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A comparative study of iron deficiency in the Indian and the African in Durban.
(1963) Mayet, Fatima G. H.
The thesis is comprised of a comparative study of iron metabolism with particular reference to iron deficiency in the Indian and the African; Europeans were included when naterlal was available. Fifty four patients with iron deficiency anaemia were studied. There ware 43 Indians as compared with 11 Africans although the overall proportion of Indians to Africans admitted to the same ward was 1 : 4. Amongst the Indians the commonest cause of anaemia from blood loss was peptic ulceration (6 patients); while 3 had cirrhosis of the liver, one had hookworm anaemia and one was a case of ulcerative colitis. Gynaecological lesions were found in 2 patients, one had a proliferative endometrium and the other had endometrial polypi. Idiopathic iron deficiency anaemia was found in 60.5% of the Indian patients (both male and female). Amongst the Africans on the other hand, there were 2 cases of hookworm anaemia and 2 of cirrhosis of the liver while peptic ulceration was suspected in one patient who alao had amoebic dysentery and urinary hllharsiesis. None of the Africans had Idiopathic iron deficiency anaemia with the possible exception of one who had 4 Caesarean sections in rapid succession. There were 175 Indians, 175 Africans and 139 Europeans who were studied haematologlcally during pregnancy. The Incidence of iron deficiency anaemia among them was 26.7%, 2% and 4% respectively. The third aspect of the thesis is confined to an analysis of necropsy materiel for iron stores. Two hundred Africans and 58 Indians were studied. It was found that the incidence of *siderosis" in the African was high. There was a significant difference in the iron concentrations in the stores of the 2 racial groups. It was concluded that iron deficiency anaemia is common in the Indian. Diet appears to play an important role in its production.
The Clinico-pathological manifestations of schistosomiasis in the African and the Indian in Durban.
(1964) Bhagwandeen, Surridhine Brumdutt.; Elsdon-Dew, R.
Abstract available in PDF.
The pathological aspects of heart failure in the Natal African.
(1967) Kallichurum, Soromini.; Wainwright, J.
The aims and objects of this work, as outlined in the introduction, were to a s s e s s the necropsy incidence of deaths due to heart failure in the African in Durban, to a s s e s s the necropsy incidence of the various aetiological types of heart failure with particular reference to right ventricular hypertrophy and failure, and to compare and contrast the incidence, complications, morbidity and mortality of heart disease in the Natal African with the same in other African and racial groups, both in South African and elsewhere. Many of the points emerging from this work merely confirm what has long been known, but others refute previous concepts. The all-age average necropsy incidence of deaths from heart failure in the African in Durban is of the order of 8%. This percentage does not, unfortunately, lend itself to straight comparison with most other series because of the high infant mortality shown in the present study. However, in considering deaths due to heart failure in the 10-plus age groups, the African still shows a lower mortality from heart disease in comparison with figures obtained for Indians or those reported for the Coloured and White races in South Africa. There are six major causes of heart disease in the African, which in order of frequency are, rheumatic heart disease, hypertensive heart disease, cardiomyopathy, cor pulmonale, pericarditis, and syphilitic heart disease. While little difference is apparent in the incidence of rheumatic and hypertensive heart disease, and possibly cor pulmonale, among the various races, cardiomyopathy, pericarditis and syphilitic heart disease are far more important causes of heart failure in the African by contrast with the other racial groups in South Africa. Although coronary a r t e r y disease is by comparison very uncommon in the African, cardiomyopathy, pericarditis, and syphilitic heart disease together claim as many deaths from heart failure in these people as does coronary heart disease among the Indian and White races in the Republic. Except for minor variations in the incidence of certain aetiological types, and the geographical distribution of endomyocardial fibrosis and cardiomyopathy/. . cardiomyopathy, the g e n e r a l p a t t e r n of h e a r t d i s e a s e among the Africans in Natal a p p e a r s to be s i m i l a r to that r e p o r t e d from other P r o v i n c e s in South Africa and most other c o u n t r i e s on the continent. Rheumatic h e a r t d i s e a s e is r e s p o n s i b l e for 21. 