Vol 2 - Cont. J. Med Res.re

8/9/2019 Vol 2 - Cont. J. Med Res.re

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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.

1Okagbare T. E. and

2Emudianughe T. S.

1Department 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(46-

62%) 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.


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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

Central

hospital

Warri

Central

hospital

Sapele

Central

hospital

Agbor

Federal Medical

Centre Asaba

Total

Bacterial infection

Acute dento-alveolar abscess 24 25 25 24 24 122

Pericoronitis 14 13 13 15 15 70

Lateral periodontal abscess 7 5 7 6 7 32

Post-extraction infection 5 7 6 6 5 29

Acute ulcerative gingivitis 5 4 6 4 5 24

Cellulites 4 4 2 4 3 17

Salivary gland infection 1 2 1 1 1 6

Total 60 60 60 60 60 300

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


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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, % Duration prescribed, %

Acute infection Amp Pen Metr Eryth 3 days 5 days 7days

Acute dento-alveolar abscess 69 13 9 9 5 91 4

Lateral periodontal abscess 63 11 19 7 8 89 3

Post-extraction infection 63 6 21 10 7 82 6

Pericoronitis 58 4 32 6 10 81 9

Acute ulcerative gingivitis 5 1 92 2 46 44 10

Salivary gland infection 41 10 38 11 2 88 10

Cellulitis 6 91 2 1 69 26 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,


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although it is recommended that its usage should be restricted, unless specifically indicated by bacterial

culture, due to the possibility of inducing colitis (Mehrohofet 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 Ludwigs 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.


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REFERENCESChow A W, Roser S M, Brandy F A, (1978). Orofacial odontogenic infections. Ann. Intern. Med; 88:392-

402.

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 oforofacial 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 @yahoo.com


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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 of1Anatomy and

2Radiology. College of Health Sciences. Usmanu Danfodiyo University,

Sokoto, Nigeria.

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 orpituitary 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 dimensionsof 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,


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the sella is bounded by the dorsum sellae and the posterior clinoid processes; its lateral margins are thecarotid 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 ofthe 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).


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The dorsum sellae: - The dorsum sellae is the vertical posterior boundary of the sella and is formed by twolateral 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 13 year old boy with Cushings syndrome due to an adrenocortical adenoma (Steinbach et al.,

1963). A small sella was also reported in Sheehans 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 andGemzell, 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, Nelsons 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


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Erosion of undersurface of anterior clinoid processes and chiasmatic sulcusErosion 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, Hunters 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:


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Destruction of top of dorsum may include loss of those rough elements of bone that are the site ofattachment 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 theirligaments, 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). Inabout 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).


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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 theattention 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).


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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;131:99-

104.

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, 343-

359.

Chummy S. and Sinnatamby (2004). (Editors) Lasts 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: 989-

1008.

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, AJRAm. 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. AJRAm. 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 (Sheehans

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 Cushings 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.



Corresponding Author:

Dr. A.D. Zagga,Department of Anatomy, College of Health Sciences, Usmanu Danfodiyo University, PMB 2346, Sokoto,

Nigeria.

E mail:[email protected]

Fax: +234-80-231514.


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POST PRANDIAL BLOOD PRESSURE CHANGES IN PATIENTS WITH CHRONIC RENAL

FAILURE DURING HEMODIALYSIS.

Onyemekeihia UR1, Esume CO

2, Bamgboye LE,

3Anyanwu BE

4

1Department of Medicine, Nephrology Unit, Central Hospital, Warri.

2Department 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 thepatients 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


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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 rateand 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

TIME(HR) TEST(MMHG) CONTROL(MMHG)

0 171 23

----- -----

94 14

169 23

----- -----

92 18

1 168 23

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

92 15

168 22

---- ------

91 12

2 169 31

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

94 19

176 27

----- ------

95 16

3 169 28

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

93 18

176 26

----- ------

93 17

4 169 24

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

92 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 foods 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 Parkinsons 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 1 hr 2 hrs 3hrs 4hrs

TEST Males

96

167

14

25

92

165

17

24

94

163

20

31

94

166

19

25

91

167

16

22

Females

90

173

15

22

91

172

14

23

94

175

19

31

93

172

16

31

93

172

16

25

CONTROL

Males

94

166

12

23

92

164

15

25

93

167

17

25

93

169

15

22

98

176

13

26

females

90

173

16

23 91

172

19

29 95

186

16

29 94

184

19

30 97

188

17

28

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.


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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 t-

test.

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

Mean Blood Pressure for all patients was99

172

17

26MMHG, with the males having a mean blood

pressure of 94

167

16

26MMHG and the Females

93

17718

27MMHG. The Mean BP in the test and

control for both sexes was 93

169

17

27MMHG and

93

17417

25MMHG respectively.

