Diastolic Blood Pressure reduction. There was no isolated Systolic Blood Pressure Postprandial hypotension. There was increase in Blood Pressure in 9 patients (30%) of the Control. 5 of these patients (55%) had increase in Systolic blood pressure only, 2 (22%) diastolic blood pressure only; and 2(22%) a combination of Systolic Blood Pressure and Diastolic blood Pressure. There was 1 case (3%) of hypotension amongst the control. Only 2 (6%) of test group complained about weakness, but was not enough to discontinue HD. DISCUSSSION In this study we compared the effect of food on blood pressure of patients undergoing Hemodialysis using 31test subjects who ate just before or during hemodialysis and 30 control subjects who were in the fasting state during hemodialysis. When compared to the controls, there were more significant falls in blood pressure among the test group (P<0.05). Postprandial hypotension occurred in 7 (23%); while only 1% of the control had postprandial hypotension. However, there was increase in Blood Pressure in 9 (30%) Of Control; 5 (55%) Systolic blood pressure only, 2 (22%) diastolic blood pressure only; 2 (22%) Systolic Blood Pressure and Diastolic blood Pressure 2 (22%). Hypotension though a complication of hemodialysis may be worsened by eating during or before Haemodialysis. Several factors had been implicated, which could be decreased cardiac output due


Onyemekeihia UR et al: Continental J. Medical Research 2: 14 - 19, 2008

to splanchnic sequestration or decreased vascular resistance due to splanchnic vasorelaxation (Barakat et al, 1993). Although the mechanism is not fully understood, postprandial blood pressure reduction seems to be related to glucose related factors, since blood pressure only falls after oral glucose loading, but not after oral fructose, fat or protein loading. Vasoactive gastrointestinal hormones may play a role in the glucose induced vasodilation of splanchnic vasculature, but attempts to identify such hormones were unsuccessful (Jansen and Hoefnagels, 1989).It has been suggested that interference of insulin with a sympathetic response diminished by age or disease to splanchnic vasodilation, may be responsible for the postprandial fall in blood pressure in the elderly. However, vasodilator effects of insulin or a baroreflex response diminished by insulin do not seem to be involved (Jansen and Hoefnagels, 1989, 1990). The immediate cause of hypotension during dialysis is intravascular hypovolaemia which is related to the procedure itself (Shibagaki et al, 1998). To analyze the effects of food intake during hemodialysis on blood volume of the large vessels quantitatively, Shibagaki et al, (1998) monitored Hematocrit of the arteriovenous shunt blood continuously in the patients treated with hemodialysis regularly and estimated blood volume. They reported that food intake during hemodialysis decreases blood volume of the large vessels transiently but significantly. Blood pressure is dependent on blood volume especially in black subjects in whom hypertension is volume dependent. From our results, Diastolic Blood pressure seems to be mostly affected in postprandial hypotension during haemodialysis which is in consonance with work done by Sherman et al (1998). Males seem to be more affected by postprandial hypotension though the difference is not significant (P>0.05, Table 2). This may imply a sex difference in the pathophysiology of postprandial hypotension and requires further investigation. The hypotension is more marked the longer the patients stay on the dialysis machine as our results showed more significant difference in systolic blood pressure during the fourth hour (Table 1). Patients may be symptomatic of postprandial hypotension. Hypotension during dialysis may induce minor but troublesome side effects in the patient, such as nausea, vomiting, and dizziness, but may also lead to more serious complications, such as cardiac or cerebral ischemia. There are dialysis patients who hardly suffer from hypotensive episodes. However, HD-associated hypotension is especially frequent in elderly people and in those patients with a compromised cardiovascular system. Particularly the latter group, hypotension may have serious consequences (Reed and Devous, 1985). In our study, only 2 (6%) of test group complained about weakness, but was not enough to discontinue HD. Eating has adverse effects on the hemodynamics of circulation during hemodialysis and should be avoided in patients with intradialytic hypotension. (Zocalli et al, 1989). All physicians caring for chronic renal failure patients should be aware of the hypotensive effects of food ingestion during haemodialysis. Postprandial hypotension should be considered in the evaluation of syncope, falls, dizziness and other cerebral ischaemic symptoms. Consumption of meal during haemodialysis should be avoided in patients at risk of hypotension during treatment. Further studies needs to be carried out to determine the effects of sex, Body Mass Index, age, aetiology of Chronic Renal Failure, blood flow rate, type and quantity of food on Blood Pressure during hemodialysis. The limitations in the study were non uniformity in timing of meals, the type and quantity of food and blood flow rate. AKNOWLEDGEMENT The authors wish to express their gratitude to the management of Saint Nicholas Hospital, Lagos for allowing them to conduct this research with their health facility. Our gratitude also goes to all staff of the renal dialysis (SNH) unit for their meticulous and relentless efforts towards the success of this work. REFERENCES Barakat, M.M.; Nawab, Z.M.; Yu, A.W.; Lau A.H; Lng, T.S; Daugirdas, J.T (1993): Hemolytic effects of intradialytic food ingestion and the effects of caffeine. J Am Soc Nephrol.;(11):1813-8


Onyemekeihia UR et al: Continental J. Medical Research 2: 14 - 19, 2008

Hirakata, H; Onoyama, K; Hori, K; Fujimi, S; Fujishima, M (1987): The hemodynamic and humoral responses to tilting in diabetic patients on chronic hemodialysis treatment. Clin Nephrol.; 27(6):298-303. Jansen R.W. and Hoefnagels, W.H.(1989): Postprandial reduction in blood pressure after meals in the elderly. A review article. Trijdschr Gerontal Geriatr.20 (4):141-6 Jansen, R.W. and Hoefnagels,W.H.(1990):Postprandial blood pressure reduction. Neth J Med.; 37(1-2):808. Jansen, R.W and Lipsitz, LA. (1995): Postprandial Hypotension: Epidemiology, Pathophysiology, and Clinical Management. Annals of Internal Medicine. 122(4)286-95. Reed, G and Devous M. (1985): Cerebral blood flow autoregulation and hypertension. Am. J Med Sci.;285:37-44 Seyer-Hansen K. (1977): Postprandial hypotension. Br Med. J. 2:1262 Sherman R.A. Torres F. and Cody RP. (1988): Postprandial blood pressure changes during hemodialysis. Am J Kidney Dis .12(1):37-9. Shibagaki, .Y. and Takaichi,. K. (1998): Significant reduction of the large-vessel blood volume by food intake during hemodialysis. Clin Nephrol. 49(1):49-54. Zoccali, C; Ciccarelli, M; and Maggiore, Q. (1989): Postprandial alterations in arterial pressure control during hemodialysis in uremic patients. Clin Nephrol. 31(6):323-6. Received for Publication: 28/12/2007 Accepted for Publication: 24/02/2008 Corresponding Author C.O. Esume, Department of Pharmacology and Therapeutics, Delta State University, Abraka Email:


Continental J. Medical Research 2: 20 - 23, 2008 © Wilolud Online Journals, 2008.



Khalid U Khayyam1, Sazina Muzammil2, Mohd Yunus1, Zulfia Khan1 Department of Community Medicine, Jawaherlal Nehru Medical College, Aligarh Muslim University, Aligarh, UP, India 2Department of Physiology, Jawaherlal Nehru Medical College, Aligarh Muslim University, Aligarh, UP, India ABSTRACT Objective: To study addiction and psychosocial behaviour in relation to obesity in urban population. Method: A prospective study in an urban health training center of Department of Community Medicine, Jawaherlal Nehru Medical College, Aligarh Muslim University, Aligarh, Utter Pradesh, INDIA through predesign and pretested questionnaire base. Results: Individuals addicted to alcohol (2%) and pan (10.7%) were found to be more obese as compared to individuals addicted to tobacco (1.3%), pan masala (2.4%) and cigarettes (2.6%).The prevalence of obesity was more in individuals having abnormal psychosocial behaviour like withdrawn (3%), self conscious (51.1%), loneliness (5%), anxiety (14%) and depression (12%). Conclusion: The addiction of alcohol, pan and abnormal psychosocial behaviour play a role in development of obesity. KEY WORDS: Obesity, Addiction, Psychosocial behaviours, Urban population, prevalence, Body mass index.