5% of all deaths from congestive h e a r t failure in the African in Durban. The immediate and the l a t e c a r d i a c complications of r h e u m a t i c fever in the Durban African a r e , on the whole, found to be no different from those r e p o r t e d in W e s t e r n communities. The findings in t h i s study t h e r e f o r e refute the view that r h e u m a t i c h e a r t d i s e a se i s infrequent in the African after the age of 40 y e a r s , and failed to support the suggestion that the d i s e a s e affects them m o r e s e v e r e l y or that death from r h e u m a t i c heart d i s e a s e o c c u r s at an e a r l i e r age in t h i s r a c e . While it is a g r e e d that s e v e r e valvular deformity in young African subjects (under 15 y e a rs of age) o c c u r s c o m p a r a t i v e l y m o r e frequently, it must be stated that this is in no way p e c u l i a r to the African, similar lesions being o b s e r v e d in Indian s u b j e c t s of c o r r e s p o n d i n g age. Hypertensive h e a r t d i s e a s e is common among the African in Durban, accounting among t h em for 18. 9% of all deaths from congestive h e a r t f a i l u r e. While both e s s e n t i a l and secondary forms of h y p e r t e n s i o n occur in the local indigenous population, the former appears to be m o r e common, with a peak incidence in the seventh decade of life. Secondary hypertension, mostly r e n a l in origin, is an i m p o r t a n t cause of h y p e r t e n s i v e congestive c a r d i ac f a i l u r e in the fourth decade. The wide v a r i a t i o n s in the type of h y p e r t e n s i on r e p o r t e d from the different regions in Africa, and the doubt e x i s t i n g as r e g a r ds the significance of focal lesions in the kidneys, point towards the need for g e n e r a l l y accepted c r i t e r i a in the diagnosis of r e n a l hypertension, p a r t i c u l a r ly with r e g a r d to chronic phylonephritis. Cardiomyopathy c l a i m s 15. 8% of all deaths from congestive heart f a i l u r e in the local African population. While many of the pathological changes o c c u r r i n g in the h e a r t in t h i s d i s e a s e were found to be s i m i l a r to those of other i n v e s t i g a t o r s , c e r t a i n f e a t u r e s , relating to c a r d i a c hypertrophy and s t r u c t u r a l a l t e r a t i o n s in the pulmonary v e s s e l s , have been e s p e c i a l ly i n v e s t i g a t e d / . . . investigated and results obtained in this series of cases show that whereas pure right ventricular hypertrophy is uncommon in cardiomyopathy biventricular hypertrophy with predominance of the right ventricle is the most frequent form of cardiac enlargement in such cases. Equal hypertrophy of the ventricles is the next common form of enlargement; left ventricular predominance is by far the least frequent, and no case of exclusive left ventricular hypertrophy was encountered. Although structural alterations in the pulmonary a r t e r i e s , indicating pulmonary a r t e r i a l hypertension, were observed in a large number of cases investigated, such changes were in no way specific to cardiomyopathy, since similar changes were observed in cor pulmonale due to emphysema and also in some cases of hypertensive congestive heart failure. Structural alterations in the small muscular pulmonary a r t e r i e s and arterioles were also identical with those found in emphysema. Whereas fresh pulmonary emboli and infarcts were frequently encountered and were often of such degree as to be the immediate cause of death, chronic pulmonary thrombo-embolism of an extent sufficient to have been the cause of right ventricular predominance was seldom found. It is suggested that the cause of the pulmonary hypertension and certain pathological changes in the heart in cardiomyopathy may lie in some form of exogenous toxin, possibly related to the practice of herbal medication among the African people, which acts as an a r t e r i a l vasoconstrictor in both the pulmonary and systemic circulations. This would suggest that the a r t e r i a l changes observed in the lungs are probably the result and not the cause of pulmonary hypertension. The incidence of cor pulmonale as a cause of congestive heart failure among the African in Durban is of the order of 12%. It has been shown that almost one quarter of all cases of right ventricular failure remains undiagnosed, as regards aetiology, at routine necropsy. The latter finding pointed towards the need for an investigation of the causes of right ventricular failure in the African. Such a study was undertaken and special methods of investigation w e r e / . . . were used as aids towards a more conclusive diagnosis. This study showed fibrosing lung disease, due particularly to the late complications of pulmonary tuberculosis, to be the most important cause in the production of chronic cor pulmonale in the African in Durban. The development of cor