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


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18


to splanchnic sequestration or decreased vascular resistance due to splanchnic vasorelaxation (Barakat etal, 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 troublesomeside 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 hardlysuffer 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 aboutweakness, 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.

AKNOWLEDGEMENTThe 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


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Hirakata, H; Onoyama, K; Hori, K; Fujimi, S; Fujishima, M (1987): The hemodynamic and humoralresponses 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):80-

8.

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: 28/12/2007Accepted for Publication: 24/02/2008

Corresponding Author

C.O. Esume,

Department of Pharmacology and Therapeutics, Delta State University, Abraka

Email: [email protected]


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AN EPIDEMIOLOGICAL STUDY OF ADDICTION AND PSYCHOSOCIAL BEHAVIOUR AND RISK

OF OBESITY IN URBAN POPULATION

Khalid U Khayyam1, Sazina Muzammil

2, Mohd Yunus

1, Zulfia Khan

1

1Department of Community Medicine, Jawaherlal Nehru Medical College, Aligarh Muslim University, Aligarh,

UP, India2Department 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 behaviourplay 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 uptake 2. 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 self-

esteem are noted in obese when they loose weight. As a consequence of


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

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

Subjects

Alcohol Tobacco Smoking Pan-Masala Pan Drug None

Obese

(n=458)

9

(2.0)

6

(1.3)

12

(2.6)

11

(2.4)

49

(10.7)

0

(0)

371

(81.0)

NonObese

(n=3535)

27(0.8)

184(5.2)

177(5.0)

169(4.8)

254(7.2)

0(0)

2724(77.0)

Chi square

1 d. f

7.08 13.8 5.37 5.62 6.84 0 3.61

P 0.01 0.001 0.05 0.02 0.01 0 0.10

Figure in bracket indicates percentage of the value above it.

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/ height

2

(kg/m2) was used as an index of relative weight. Persons with BMI>30 kg/m

2were 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.


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DISCUSSIONIn 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

Subjects

Withdrawn Self

consious

Loneliness Emotional

deprivement

Anxiety Depression None

Obese(n=458)

14(3.0)

234(51.1)

23(5.0)

9(2.0)

64(14.0)

55(12.0)

59(12.9)

Non Obese

(n=3535)

61

(1.7)

424

(12.0)

141

(4.0)

70

(2.0)

353

(10.0)

389

(11.0)

2097

(59.3)

Chi square 1

d. f

3.19 455.0 0.98 0.0 6.72 0.38 350.83

P 0.1 0.001 0.5 N.S. 0.01 N.S. 0.001

Figure in bracket indicates percentage of the value above it.

NS = not significant

Carl9, Hammer

10, Bruch

11, David

12and Judith

15also 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 anxietyhad 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. HealthMedia 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 rangeevaluation 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.



Corresponding Author

Dr. Khalid U Khayyam

HOD, Epidemiology and Public Health, LRS Institute of TB & Resp. Diseases,

Sri Aurobindo Marg New Delhi-110030. India

E-mail: [email protected]




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DIETARY GUIDELINES FOR GOOD HEALTH

Francis Olawale Abulude

Department of General Studies. Federal College of Agriculture, Akure 340001, Ondo State. Nigeria.

(Email: [email protected])

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) worldover 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 bloodpressure, 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 peopleto 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


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

ii. Vegetableiii. Bread, Cereal, Rice and Paste

iv. Milk, yogurt and cheese

v. 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 promotetooth 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 fromeating 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 1 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 gastrointestinaltract. 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 14-20Vit B-6 mg 1.3-20

Vit B-12 g 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 g 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 - 15Chloride 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 44-56Sugar 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 foods 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 foods 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 Publishersand 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). Teachers 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.


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CORRELATION OF SERUM URIC ACID WITH MATERNAL AGE, PARITY AND SEVERITY OFBLOOD PRESSURE IN PREECLAMPTIC PREGNANCIES

Sazina Muzammil1, Khalid Umer Khayyam

2, Nayyar Parvez

3

1Department 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 Pharmaceutics,

Advance Institute of Phamacy,MD University. Rohtak,Faridabad,Haryana,INDIA.

ABSTRACT

Maternal serum uric acid was determined in 30 preeclamptic and 20 normalpregnant females in their third trimester. Serum uric acid was 3.52 0.75 in normal

pregnancies and 6.03 1.67 in preeclamptic pregnancies. This increase in serum

uric acid was highly significant (P


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Sazina Muzammil et al: Continental J. Medical Research 2: 24 - 34, 2008

associated renal/hepatic/cardiac disorder; metabolic disorders; concomitant severe complications ofpregnancy, pregnancy less than 28 wks o

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