INTRODUCTION Obesity is a very complex disorder in which multiple causative factors are potentially operative1. Any factor (eg. genetic, metabolic, psychological, social or environmental) which increase energy uptake or decreases energy expenditure can lead to positive energy balance and hence obesity. The body has excellent physiological defenses against the depletion of body energy stores, but it has weak defense against the accumulation of excess energy stores. Studies have shown that addiction to a particular substance like tobacco, alcohol, etc. and psychosocial behaviour can contribute to obesity. Some alcoholic beverages such as beer and wines are carbohydrates and they increase calories uptake2. Suter et al3 point out that as an energy source, unlike other sources of energy, alcohol cannot be stored in body and appears to have absolute priority in metabolism. This takes place at expense of other metabolic pathways, including the suppression of lipid oxidation, which appears to be a critical factor in the development of positive energy balance. Cigarettes smokers tend to have less weight as compared to non-smokers and ex-smokers. Studies have shown that ex-smokers tend to gain weight after quiting smoking4,5,6,7. The obese have a high incidence of body image problems and disturbances in perception and conceptual organization of certain physiological states8. A reduction in psychological stress and improvement in selfesteem are noted in obese when they loose weight. As a consequence of


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overweight many persons experienced job discrimination, public redicule, embarrassment, withdrawn, fear or worry.9,10,11,12 This prospective study was aimed to determine the association of addiction and psychosocial behaviour with obesity in urban population. Table 1: Distribution of Obesity According to Addiction Alcohol Tobacco Smoking Pan-Masala Subjects Obese 9 6 12 11 (n=458) (2.0) (1.3) (2.6) (2.4) Non 27 184 177 169 Obese (0.8) (5.2) (5.0) (4.8) (n=3535) 13.8 5.37 5.62 Chi square 7.08 1 d. f P 0.01 0.001 0.05 0.02 Figure in bracket indicates percentage of the value above it. Pan 49 (10.7) 254 (7.2) 6.84 0.01 Drug 0 (0) 0 (0) 0 0 None 371 (81.0) 2724 (77.0) 3.61 0.10

MATERIAL AND METHODS This prospective study was carried out in and around urban health training center of Department of Community Medicine, Jawaherlal Nehru Medical College, Aligarh Muslim University, Aligarh, Utter Pradesh, INDIA. At screening, weight and height were measured, and Body Mass index (BMI) calculated as weight/ height2 (kg/m2) was used as an index of relative weight. Persons with BMI>30 kg/m2 were considered obese and those with BMI between 20-24.9kg/m2 were considered non obese. Total persons screened were 3993, out of which 458 were obese and 3535 were found non- obese. Information on lifestyle characteristics and psychosocial behavior was received by pre-designed questionnaire. Addiction: Alcohol/ tobacco chewing/ smoking/ pan masala/ pan/ drugs/ none Psycho- social behaviour: Withdrawn/self-conscious/ loneliness/ emotional deprivement/ anxiety/ depression/ none. Data were analysed using percentage and chi-square test. RESULTS Table 1 shows that distribution of obese and non-obese in accordance with the addiction. Obesity was more prevalent in individuals who were less addicted to tobacco (1.3%), smoking (2.6%) and pan masala (2.4%). Addiction to alcohol (2%) and pan (10.7%) was more prevalent among obese as compared to non-obese. Table 2 shows the distribution of obese and non-obese subjects in accordance with psychosocial behaviours. The prevalence of obesity was more in individuals having abnormal psychosocial behaviours like withdrawn (3%), self conscious (51.1%), loneliness (5%), anxiety (14%) and depression (12%) as compared to non-obese.


Khalid U Khayyam et al: Continental J. Medical Research 2: 20 - 23, 2008

DISCUSSION In the present study we found that obesity was more prevalent in those consuming alcohol and pan as compared to those addicted to tobacco and smoking .The findings are similar to other studies. Garrow et al4, James6, Garrison7 , Glanser et al5 found that people who smoke cigarettes tend to be less in weight than non-smoker and ex-smoker tend to gain weight. Goya and Gerald13 demonstrated a positive relation between alcohol consumption and body weight irrespective of type of drink consumed. In prospective analysis, heavy drinking was associated with increased weight gain, and this was most apparent in men who had never smoked. In individuals who already have hypertension, even moderate consumption of alcohol readily increases serum triglyceride leading to obesity14. Table 2: Distribution of Obesity According to Psycho- Social Behaviour Withdrawn Self Loneliness Emotional consious deprivement Subjects Obese (n=458) Non Obese (n=3535) Chi square 1 d. f 14 (3.0) 61 (1.7) 3.19 234 (51.1) 424 (12.0) 455.0 23 (5.0) 141 (4.0) 0.98 9 (2.0) 70 (2.0) 0.0

Anxiety 64 (14.0) 353 (10.0) 6.72

Depression 55 (12.0) 389 (11.0) 0.38

None 59 (12.9) 2097 (59.3) 350.83

P 0.1 0.001 0.5 N.S. Figure in bracket indicates percentage of the value above it. NS = not significant




Carl9, Hammer10, Bruch 11, David12 and Judith15 also observed that obese individuals experienced more tension and anxiety over their body image, and psychosocial stress decreases when they loose weight. No difference was found between mental health score of overweight and normal weight persons, but anxiety had a definite role in those people who were trying to loose weight. REFERENCES Anderson L, Dibble MV, Turkki PR, Mitchell HS, Rynbergen HJ.(1982): Weight control. Nutrition in health and disease, 17th Edn : 407- 482. Bruch M.(1973): The Psychological handicaps of the obese. Obesity in perspective. Washington DC, 2 (2), V.S. Govt. Printing Office . Carl C, Seltzer and Jean Mayer.(1971): Body build (somatotype) distinctiveness in obese women. Journal Am. Dietetic Ass. 55 (5): 454-458. David Heber, Elizabeth Somar.(1986): The health risk of obesity. Weight loss and nutrition. Health Media of American Editorial Board. 53-58. Garrow JS, James WPT, and Ann Ralph.(1993): Obesity: Human nutrition and dietetics. Churchill Livingstone. 9th Edn : 465- 479. Gassison RJ, Feinleib M, Castelliw P, Mc Nammara PM.(1983): Cigarettes smoking as a confounder of relationship between relative weight and long term mortality, JAMA, 249:2199-2203. Glanser SC,Glauser EM, Reidenberg MM, Rusy BF, Tallaride RJ.(1970): Metabolic changes associated with the cessation of cigarettes smoking. Arch. Environment Health, 20 : 377.


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Hammar SL, Campbell C, Campbell V, Woolley J.(1971): Treating adolescent obesity. Long range evaluation of previous therapy. Clin. Pedia. 10 : 46. James WPT. In Weatherall DJ, Ledingham JGG, Warrel DA. (1987): Obesity oxford textbook of medicine, London Oxford. 8 : 35-51. Jonathan J Braunstein. (1971): Management of the obese patient. Medical Clinic of North America, 55 (2) : 391-401. Judith Rodin.(1993): Cultural and psychosocial determinants of weight concern. Ann. Intern. Med,119 (7) Part 2: 643-645. Mayer Mendelson. (1964): Psychological aspects of obesity. Med. Clin. North America. 48: 1373 1385. Nestel PJ, Simons LA, Homma Y.(1976): Effect of ethanol on bile acid and cholesterol metabolism. Am. J. Clin. Nutr. 29 : 1007. S Goya Wannamethee and A Gerald Shaper.(2003): Alcohol, body weight and weight gain in middle aged men. Am. J. Clin. Nutrition. 77 (5) : 1312-1317. Suter PM, Hasler E, Vetter W. (1997): Effect of alcohol on energy metabolism and body weight regulation: Is alcohol a risk factor for obesity? Nutr Rev, 55 : 157-71.

Received for Publication: 28/03/2008 Accepted for Publication: 24/06/2008 Corresponding Author Dr. Khalid U Khayyam HOD, Epidemiology and Public Health, Sri Aurobindo Marg New Delhi-110030. India E-mail: Continental J. Medical Research 2: 20 - 23, 2008 © Wilolud Online Journals, 2008.









Continental J. Medical Research 2: 24 - 27, 2008 © Wilolud Online Journals, 2008.