pulmonale in such cases depends not only on the presence of pulmonary parenchymal damage by fibrosis, but also on the associated pleural thickening, adhesions between chest cage and diaphragm, emphysema, and the curtailment of the pulmonary a r t e r i a l bed. In this series, all cases of fibrosing lung disease with cor pulmonale investigated for cardiac hypertrophy by means of separate weighing of the ventricles, showed evidence of pure right ventricular enlargement, indicating no significant chronic burden on the left ventricle of a diastolic overload through bronchial shunting. Thrombo-embolic cor pulmonale, hitherto believed to be r a r e in the African, emerges as the most important cause of acute cor pulmonale and the second most common cause of the more chronic varieties of the disease. The usual pathological type of pulmonary thrombo-embolic disease observed in this study is one in which fairly large pulmonary a r t e r i e s , as opposed to those of microscopic size, were involved and in consequence infarction was frequent. The lack of completely organised lesions, and the relatively small increase in total heart weights (majority below 400 Gms) suggest a rapid course in these cases, measured in months rather than in years. The usual source for pulmonary emboli was found to be the veins draining the lower limbs, particularly the deep calf veins. Whereas a predisposing factor for the development of venous thrombosis was found in just over half the number of cases investigated, in 44% of all cases of thrombo-embolic cor pulmonale in this study no cause was found at necropsy for the peripheral venous thrombosis. Of the predisposing causes encountered a posteriorly placed amoebic liver abscess emerges as an interesting aetiologic factor in the development of thrombo-embolic cor pulmonale because of its ability to produce hepatic vein and inferior vena caval thrombosis. Emphysema, usually in association with chronic bronchitis, was found to be the third most common cause of chronic cor pulmonale among Africans/ . . . Africans in Durban, and was encountered mainly in its mixed form (centrilobular and panlobular). Although structural alterations in the pulmonary a r t e r i es were noted in a significant number these were sometimes of insufficient degree to be the cause of pulmonary hypertension, thereby suggesting some other factor in the production of a raised pulmonary a r t e r i a l p r e s s u r e . Results of separate ventricular weighing in these cases show exclusive right ventricular hypertrophy, again indicating strain solely on the right ventricle. Bilharzial cor pulmonale, although one of the r a r e r causes of cor pulmonale in the African in this series, is suspected to be probably more frequent than hitherto believed. The lack of obvious macroscopic changes in the lungs of such cases is stressed, and while this may account for omissions in diagnosis, a sudden recent increase in the incidence of bilharzial cor pulmonale might also suggest that the disease is becoming more severe. Primary pulmonary hypertension as a cause of cor pulmonale in the African is r a r e , being suspected in only one case in this series. In keeping with the generally high incidence of infective diseases in the African, pericarditis as a complication of tuberculosis and hepatic amoebiasis, and the cardiac complications of syphilitic aortitis still occupy major positions among the causes of congestive heart failure in this population; together accounting for 12.4% of all deaths from congestive heart failure. Tuberculosis and amoebiasis are important not only in the production of p e r i c a r d i t i s , but, as mentioned, also play an important part in the development of cor pulmonale. Syphilitic heart disease, besides being a significant factor in the production of congestive heart failure, is the most important cause of a sudden cardiac death in the African. In conclusion it may be said that while little can be achieved with regard to the control of diseases for which no cause has as yet been found, the elimination of infective conditions such as tuberculosis, amoebiasis and syphilis will result in a significant drop in the incidence of death and disability from heart failure in the African in Natal.
Assisted respiration in the treatment of neonatal tetanus.
(1967) Thambiran, A. K.
A study of some aspects of senescence in embryos of zea mays L.
(1968) Berjak, Patricia.; Villiers, T. A.
Abstract available in PDF file.
The oxygen consumption in tetanus neonatorum.
(1968) Desai, S. D.; Adams, E. B.; Ripley, S. H.
No abstract available.
Observations on the effects of some environmentally induced mental stresses on the heart.
(1973) Meeran, Mooideen Kader.
No abstract available.
The effects of nerve stimulation on pacemaking activities of biological tissues.
(1973) Bhagat, Chotoo Ichharam.; Reid, John Victor Oswald.