DIETARY GUIDELINES FOR GOOD HEALTH Francis Olawale Abulude Department of General Studies. Federal College of Agriculture, Akure 340001, Ondo State. Nigeria. (Email:

ABSTRACT The risk of developing obesity, diabetes, high blood pressure, alcoholism and heart disease is on the increase in Nigeria, the main cause could be the eating behavior of the populace. Varieties of private and government organizations (WHO, Cancer Society, Heart Associations, Academy of Sciences and Ministries of Health) world over have recommended dietary guidelines which are not difficult to implement and inexpensive. This paper discussed the dietary guidelines which would encourage people to modify their eating behavior in ways that are both healthful and pleasurable. KEYWORDS: WHO, Heart Association, Food and Nutrition Board, Diet, High blood pressure, Stroke INTRODUCTION The dietary guideline is known to be a total intake over a day or week, not to a single meal or certain foods. These are designed to promote adequate carbohydrate, vitamin, protein and mineral intake. It also emphasizes changes that will reduce the risk of cirrhosis of the liver, obesity, hypertension, stroke, heart disease, alcoholism, arteriosclerosis and diabetes. In Nigeria, it is unfortunate the economic situation has not permitted the populace to eat adequate and nutritious foods and lack of good guide did not make people to consider their state of health. Dietary guidelines have been set by a variety of private and government organizations. These guidelines are designed to reduce the risk of developing certain diseases. One of the regulating bodies, Food and Nutrition Board of the Nation Academy of Sciences, USA recommended intakes of nutrients that meet the needs of almost all healthy people of similar age and gender. The recommended dietary allowances (RDA) have become the premier nutrients standard in both the United States (U.S) and the World. More than 40 countries now have their own RDA, but many other countries use the US RDA. These RDA are just allowances and not requirements some people need less or more than the amount of nutrients. They are updated about 4-5years (Table 1). The RDA has got many uses which include, food labeling, food and nutrition information and education, clinical dietetics, nutrient supplements and special dietary food, sample diet for food programs, guide for food selection programs, planning and obtaining food supplies for groups, evaluation of dietary survey data and other scientific research, developing new or modified food products just to mention a few. The RDA outlined in Table1 is provided with ranges to allow people to determine their unique requirements. This paper is aimed highlight the RDA intakes of nutrients that meet the needs of healthy people. THE DIETARY GUIDELINES A close look at each of the summarized guidelines would aid diet planning. 1. Eat a variety of foods It is ideal to consume a variety of foods and one way to balance ones diet is to select from these five major groups everyday. The groups are: i. Fruit


Francis Olawale Abulude: Continental J. Medical Research 2: 24 - 27, 2008

ii. iii. iv. v.

Vegetable Bread, Cereal, Rice and Paste Milk, yogurt and cheese Meat, poultry, fish, dry-beans, eggs and nuts.

Women and adolescent girls need to eat more calcium rich and iron-rich foods. A meal consisting of beans with gari accompanied by a glass of milk or cheese and an orange cover all groups. Fats, oils, and sugar/ sweets can be added to the diet in moderation just to increase its flavor and help deliver some nutrients. 2. Eat a diet low in fat, saturated fat and cholesterol It is advisable to choose a low fat option among foods to leave room for the recommended servings from the five groups. Meat, milk and its products are source of saturated fats in most diet, while dietary cholesterol is derivable from animal sources. It is recommended that fats, oils, sweet should be used sparingly. Intake of yogurt, milk and cheese should be encouraged. If one prefers whole milk or low-fat or non-fat milk, one should cut or reduce the fat elsewhere in meals. “Moderation” should be the watch than “elimination” of some groups. 3. Balance food intake with physical activity- maintains or improves your weight It is advisable to do 30 minutes or more of moderate physical activity daily such as walking, bicycle riding, rope skipping, jumping, just to mention a few. Less time should be devoted to sedentary activities such as sitting. High-fat foods contain more energy per serving than other foods and may increase the likelihood of weight gain. Generally, the more the weights gain for ones height, the higher the weight - related risk. It is recommended that when weight loss is needed, this must be done slowly. A visit to the gymnasium for physical exercise would be ideal. 4. Eat a diet moderate in sugars Maintaining a nutritious diet and a healthy weight is crucial and so sugars should be eaten in moderation by most healthy people and sparingly by people with low energy needs. Both sugars and starches can promote tooth decay, the more they are consumed and the longer they reside in the mouth the greater the risk for tooth decay. It is advisable to wash and rinse the mouth after each meal. 5. Eat plenty of grain products, vegetables and fruits Most fruits and vegetables are naturally low in fat and provide many essential nutrients. Eat more of these along with more grain products. (Bread, cereals, rice etc). A high carbohydrate diet is based largely on plant foods that contain starch. The only plant exception is fruit which contains glucose, fructose, sucrose, as well as pectin. From the health point of view a high carbohydrate diet consisting largely of plant foods is a diet that is rich in fiber, nutrients, vitamins, saponin and essential fatty acids. 6. Eat a diet moderate in salt and sodium Salt and other sodium containing ingredients are often used in food processing. Many dietary and lifestyle choices influence blood pressure. There is no way at present to tell who might develop hypertension from eating too much sodium. Consumption of less salt or sodium is not harmful and is recommended for the healthy normal adult. 7. Drink alcoholic beverages in moderation Alcoholic beverages are known to supply energy, but few or no nutrients. They are the third contributor to energy intake for adults in the United State. Moderate intake is associated with a reduce risk of certain forms of heart disease, stroke, cancer, liver and pancreases disease, accidents, birth defects, death by other causes, risk for hypertension, heart failure. A moderate intake consists of two or fewer servings of 12 once of beer, 5 ounces of wine and 1½ once of distilled spirits per day. It is advisable to drink alcohol with meals. People with certain medications, children, pregnant women and those who plan to take part in activities that require special attention or skill like driving should not drink. People with alcoholism usually


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have unbalanced diets, which can impair absorption of vitamins and minerals from the gastrointestinal tract. An associated problem Table1. Recommended Dietary Allowance (Per day) Nutrient Unit People above 4 years Old Vit A Retinol equivalents 800-1000 Vit D International Units 200-400 Vit E International Units 8-30 Vit K mg 60-80 Vit C mg 60 Folate mg 0.4 Thiamin mg 1.1-1.5 Riboflavin mg 1.1-1.7 Niacin mg 14-20 Vit B-6 mg 1.3-20 Vit B-12 µg 2.4-6.0 Biotin mg 0.03-0.3 Pantothenic acid mg 5-10 Calcium g 1.0 Phosphorus g 0.7-10 Iodide µg 150 Iron mg 10 -18 Sodium mg 500 Magnesium mg 310 - 420 Copper mg 1.5 – 3.0 Fluoride mg 3.1 – 3.8 Zinc mg 12 - 15 Chloride mg 750 - 3400 Manganese mg 2.0-50 Potassium mg 2000 Selenium mg 55-70 Chromium mg 50-200 Molybdenum mg 75-250 Carbohydrate g 50-100 Fats/oils g No RDA but min of 4% of total energy intake Fiber g 20-35 Protein g 44-56 Sugar g 70-80 Water ml 1ml/Kcal expended a day Source: Wardlaw (1999). is poor metabolism. Alcohol consumption decreases the absorption of many B vitamins, such as thiamin, riboflavin, niacin and folate. All of these vitamins are important in maintaining proper metabolic and nervous system function FOOD LABELS TO PLAN HEALTHY DIETS. Nutrition labeling is intended to give information concerning the energy, protein, fat, carbohydrate, minerals and vitamins contained in a given amount of food and consumers have more nutrition information in food labels. It is possible to determine which foods are healthful, a consumer can know how a particular food fits into their daily nutrition needs. On the labels, important information like fat, cholesterol, saturated fat and sodium are highlighted. It is advisable to use them to make wise choices among foods. It is


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recommended that regulatory bodes like National Agency for Food and Drug Administration and Control (NAFDAC) should enforce the use of labels on food packages in Nigeria. Nutrient Density Guide in Food Choice Nutrient density is the ratio formed by dividing a food’s contribution to nutrient needs by its contribution to energy needs. When its contribution to nutrient needs exceeds its energy contribution the foods are considered to have a favorable nutrient density. To determine the nutrient density of a food, this is simply by comparing its vitamin or mineral content with the amount of energy it provides. A food is said to be nutrient dense if it provides a high amount of a nutrient for a relatively small amount of kcals. The higher a food’s nutrient density the better it is as a nutrient source. Generally, nutrient density is assessed with respect to individual nutrients, for example; many fruits and vegetables have high content of vitamin C compare with their modest energy content. (They are nutrient dense foods for vitamin C), nonfat milk is much nutrient dense than sugared soft drink for many nutrients. Nonfat milk has more protein, vitamin A, thiamin, riboflavin and calcium than soft drink. Nutrient dense foods, such as nonfat and low-fat milk, lean meat beans, oranges, carrots, whole bread and whole-grain breakfast cereals do help balance less nutrient dense foods such as cookies and potato that many people like to eat. Eating nutrient dense foods can aid diet planning for people who tend to consume little food including some older people and those following weight-loss diets. CONCLUSION This paper has highlighted the RDA intakes of nutrients that meet the needs of healthy people, but do not take into account special needs that may require individual adaptation (physical activity, climate, aging and clinical problems). However, it is important to follow the dietary guidelines in order to promote the relationship between nutrient intake and high wellness, longevity and chronic disease prevention. REFERENCE Atherton H.V and Newlander J.A (1987). Chemistry and testing of diary products. 4th ed. CBS Publishers and Distribution. Indiana. Pp 376. Christie J.S. (1991). Food for vitality. Bantam ed. Transworld Publisher Ltd. London. Pp.35-76. Fellows P. (1997). Traditional foods-processing for profits. Intermediate Technology Publishers. UK. Pp 27-193. Food and Nutrition Board (1981). National Academy of Sciences – National Research Council: Recommended dietary allowances, Revised, Washington, DC. McBean L (1996). The dietary guidelines: change and implications. Dairy council Digest.67:7 Nieman D.C. Butteworth D.E and Nieman C.N (1992). Nutrition. 1st ed. Wm. C. Brown publishers USA. Pp. 45-50 Revised Nuffield Advance Science Chemistry (1984). Teacher’s guide to food science. A special study. Published for Nuffield-Chelsea Curriculum Trust. Longman Group, UK. Ltd.pp.16-17 Trust well A.S (1987). Evolution of dietary recommendations, goals and guidelines. American Journal of Clinical Nutrition. 45:1060-72 Wardlaw G.M (1999). Perspectives in nutrition. 4th ed. International edition. WCB-McGraw-Hill Companies Inc, USA. Pp 51-532.


Continental J. Medical Research 2: 28 - 34, 2008 © Wilolud Online Journals, 2008. CORRELATION OF SERUM URIC ACID WITH MATERNAL AGE, PARITY AND SEVERITY OF BLOOD PRESSURE IN PRE–ECLAMPTIC PREGNANCIES Sazina Muzammil1, Khalid Umer Khayyam2, Nayyar Parvez3 Department of Physiology,Hamdard Institute of Medical Science, Jamia Hamdard,Hamdard Nagar,New Delhi-110062,INDIA. 2Department of Epidemiology and Public Health,Lala Ram Institute of Tuberculosis and Respiratory Diseases,Sri Aurobindo Marg, New Delhi-110030,INDIA. 3Department of Pharmceutics,Advance Institute of Phamacy,MD University. Rohtak,Faridabad,Haryana,INDIA.

ABSTRACT Maternal serum uric acid was determined in 30 pre- eclamptic and 20 normal pregnant females in their third trimester. Serum uric acid was 3.52± 0.75 in normal pregnancies and 6.03 ± 1.67 in pre- eclamptic pregnancies. This increase in serum uric acid was highly significant (P<0.001). There was no influence of parity and maternal age on serum uric acid. Serum uric acid levels increased significantly from 5.05±0.89 to 7.49±1.50 with increase in mean arterial pressure above 115 mmHg in pre –eclamptic pregnancies. (P<0.01) KEYWORDS: Serum uric acid,Eclampsia, Pre-eclampsia,Hyperuricaemia, Maternal age, Parity, Mean arterial pressure. INTRODUCTION Possible biochemical indices of pre-eclampsia have been sought for many years. Amongst the many markers which have been investigated, perhaps serum uric acid has been considered the most reliable. The relationship between hyperuricaemia and pre-eclampsia was first noted (Slemons and Bogert 1917) and it is now principally agreed that hyperuricaemia is a characteristic of pre-eclampsia (Hill et al 1978). Serum uric acid is also a reliable index of foetal welfare when pregnancy is complicated by pre-eclampsia, prognosis of foetus is poor irrespective of level of blood pressure (Verma 1982). Serum uric acid is one of the parameter used in early diagnosis of pregnancy induced hypertension, and a level of 5.5mg% or more can be taken as a warning sign of pregnancy induced hypertension and is associated with increased perinatal morbidity and mortality (Ranjan et al 1996; Lim et al 1998). Various studies have demonstrated a correlation between serum uric acid and pre-edampsia (Voto et al 1988; Koike et al 1997; Garrone et al 1997 and D’ Anna et al 2000) but information about the influence of maternal age, parity and mean arterial pressure on serum uric acid in pre-eclamptic pregnancies is scanty. The present study has examined the serum uric acid concentration in pre-eclamptic and normal pregnant females in the third trimester of pregnancy. The influence of maternal age, parity and mean arterial pressure on uric acid is studied. MATERIALS AND METHODS The present study was conducted on proven cases of pre-eclampsia. Thirty pre-eclamptic females in third trimester of pregnancy were selected from Inpatient and Outpatient Department of Obstetrics and Gynaecology, Jawaherlal Nehru Medical College,Aligarh Muslim University, Aligarh, Uttar Pradesh, INDIA, in a period of one year ( March 2002 to February 2003). Exclusion criteria were


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associated renal/hepatic/cardiac disorder; metabolic disorders; concomitant severe complications of pregnancy, pregnancy less than 28 wks or more than 41 weeks, multiple pregnancy and any medication during pregnancy except vitamins, iron and calcium (Farah et al 1993). Previously healthy normotensive females were considered to have pre-eclampsia if their blood pressure after 20 weeks of pregnancy was raised to >140/90 mmHg or had mean arterial pressure Continental J. Medical Research 2: 24 - 29, 2008 (Diastolic pressure + 1/3 pulse pressure) of more than 110mmHg. The increase in blood pressure had to be present on at least two occasions 6 hours apart along with proteinuria of more than 300mg/day or 100mg/dl. Twenty females with normal pregnancies in third trimester were matched on an individual basis for same parameters and were taken as controls. Table 1. Serum uric acid (mg/100ml) in normal and pre-eclamptic pregnancies: Normal pregnancy (n=20) Pre- eclampsia (n=30) Uric acid (mg/100ml) Age <25 yrs >25 yrs Parity Primipara Multipara MAP 110-115 mmHg >115 mmHg * P<0.001 ** P<0 5.05±0.89** 7.49±1.5 3.78±0.63 3.26±0.8 5.73±1.49 6.32±1.85 3.48±0.64 3.56±0.81 5.58±1.07 6.4±1.97 3.52±0.75 6.03±1.67*

All females were between 20-40years of age (mean age 25.53±3.9 years). Estimations of serum Uric acid: Phosphotungstate Method (Brown 1945 and Martinek 1970) Test principle Uric acid in alkaline medium reduces phosphotungstic acid to “Tungsten Blue” a blue coloured complex which is measured calorimetrically. Procedure Preparation of working solution: 0.5 ml of stock uric acid standard was diluted to 50 ml with distilled water and mixed well. Step A : Deproteinization of sample


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I ml of serum and 8 ml of distilled water was taken in clean, dry test tube to which 0.5 ml sulphuric acid, 2/3 N (Reagent 1) 0.5 ml sodium tungstate and 10% W/N (reagent 2) was added, mixed well and allowed to stand for 10 minutes and then centrifuged. Step B : Three dry and clean test tubes serving as blank ‘B’, standard ‘S’ and test ‘T’ were taken. 1 ml of sodium carbonate, 14% W/N (Reagent 3) and phosphotungstate (Reagent 4) were added to three test tubes. Then 3 ml of supernatant filtrate (from step A) was added in test ‘T’ test tube, 3 ml of working reagent was added in standard ‘S’ test tube and 3 ml distilled water in blank ‘B’ test tube. Contents of all three test tubes were mixed and allowed to stand in dark for 15 minutes. Optical density (OD) of blank (B), standard (S) and test (T) were measured against distilled water on colorimeter using red filter or at 710 nm wave length.


Uric acid (mg/100 ml)

8 6 4 2 0 Normal pregnancy (n=20) Pre-eclamptic pregnancy (n=30)

Figure 1 : Serum uric acid in normal and pre-eclamptic pregnancies
Calculation Serum uric acid (mg/100ml) = O.D test – O.D. Blank ------------------------------------- X 10 O.D. standard – O.D. blank Statistical Analysis Values were expressed as mean ± SD. Statistical analysis was done using student ‘t’ test. Results were considered significant if ‘p’ valve was <0.05. Correlation between serum uric acid and mean arterial pressure was determined by co-efficient of correlation (r). RESULTS The comparison of serum uric acid in normal and pre – eclamptic pregnancies is shown in Table 1 ( Fig – 1). There was a highly significant increase in serum uric acid from 3.52±0.75 in normal to 6.03 ± 1.67 in pre- eclamptic pregnancies (p<0.001). Serum uric acid in two age group (below 25 years and above 25 years) in normal and pre-eclamptic pregnancies is shown in Table 1. There was no significant changes in two age group (P>0.05) both in normal and pre- eclamptic pregnancies. Uric acid levels were studied in two parity groups i.e. primiparous and multiparous. No significant change (P>0.05) was seen in two parity groups.