The effects on the cardiac cycle length of stimulating the vagus nerves with single supramaximal electrical shocks depended upon when they were stimulated during the cycle. A maximum prolongation of the cardiac cycle was obtained when the vagi were stimulated 167 msec (SD±64) after the peak of an electrocardiogram P wave. The interval between a P wave and the subsequent vagal stimulation was called Pl-St interval. Pl-St(max) was the Pl-St interval at which maximum prolongation of the cardiac cycle occurred. Pl-St(max) increased significantly (p (0.001) with longer cardiac cycles. When the Pl-St intervals were shorter or longer than 167 msec (SD±64) the effects of vagal stimulation were less. The latent period for the effects of vagal stimulation was 195 msec (SD±32) The latent period also increased significantly (p(O.Ol) with longer cardiac cycles. The rise time of the vagal effect, obtained by subtracting (Pl-St(max)+ latent period) from the control cardiac cycle length, was 124 msec (SD+31) and occurred between Pl-St intervals of 167 msec (SD±64) and 291 msec (SD±70). The rise time did not vary with cardiac cycle length (p) 0.1), but the magnitude of the maximum response to vagal stimulation was inversely proportional to rise time (p <. 0.02). The peak response to vagal stimulation must have occurred when the vagal effects pegan somewhere in the middle of diastolic depolarization of the pacemaker cells in the S-A node. The reasons for this were discussed. The half-decay time for the effects of vagal stimulation was 210 msec (SD±102). The slope of the curve relating the prolongation of the cardiac cycle length to Pl-St is positive at Pl-St intervals less than 167 msec (SD±64) and negative at Pl-St intervals between 167 msec (SD±64) and 291 msec (SD±90). The positive slope ranged from 0.13 to 0.48 with a mean of 0.23. The paradoxical responses of the S-A node to vagal inhibitory input obtained by Reid (1969), Levy et al (1969)and Dong and Reitz (1970) would be explained by the dependence of the cardiac cycle length upon the time of arrival of vagal stimulus in relation to the previous P wave and upon the slope of the curve relating the prolongation of the cardiac cycle length to Pl-St interval being positive and between zero and two at Pl-St intervals less than 167 msec (SD±64. The effects of single shock stimulation of the vagus nerves persisted for 3.890 sec (SD+l.255)7 the number of cardiac cycles involved varied between 5 and 11. The duration of the effects of vagal stimulation did not depend upon when during the cardiac cycle the vagi were stimulated. A "dip" in the response to vagal stimulation was present in all the experiments. The possibility of the "dip" phenomenon being due to simultaneous stimulation of the sympathetic fibres in the vago-sympathetic trunk was ruled out. It is suggested that the "dip" phenomenon may be due to transient accumulation of K+ in the interstitial fluid surrounding the pacemaker cells in the S-A node.There was no paradoxical response of the smooth muscle in the distal colon of the adult rabbit when the frequency of sympathetic inhibitory input was continuously increased. A paradoxical response in the frequency but not in the size of the contraction of the smooth muscle was obtained when the sympathetic nerves were stimulated with bursts of stimuli, each burst consisting of 5-40 impulses, 10 msec apart. One may conclude from this that the delay of the next spontaneous contraction but not the inhibition of the size of smooth muscle contraction is dependent upon the arrival time of a burst of stimuli during a contraction cycle. This was confirmed in an experiment when the sympathetic nerves were stimulated with single bursts of stimuli applied at different times during the contraction cycle. It is unlikely that such a paradoxical response would occur under physiological conditions as this would require the natural sympathetic efferent discharges to the smooth muscle to occur in regular bursts, each burst consisting of impulses at a high frequency. Stimulation of the sympathetic nerves at 3, 5, 10 and 25 PPS caused an inhibition of the size and frequency of smooth muscle contraction in the distal colon of the newborn rabbit. Assuming that the cholinergic fibres are excitatory there is therefore no evidence for the sympathetic fibres to the distal colon being cholinergic in the newborn rabbit. This is contrary to Burn's (1968) report of the sympathetic fibres being motor and cholinergic to the small intestinal smooth muscle in the newborn rabbit.The heart rate increased rapidly at the onset of exercise and then more gradually over the rest of the exercise period. The initial increase in the heart rate during exercise was not affected by adrenergic blockade but the subsequent increase in heart rate was significantly reduced by adrenergic blockade. Hence the increase in heart rate at the onset of exercise is due primarily to a decrease in the cardiac vagal efferent discharge, whereas the subsequent increase in heart rate is due to both a further decrease ln vagal discharge and an increase in sympathetic discharge to the S-A node. In almost all the sub jects there was initially a rapid decline in the heart rate in the post-exercise period, but subsequently the heart rate returned to resting levels in a variety of ways. These were classified into 5 types. Of particular interest to the present study was the Type V pattern of heart rate change. This was characterised by an increase in heart rate of 6 beats or more per minute during the post-exercise period, with or without superimposed arrhythmia. The Type V pattern may be the equivalent of the paradoxical responses to inhibitory input demonstrated in animal experiments i.e. an increase in the heart rate with increasing vagal stimulation frequency. Type V pattern occurred more frequently at mild exercise levels (4 out of 14) than at moderate exercise level (lout of 14) and also more frequently in adrenergic blocked individuals (11 out of 28) than in control subjects (5 out of 28) It is suggested that the sympathetic effects on the P-R interval and arterial baroreceptor modulation of vagal efferent discharge protect again st the occurrence of paradoxical responses to vagal inhibitory input. They may do so by confining the vagal discharge to the rise time of vagal effect during the cardiac cycle. On the other hand the Type V pattern in p-adrenergic blocked individuals may be due to a decrease in the vagal discharge, in which case Type V pattern would not be a paradoxical response. The changes in minute ventilation in the post-exercise period were also variable. Besides a gradual decline in minute ventilation there were also gradual increases and sudden increases and decreases in minute ventilation. These may represent a form of paradoxical response to increasing inhibitory input and decreasing excitatory input to the respiratory neurones in man. However, all the changes in minute ventilation could also be explained by fluctuating excitatory and inhibitory neural input to the respiratory neurones.