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Pre – eclamptic females were divided into two groups according to (MAP) mean arterial pressure (i) MAP 110-115 mmHg (ii) MAP> 115 mmHg. The normal pregnant females had mean arterial pressure below 110 mmHg. Uric acid levels increased significantly from 5.05 ± 0.89 to 7.49 ± 1.50 with increase in mean arterial pressure above 115 mmHg (P<0.01) (Table 1, Fig 2) Fig 3 is showing the correlation between mean arterial pressure and serum uric acid. There was a direct positive association between serum uric acid and mean arterial pressure (r= 0.8, P<0.001) which was highly significant. DISCUSSION The present study demonstrated that serum uric acid levels were significantly elevated in pre-eclamptic pregnant females as compared to normal pregnant females. There was no effect of maternal age and parity in both groups on uric acid levels. But uric acid levels increased significantly in pre-eclamptics with rise in mean arterial pressure more 115 mmHg. Strong positive correlation was seen between serum uric acid and mean arterial pressure.

10 9 8 7 6 5 4 3 2 1 0

Uric acid (mg/100ml)

Figure III : Correlatio

MAP 110-115 mmHg (n=18)

MAP >115 mmHg (n=12)

Figure 2: Comparison of serum uric acid in pre-eclamptic women with 2 levels of mean artesial pressure (MAP) It has been more than 60 years since association between hyperuricaemia and toxemia was first noted1 During that time the theories advanced to explain this relationship have included, placental production of uric acid (Fadel et al 1969) starvation (Diekmann 1952) lactic acidosis (Handler 1960), excessive muscle exertion (Crowford 1941) hepatic damage (Cadden and Stander 1939) decreased glomerular filtration rate (Schaffer et al 1943) and renal cellular damage (Treadwell and Dixon 1961). In normal pregnancy glomerular filtration rate increases in first trimester and then remains stable until term. The clearance of uric acid, however continues to change as pregnancy advances. Upto 16 weeks of gestation there is decline in serum uric acid concentration and increase in execration of uric acid. From 16th –36th weeks serum uric acid increases whereas excretion remains constant (Hytten and Lind 1973). In pregnancy induced hypertension there was impaired glomerular filtration rate and an increased tubular reabsorption of uric acid, leading to impaired uric acid clearance and thereby increasing serum uric acid concentration. Although both glomerular filtration rate and clearance of uric acid were shown to decrease in pre-eclampsia, there was no direct correlation between glomerular filtration and renal handling of uric acid (Chesley and Williams 1945).


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Increased oxidative stress and formation of reactive oxygen species had been proposed as another contributing source of hyperuricaemia noted in pre- eclampsia (Many et al 1996). Although hyperuricaemia is an acknowledged characteristic of pre- eclamptic toxaemia, (Plass 1924) did not consider the level of uric acid to be an index of severity of disease (Pitchard and Stone 1967) found no evidence to suggest that those with highest serum uric acid were more seriously ill. According to some worker increased accumulation of lactic acid might lead to decrease excretion of uric acid and thereby resulting hyperuricaemia associated with pre – eclampsia (Stander and Cadden 1934; Quick 1932). It was demonstrated that a significant but week correlation between serum uric acid levels and blood pressure (Lim et al 1998) but another study showed a highly significant positive correlation as was also shown in this study (Hickman et al 1982).

Blood Pressure (BP) Figure 3 : Correlation of mean arterial pressure with uric acid REFERENCES: Brown J,(1945): Estimation of serum uric acid. Clin. Chem . 15-20 Cadden JF, Stander HJ,(1939): Uric acid metabolism in eclampsia. Am. J. Obstet Gynecol ; 37 : 37 47. Chesley LC, Williams LO,(1945): Renal glomerular and tubular function in relation to hyperuricaemia of pre- eclampsia and eclampsia. Am. J. Obstet Gynecol ; 50 : 367-375. Crawford MD,(1941): Plasma uric acid and urea findings in eclampsia. J. Obstet. Gynecol. Br. Empire ; 48 : 60-72. D’ Anna R, Baviera G, Scilipoti A, Leo R,(2000): The clinical utility of serum uric acid measurement in pre – eclampsia and transient hypertension in pregnancy. Panminewa Med ; 42: 101-3. Diekmann WJ,(1952): The toxemias of pregnancy. Second edition. St. Louis, CV Mosby Company.62-74


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Fadel HE, Sabour MS, Mahran M, El- Din DS,(1969): Serum uric acid in pre – eclampsia and eclampsia. J . Egypt. Med. Assoc. ; 52 : 12-23. Farah Khaliq, Usha Singhal, Zakia Arshad, Mubarak Hussain,(1993): Thyroid function in pre eclampsia and its correlation with maternal age, parity, severity of blood pressure and serum albumin. India. J. Physiol. Pharmacol. ; 43 (2) : 193-198. Garrone C, Broso P,(1997): Uric acid and pre – eclampsia. Minerva Ginecol, ; 49: 213-16. Handler JS,(1960): The role of lactic acid in reduced excretion of uric acid in toxemia of pregnancy J. Clin. Invest. ; 39 : 1526-1532. Hickman PE, Michael CA, Potter JM,(1982): Serum uric acid as a marker of pregnancy induced hypertension. Aust. NZ. J. Obstet. Gynaecol ; 22 : 198-202. Hill LM, Furness C, Dunlop W,(1978): Diurnal variation of serum urate in pregnancy. Br. Med. J. ; 2 : 1520. Hytten FE, Lind T,(1973): Diagnostic Indices in pregnancy. Switzerland Ciba Geigy.151-206 Koike T, Ogawa S, Kuwata T, Sato I,(1997): Evaluation of serum uric acid level preceding the clinical manifestation of pre – eclampsia in twin pregnancies. Gynecol. Obstet. Invest. ; 44 : 97-101. Lim KH, Friedman SA, Ecker JL, Kaol,(1998): The clinical utility of serum uric acid measurement in hypertensive disease of pregnancy. Am J Obstet Gynecol ; 178 : 1067-71. Many A, Hubel CA, Roberts JM,(1996): Hyperuricemia and xanthine oxidase in pre- eclampsia. Am. J. Obstet Gynecol ; 174: 288-91. Martinek J,(1970): Clin. Chem.18-27 Pitchard JA, Stone SR,(1967): Clinical and laboratory observations on eclampsia. Am. J. Obstet Gynecol ; 99 : 754-765. Plass ED,(1924): Non protein nitrogenous constituents of blood in eclampsia and allied conditions. JAMA ; 82 : 266-269. Quick AJ,(1932): The relationship between chemical structure and physiological response. III. Factor influencing execration of uric acid. J Biol. Chem. ; 98 : 157-169. Ranjan Mustaphi, Sarala Gopalan, Lakhbir Dhaliwed, AK Sarkar,(1996): Hyperuricaemia and pregnancy induced hypertension. Indian J. Med. Sci, ; 50 : 68-71. Schaffer NK, Dill LV, Cadden JF,(1943): Uric acid clearance in normal pregnancy and pre eclampsia. J. Clin. Invest. ; 22: 201-206. Slemons JM, Bogert LJ.(1917): The uric acid content of maternal and fetal blood. J. Biol. Chem, ; 32 : 63-69 Stander HJ, Cadden JF,(1934): Blood chemistry in pre – eclampsia and eclampsia. Am. J. Obstet. Gynecol ; 28 : 856-871. Treadwell BLJ, Dixon AS,(1961): Perpeural hyperuricaemia. Ann. Rham. Dis. ; 20 : 186-188.


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Varma TR,(1982): Serum uric acid levels as an index of fetal prognosis in pregnancies complicated by pre existing hypertension and pre-eclampsia of pregnancy. Int. J. Gynaecol. Obstet. ; 20 : 401. Voto LS, Illia R, Darbon Grosso HA, Imaz FU, Margulies M,(1988): Uric acid levels : a useful index of severity of pre-eclampsia and perinatal prognosis. J. Perinat. Med. ; 16 : 123-6. Received for Publication: 28/06/2008 Accepted for Publication: 24/07/2008 Corresponding Author Sazina Muzammil, Department of Physiology, Hamdard Institute of Medical Science, Jamia Hamdard,Hamdard Nagar, New Delhi – 110002, INDIA.


Continental J. Medical Research 2: 35 - 38, 2008 © Wilolud Online Journals, 2008.

THE VIRULENCE OF PLASMODIUM FALCIPARUM INFECTION IN HUMAN HOST Anyanwu, E.B. 1, Onyesom, I2., Okperi, B3., Awusi, V.O. 3, Mabiaku, T.O3. Umukoro D.O.3 Department of Family Medicine, 3Department of Paediatrics Faculty of Clinical Medicine, 2Department of Medical Biochemistry, Faculty of Basic Sciences, Delta State University. Abraka, Nigeria. ABSTRACT Malaria causes an acute febrile illness which may be characterized by periods of fibrile paroxysms. The severity and course of an attack of malaria depends on species and strains of the infecting parasite. Mankind is infected by four species of the genus Plasmodium but Plasmodium falciparum is associated with the highest degree of parasitaema due to high yields of merozoites per schizonts. The malignancy of Plasmodium falciparum is peculiar to that species. This review highlights some of the reasons why infection by Plasmodium falciparum may be malignant and more virulent than the other plasmodia species. KEYWORDS: malaria parasite, virulence, merozoite, sequestration. INTRODUCTION Malaria is the most important parasitic disease of man. The human disease is a protozoa infection of red blood cells which is transmitted by the bite of blood-feeding female anopheles mosquito (White, 1996) Malaria is found throughout the tropical region of the world, most of the Sub – Saharan Africa, South America, South East Asia and the Western Pacific Areas (Lucas, and Gilles, (1987), Gilles, (1993a). Malaria transmission occurs in more than 100 countries of the world. More than one billion inhabitants of these countries are exposed to risks of malaria infection. The estimated annual global incidence of malaria is over two million cases (White, (1996), Strickland, (1991). Malaria is highly endemic in Nigeria and is one of the major causes of ill- health and deaths. The risk of malaria exists throughout the country but is greater in the rural areas. Malaria leads to about 10 percent deaths in children under five years of age and similarly, it causes about five percent of death in Uganda (National Malaria and Vector Control Division , (1991), Bitawaha et al, 1997). The causative agent of this parasitic disease is Plasmodium. In nature, malaria is transmitted from man to man by a female anopheles mosquito while taking a blood meal. About 60 species of anopheles mosquitos are important vectors and are found most frequently in tropical and sub – tropical regions. About 40 species have been identified in Nigeria, but the major vectors of human malaria are Anopheles gambiae, Anopheles arabiense, Anopheles funestus, and Anopheles melas. Out of the six zoo-geographical regions of the world, the most important vector in the Afro – Tropical zone including Nigeria is the Anopheles gambiae (Service, 1993). Mankind is infected by four species of the genus Plasmodium. These are Plasmodium falciparun, Plasmodium ovale, Plasmodium vivax and plasmodium malaria. Plasmodium ovale has been reported predominantly from East and West Africa. It is uncommon outside Africa. Plasmodium vivax is the major species in the temperate zones, Central America, and the Indian subcontinent. But Plasmodium falciparum has increased in India over the last decades. This is due to the transfer of anopheles mosquitoes on board of aircraft during stop – over’s in endemic zones. This is why



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International regulations sanctions the spraying of planes with insecticides in malaria zones before take off (Bouree et al, 1993). Plasmodium malaria is less common but is found in most areas especially in West and Central Africa. Plasmodium falciparum predominates in the Sub – Saharan Africa, Papua New Guinea and Haiti (Isselbacher et al, 1994) The severity and course of an attack of malaria depends on the species of infecting parasite, on the age of the patient, state of immunity, general health and nutritional status of the patient. Falciparum malaria is responsible for almost the entire 2 million deaths attributed to malaria each year worldwide. Of all the species of plasmodia, Plasmodium falciparum is the most highly pathogenic, and is associated with malignant type of malaria. It is the chief infection in areas of endemic malaria in Africa, and in a non- immune patient, it usually runs an acute course. Such course could be fatal unless promptly treated with specific drugs. Plasmodium falciparum is associated with the heaviest degree of parasitaemia. Infection with human malaria begins when the feeding female anopheline mosquito inoculates plasmodial sporozoites into the human host (Table 1). These migrate into the liver cells and the process of asexual reproduction called pre – erythrocytic schizogony starts. This process result into schizonts which enlarge, while the nucleus and cytoplasm divides to form thousands of merozoites, which eventually leads to the rupturing of the liver cells. This process librates thousands of merozoites into the circulation to penetrate red blood cells. The sporozoites of Plasmodium falciparum yields about 30,000 – 40,000 merozoites per sporozoite, while the merozoites yield per sporozoite is lower in the other species (Gilles,1993b). Also, the nuclear division is faster in the Plasmodium falciparum species. Table 1: Some comparative character of sporogonic and schizogonic stages of four species of human plasmodium of pre – Hypnozoite Number of Species Duration of Duration merozoite in presporogony in erythrocytic stage in human erythrocytic anopheles (at 280C) schizont P. vivax 8-10 days 6-8days + 10, 000 P. malaria 14-16days 14-16days 0 15, 000 P. ovale 12-14days 9days + 15, 000 P.falciparum 9-10days 5½ – 7days 0 30, 000 Source: Gilles, (1993b) The malignancy of falciparum malaria is peculiar to that species. The merozoite emerging from the liver are considerably more numerous than those of the other species. Also, the merozoites of Plasmodium falciparum appear to enter the erythrocytes more efficiently than the merozoites of the other malaria parasites. Plasmodium falciparum is the only human malaria parasite that is found in equal numbers in erythrocyte of all ages. Plasmodium vivax for example, invades primary the reticulocytes, while Plasmodium malariae seems to prefer the older, natural red blood cells (Gilles, 1993b). Again, the severity of malaria infection caused by Plasmodium falciparum is made even worse by the increasing resistance to commonly used anti-malaria drugs. Resistance to chloroquine has been documented in most countries with falciparum transmission over the last two decades and resistance to other alternate


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anti-malarial drugs has followed in many counties of the world (Olatunde, (1977), Eke, (1979), Salako, and Fedeke-Aderounmu, (1987), Oduola (1992), Hagos (1993). Some prior treatment is extremely common, particularly in developing countries where drugs such as chloroquine are sold across the counter for treatment of fevers and suspected malaria. This action has helped in a very large way in spreading resistant strains of falciparum malaria. Another factor that aids the virulence or malignancy of Plasmodium falciparum is the process of sequestration of parasitized red blood cells. At about 24-26 hours of development of the parasite in the human host, the falciparum parasite which has infected red blood cells disappears from the circulation by attachment or cycle-adherence to the wall of venules and capillaries in vital organs vis-a-vis, brain heart, placenta, spleen, intestine and bone marrow (Gilles , 1993). It has been demonstrated that sequestration of red blood cells containing mature forms of the parasites in capillaries and post-capillaries venules appears to be a constant feature of severe falciparum malaria (Macpherson et al, 1985). Most of the fatal cases show blocking or occlusion of the capillaries by clumps of red blood cells harbouring developing parasite, huge number of which can be seen in smears and sections of post-mortem materials. This process of sequestration leads to reduction in the supply of oxygen and other nutrients to the affected organs. Notably, sequestration is not seen in the other relatively bargain human malaria. REFERENCES Bitawaha, N., Tumwesigye, O. Kabariime P., Tyebwa, A.K.M., Tumwesigye, S., and Ogwal-Okeng, J.W (1997). Herbal Treatment of Malaria-four cases reports from Rukararewe Partnership Workshop for rural development (Uganda). Tropical Doctor ; 27 (Suppl 1): 17-19. Bouree, P., Taugourdeau, P.H., Ng-Anh Van. Malaria (1993). In: Bouree, P., Taugoudeau, P.H. (Eds). Malaria, Smithkline Beacham Pharmaceuticals Bibliography;. p. 1-40. Eke, R.A (1979). Possible Chloroquine Resistant Plasmodium Falciparium in Nigeria. A J Trop Med Hyg; 28 (6); 1074-1075. Gilles. H.M (1993a). Epidemiology of Malaria. In: Gilles, H.M. and Warrel, D.A (Eds). Bruce-Chwatts Essential Malariology. 3rd edition. Great Britain, Edward Arnold (Publisher);. pp. 124-164. Gilles, H.M (1993b). The Malaria Parasite, In: Gilles H.M., and Warrel, D.A (eds). Bruce- Chwatt’s Essential Malariology. Great Britain, Edwin Arnold (Publisher),. pp. 12-34 Hagos, B., Khan, B., Ofulla, A.V.O., Kariuki, D., and Martin, S.K (1993). Responses of Falciparum malaria to Chloroquine and three-second line antimalaria Drugs in a Kenya Coastal School Age Population. East Afr Med J.; 70 (10); 620-623. Isselbacher, K.J., Braunwald, E., Wilson, J.D., Martin, J.B., Fauci, A.S., and Kasper, D.L. (1994) (Eds). Protozoal infection: Malaria. In: Harrison’s Principles of Internal Medicine. 13th edition. McGraw – Hill Inc. USA;. pp. 307 – 310 Lucas, A.O., and Gilles, H.M (1987). The Protozoal Disease, Malaria. In: Luca, A.O., and Gilles, H.M. (Eds). A Short Textbook of Preventive Medicine for the Tropics. 2nd edition. ELBS;. pp. 189-196. Macpherson, G.G., Warrel, M.J., White N.J., Looareesuwan, S., and Warrel, D.A (1985). Human Cerebral Malaria. A quantitative ultrastructure analaysis of parasitized erythrocyte sequestration. AJP , 119 (3); 385 401. National Malaria and Vector Control Division, Department of Disease Control and International Health,


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FMOH (1991). Malaria in Nigeria: Epidemiology and Control. Nig. Bull Epidemiol .; pp. 2-19. Oduola, A.M.J., Sowunmi, A., Milhouse, W.K., Kyle, D.E., Markin, R.K., Walker, O (1992). Innate Resistant to new Antimalarial Drugs in Plasmodium Falciparum from Nigeria. Trans Roy Soc Tropl Med Hyg; 86, 123-126. Olatunde, A (1977). Chloroquine Resistance Plasmodium Falciparum and Malaria in Africa. Trans Roy Soc Tropl Med Hyg, 71 (1) , 80-81 Salako, L.O., and Fedeke-Aderounmu, A (1987). In-vitro Chloroquine and Mefloquine Resistant Plasmodium Falciparum in Nigeria. The Lancet,; pp. 572-573. Service, M.W (1993). The Anopheles Vector. In: Gilles, H.M., and Warrel, D.A. (Eds) Bruce-Chwatt’s Essential Malariolgy. 3rd edition. Great Britain, Edward Arnold (Publisher);. PP. 96-123. Strickland, G.T (1991). Infections of the Blood and Reticuloendothelial system Malaria. In: Strickland, G.T. (Ed), Hunter’s Tropical Medicine. 7th edition. Philadelphia; W.B. Saunder’s Company;. pp. 584-614. White, N.J (1996). Malaria. In: Cook, G.C. (Ed); Manson’s Tropical Disease. Saunder’s Company;. Received for Publication: 28/09/2008 Accepted for Publication: 04/12/2008 Corresponding Author Anyanwu, E.B. Department of Family Medicine, Faculty of Clinical Medicine, Delta State University. Abraka, Nigeria. 20th edition. London; WB


Continental J. Medical Research 2: 39 - 38, 2008 © Wilolud Online Journals, 2008. EVALUATION OF MATERNAL MORBIDITY RATE AMONG WOMEN IN PERI-URBAN AREA OF ENUGU STATE, CAUSES, EFFECTS AND SOLUTION. Momoh, M. A and 2 Ejike, M. O. Department of Pharmaceutics, University of Nigeria, Nsukka, 2School of Nursing and Midwifery, Bishop Shanahan Hospital Nsukka ABSTRACT Maternal and morbidity has been evaluated in this research, questionnaire were used to elicit response from the sample study. Poor antenatal visit, road and lack of qualified health personnel were implicated. The women with greatest risk of maternal death are those who are over 35 years, poor antenatal visit and lack of education or / and large families are also a major factor. The main causes of maternal mortality are anaemia, post-partum sepsis and malaria. Other causes include delay in arriving at the hospital, eclampsia, ruptured uterus, sexually transmitted infections including HIV, and the use of harmful traditional drugs. We therefore recommended that maternal care should be free and health be provide with adequate skill personnel. KEY WORDS: morbidity, maternal, women, rate, evaluated


INTRODUCTION A new millennium has started, and pregnancy, childbirth and abortion continue to be unnecessarily hazardous for the majority of the world’s women. In spite of a century of accumulated knowledge about why maternal deaths and morbidities occur and what needs to be done to avert them, nearly, 600,000 women are still dying each year in developing countries, and preventing these deaths and diseases seem to be as elusive as ever in many countries, especially African countries Nigeria inclusive (Abdullahi SA et al, 2005). Many inter-related factors contribute to maternal and morbidity rate among women in Nsukka zone of Enugu State. Women’s low status and lack of decision-making power are important under-lying factors. Women and their families need information in order to recognize the signs of complications; they need to be able to access care when complications develop and the resources to reach an appropriate care facility in time. The short period of time from the development of a serious complication to death means care must be available close to women’s homes or reachable further away by a quick and affordable means of transport. There is need for functioning health care facilities with well-trained health providers. Maternal death is defined as “death of a woman while pregnant or within 42 days of termination of the pregnancy, irrespective of the duration or the site of the pregnancy, from any cause related to or aggravated by the pregnancy or its management, but not from accidental or incidental causes”, according to the World Health Organization’s tenth version of the International Classification of Diseases (Hill K, 2001). A maternal mortality ratio (MMR) is the number of maternal deaths per 100,000 live births. Direct maternal deaths are those resulting from obstetric complications and indirect maternal deaths are those resulting from diseases, aggravated by the physiological effects of pregnancy (Abou Z,1997). Several deaths have resulted from poor health services and it equally affected the economy of the area. This study is to evaluate the causes of maternal and morbidity rate among women in Nsukka zone of Enugu State. METHODS The research method adopted for this study is the demographic and health surveys research design. This is because maternal mortality and morbidity ratio is calculated directly from the information obtained from


respondents. Hence only a sample of the population was used for the study. Three hundred respondents who were interviewed formed our sample size for this study. To ensure the content validity of the instrument, three experts in reproductive issues went through the interview question constructed. Items accepted by two or three experts were included in due final interview schedule. The sample of the study was drawn from the private and public hospitals from the zones on their antenatal visit. A total number of three hundred 300 people were selected for the study. These were patient from the zone that attend clinic at a missionary hospital in nsukka between 2006/2007. Questionnaire and oral interviews were used as a means to obtaining information from the sample subjects. The interview questions were administered randomly to selected people and answers to questions subsequently transformed into the ratio through a series of simple mathematical calculations. RESULTS Data collected were analysed with respect to the twelve research questions that guided the study under the headings Yes or No. A total of three hundred and twenty (320) questionnaires were distributed, three hundred (300) representing 94% of total number of all questionnaires distributed were completed and returned. To ensure anonymity and confidentiality, no names were recorded

Table 1. Characteristics of women enrolled in the study


Number % women of women response (15-43 yr) 195 210 285 160 65% 70% 95% 53.3%

Age (yr),

Attend any form of education Able to read Married Gainfully employed


Table 2. Response from the participants

Questions NO

Response YES

1. Sample population (n= 300) 2. Do you like to deliver in the hospital 122(40.6%) 3. Does screening identify most of the women who will develop complications during labour 100(33.3%) and delivery? 2. Can the training of traditional birth attendants (TBAs) make positive change? 4. For women, who do not wish to be pregnant, can family planning and safe abortion program make an important Contribution to safe Motherhood? 5.Can HIV/AIDS complicate pregnancy and childbirth 6. Do poverty and gender discrimination contribute to the increase of maternal mortality and morbidity rate? 7. Does anemia contribute to maternal mortality and morbidity rate 8. Have improvements in roads and transport facilities reduced maternal mortality and morbidity? 9. Has expenditure on transport any effect on maternal morbidity and mortality rate in the area? 10. Do some women have a high likelihood of getting seriously ill during pregnancy? 110(36.7%) 178 (59.3%)

200 (66.7%)






56(18.7%) 30(10%)

244(81.3%) 270(90%)








Table 3. Means of transport used by pregnant women in the study area. Mode of transportation Number Percentage On foot Animal Own car/bus/taxi Friends/bike Ambulance Commercial motor bike Others NURTW bus Total 39 06 22 11 00 300 13.0 2.0 7.3 3.7 00.0 100.0 86 00 44 92 28.6 00.0 14.7 30.7

Private commercial bus Discussion In question 2, 100(33.3%) respondents responded Yes and 200 (66.7%) responded No to the question (Does screening identify most of the women who will develop complications during labour and delivery”. One of the respondent who responded No to the question said that screening does not work it does not identify most of the women who will develop complications during labour and delivery. In fact, screening cannot work for purely mathematical reasons have nothing to do with the quality of care provided or the


skill of the personnel. There are two major mathematical reasons why screening of pregnant women cannot predict obstetric complications. One reason is that very accurate screening tools do not exist (Kasongo project team , 1984). Even if we had better screening tools, however, prediction would still be very poor, because the incidence of specific complications is fairly low. Therefore, in assessing the possible efficacy of a screening test, we need to consider the value of a screening for the major complications individually. The more common the condition, the more accurate screening is. Haemorrhage is the most common of the serious obstetric complications. Women’s reported poor “compliance” with advice to come to the hospital for delivery because they are at “high risk is sometimes interpreted as evidence that they prefer to deliver at home. However, we wondered how much of women’s reluctance to follow this advice comes from their understanding that the results of antenatal screening are more often wrong than right. In addition, women are also aware that many health facilities including hospitals, are not able to treat serious complications, for a variety of reasons–the physician is not there, there is no blood or anesthesia, etc. so why go to the trouble at expanse of going to the hospital at all? Screening cannot work. This statement still seems like heresy, although it is much more widely accepted that it was few years ago, as shown for example by this statement from the official Safe Motherhood Website: “Every pregnancy faces risk”. During pregnancy, any woman can develop serious, life-threatening complications that require medical care. Because there is no reliable way to predict which woman will develop these complications, it is essential that all pregnant women have access to high quality obstetric care. Responding to the question on table 2, “Can the training of traditional birth attendants (TBAs) reduce post-partum infection by encouraging cleanliness and discouraging dangerous practices?”190(63.3%) responded Yes while 110 (36.7%) responded No. A formally trained midwife who responded Yes to this question said that the training of traditional birth attendants (TBAs) is meant to reduce post-partum infection by encouraging cleanliness’ and discouraging dangerous practices like delivering a pregnant woman in a dark room. While such training may reduce these particular problems, labour and delivery will still be complicated in a certain number of cases. TBAs have neither the skills nor the equipment to treat life-threatening complications. A clear distinction should be made between TBAs and midwives who have been formally trained in the “execution of emergency measures”, who can treat a variety of complications and are a valuable part of programme to reduce maternal deaths. It has also been said that TBAs can be trained to recognize obstetric complications and refer women with complications to a nearby health facility for treatment. There are two weaknesses in this plan. First of all, the signs and symptoms of serious obstetric complications are not subtle: any bleeding during pregnancy, excessive bleeding during or after delivery; headaches in combination with swollen hands, face and feet; labour for more than twelve hours. Everyone should be taught to recognize these few danger signs, not just TBAs or pregnant women. The more difficult problem with training TBAs to refer women with complications is that there is often no feasible referral option. In fact, it is precisely in circumstances where medical treatment is least available that training TBAs is usually proposed as a solution (Fathalla M, 1997). 260 (86.7%) respondents responded yes and 40 (13.3%) responded No to the question on question 5 that says “For women who do not wish to be pregnant, can family planning and safe abortion programme make an important contribution to safe Motherhood?” A respondent who works as a schoolteacher said a woman couldn’t die a maternal death if she is not pregnant, so family planning can directly and substantially reduce maternal deaths by helping women to avoid unwanted pregnancies. Since even the best contraceptive methods fail, even with an exemplary family planning programme there will be unintended pregnancies. Therefore, access to safe, legal termination of pregnancy is of crucial importance to reducing maternal mortality as experience in Western countries has demonstrated (Filippi V, et al 1997)). Responding to the question on question 6, “Can HIV/AIDS complicate pregnancy and childbirth?” 257 (85.7%) responded Yes while 43 (14.3%) responded No. HIV/AIDS experts who responded to this question said that direct and indirect cases of maternal mortality and morbidity may be more severe or debilitating in HIV positive women, especially in those with symptomatic HIV disease or AIDS, than in women who are HIV negative. A number of studies (Mcntyre J, 2002), have found higher rates of ectopic pregnancy, bacterial pneumonia, urinary tract infections and other infections in HIV positive as compared to HIV negative pregnant women. A Rwanda study (Leroy V, 1998), found that HIV positive pregnant women had significantly more sexually transmitted infection and were also more likely to experience postpartum haemorrhage than HIV negative pregnant women. Pregnancies may also be complicated by AIDS – related conditions. In one Swiss study (WHO 2002), there were 16 cases of severe material morbidity in 153 pregnancies: 14-pneumonia, 1 pyelonephritis and 1 cerebral toxoplasmosis. AIDS – related conditions


caused appreciable material morbidity and mortality in a controlled, prospective study (Kumar RM,1998), of pregnant women with transfusion – dependent beta–thalassaemia major in India from 1990 to 1997. Among 39 women who had AIDS 31 per cent had a miscarriage by eight weeks pregnancy and 13 per cent died undelivered by 32 weeks of pregnancy from pneumocystis carinii pneumonia. In contrast, the women with asymptomatic HIV disease remained well throughout pregnancy. From the response on table 7, 244 (81.3%) responded Yes and 56(18.7) No to the question “Does poverty and gender discrimination contribute to the increase of maternal mortality and morbidity rate among women in Nsukka zone of Enugu State?” The women’s low status is reflected in their lack of control over household expenditure, including on food; spending was ordained by mothers in-law and/or husbands, a custom that was not openly questioned by respondents, as with other issues related to role and status. The role of gender differences, while important, however, should not be seen in isolation but against a backdrop of financial insecurity, a reality of rural life for many. The women are the first to work hard and the last to be self-indulgent with food or rest in the context of the wider stress of poverty, including the demands of the market economy and makes pregnancy more perilous. Responding to the question “Does anaemia contribute to maternal mortality and morbidity rate? 270(90.0%) responded Yes while 30(10.0%) responded No. In related study, it was observed that, the haemoglobin levels of women who died in 1994 – 96 were much worse than those observed in women who died a decade before. Every one of the women (100 per cent) who died from maternal cases in 2002-2006 suffered from anaemia (Hb < 10.1 gm%), while the population was 83 per cent in the earlier series. In particular, the proportion in the 2002-2006 series with very sever anaemia (Hb < 4 gm%) was three times greater, from 11 to 34 per cent (WHO 1999). When the haemoglobin level is less than 4 gm%, the risk of sudden heart failure is very high (up to 40 percent) of all cases (WHO, 1999). Available blood was preventing some of these deaths in 1983–85. However, administrative and managerial problems related to blood transfusion in acute anaemic patients have multiplied since 2002, with the advent of HIV, hepatitis B, syphilis and malarial parasites, and screening for these infections has become mandatory since then. This has frequently resulted in the hospital being unable to provide blood for transfusion because the equipment or supplies to carry out the mandatory tests were not available. Blood donation by relatives continues to be rare. All these factors have contributed to maternal deaths related to anaemia in the 2002-2005 series. In table 2, question 8, 255 (85.0%) and 98 (15.0%) responded Yes and No respectively to the question “Have improvements in roads and transport facilities reduced maternal mortality and morbidity among women in the zone? ”With the improvement in roads and transport facilities which took place in the years, and increased number of women who died in the hospital had traveled from distant places and had arrived at the hospital with the hope of surviving. Because of the hilly terrain and poor (even if approved) roads for the long distances, delays in bringing women to the hospital, leading to deterioration in the woman’s condition, were always a strong possibility in the majority of the cases. Eight women were carried manually on a cot or on someone’s back. Often, a woman would be carried on a clot or on someone’s back from her village to the nearest motorable road. Distance and lack of transport together may have contributed to far more material deaths in the community than among women who reached the hospital. Results from table 2, question 9, shows that 270 (90.0%) accepted and 30(10.0%) rejected to the question “Does expenditure on transport have any effect on maternal mortality among women in Nsukka zone?” All but those who used hospital ambulances had to hire private transport and pay for it. The exorbitant amounts they had to pay are of great concern, given that the majority of them were extremely poor. The average expenditure on transporting the dying woman in each case had doubled in the period between the studies. This may partly be due to the increased cost of fuel and the longer distances traveled. However, more families had ventured to come to the hospital from longer distances, in the hope of saving the woman’s life. We gathered that many of the families had to borrow from a local moneylender or pawn some of their belongings before undertaking the journey. The whole experience left them poorer both materially and emotionally, especially when, despite their desperate efforts, the woman’s life could not be saved. On question10, 261(87.0%) respondents responded Yes and 39(13.0) respondents responded No to the question “Do some women have a high likelihood of getting seriously ill during pregnancy?”Malaria has serious adverse effects on pregnant women. Most pregnancy–related maternal deaths are directly attributable to malaria, mostly associated with severe anaemia, HIV complicates this further. HIV may reduce pregnant women’s ability to control malaria, particularly in higher birth orders. Tuberculosis (TB) kills more women than any other infectious disease and women have a higher progression from infection to disease and a higher case – fatality rate than men (Diwan VK et al 199). Women with HIV in several sub-


Saharan African countries have been shown to be at greater risk of dying up to two years after pregnancy than HIV negative women. Table 3, shows the mode of transport used by pregnant women in study area. From the table, 36, (28.8%) respondents used their foot, none used animal, 44 (14.7%) used their own car/bus/taxi, 92 (30.7%) used Private commercial bus, 39 (13.0%) used Friends bike, 6 (2.0%) used Ambulance, 22 (7.3%) used commercial motorbike; 11 (3.7%) used other means of transport not mentioned here. None used the NURTW bus because they were not available. The result here shows that transportation is a serious factor affecting the people in the area. We therefore suggested that health resources should be focused on those in greatest need in developing countries. It is important to identify groups of women who have an increased risk of maternal mortality and develop appropriate policies to target them.

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Received for Publication: 28/09/2008 Accepted for Publication: 04/12/2008 Corresponding Author Momoh, M. A Department of Pharmaceutics, University of Nigeria, Nsukka. Email:


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