The RH Factor : a clinical and fundamental study of its significance in ISO- and Auto-Haemolytic anaemias.
(1973) Vos, Gerhardus Hubertus.; Villiers, T. A.; Bain, Peter G.
No abstract available.
Host allergic response variation in children with measles infection.
(1977) Coovadia, Hoosen Mahomed.; Smythe, P. M.
In many infections some patients recover while others die or are permanently disabled. These extremes in clinical outcome may be determined as much by the capacity of the host to eliminate the infecting agent as by the antigenic load on the individual. Children with measles who do not recover may succumb to acute complications (mainly respiratory) or chronic disease (respiratory and neurological) may develop. Analysis of immunological function antedating any of these final events would assist in understanding their pathogenesis and possibly aid in management. In order to achieve t h i s , immunological responsiveness was at f i r st studied in 24 children with acute measles and compared with that in 20 children with established chronic post measles chest disease investigated 6 - 1 6 weeks after appearance of the rash. The immunosuppressive effects of acute measles were extensive. Total white cells were reduced and this reduction was accounted for entirely by lymphopenia which was equally expressed among the major lymphocyte sub-populations studied; the function of T cells, assessed by radioisotope incorporation into phytohaemaggiutinin-transformed lymphocytes and by delayed skin hypersensitivity to dinitrochlorobenzene, was depressed. Serum IgA was reduced in acute measles patients. In contrast there was a relative sparing of the measured indices of immunity in patients with chronic post measles chest disease, with the major defect being an impaired delayed hypersensitivity reaction to dinitrochlorobenzene. There were minor alterations in complement components in both groups of patients with the evidence suggesting minimal utilisation of the alternative pathway in acute measles and classical pathway in chronic patients. High levels of heterophile antibodies to sheep red blood cells were detected in patients with chronic chest disease. (11) The results suggested that the conditions for chronicity of pulmonary disease in measles were unlikely to be determined by persistent abnormalities in the immunopathological factors enumerated, most of which were normal in chronic patients. It was not possible to interpret the findings of defective delayed hypersensitivity and complement components in patients with chronic chest disease as being either the cause or the effect of chronicity. The latter findings would have to be compared with results in children who had recovered from measles studied six weeks after onset of rash. An attempt was made to resolve this problem. Twenty-two children with measles were studied in the acute stage of the rash and six weeks later and results compared with matched controls. The above findings in acute measles were confirmed: the total lymphocyte count and major lymphocyte sub-populations were significantly below control values. At six weeks the B cell and Null cell counts were s t i ll significantly diminished. The function of T cells assessed by radioisotope uptake by phytohaemagglutinin-stimulated lymphocytes and by delayed skin hypersensitivity reaction to dinitrochlorobenzene was impaired during the acute stage and this persisted for six weeks. No important abnormalities were detected in serum immunoglobulins and complement components. Partial reversal of immunological suppression caused by measles was therefore demonstrated at 6 weeks after the appearance of rash. Demonstration of a persistently defective delayed hypersensitivity in those who recovered made i t unlikely that this anergy was important in the development of chronicity. Complement abnormalities were similarly unrelated to progression to chronic lung damage. ( Children who recovered, when studied at six weeks, appeared to be worse o f f immunologically than those with established chronic chest disease following measles. Children with chronic chest disease were studied 6 - 1 6 weeks after onset of rash, by which time the partial reversal of immune deficiency, noted at 6 weeks, would be complete. Among the group of children studied during the acute rash of measles there were five who subsequently died and one who progressed to chronic chest disease. Results in these six children were compared with those in six age-matched children who recovered from measles within a week. In the children who subsequently died or developed chronic pneumonia, immunosuppression was more pronounced during the acute rash ( i . e ., 3 - 2 0 days before death) than in the children who recovered. The absolute total lymphocyte count (T and B cells) was s i g n i f i c a n t ly lower in those who died or developed chronicity. Mean serum C, was also lower in this group. There were no significant differences between the two groups for total white c e l l s , neutrophils, Null c e l l s, cells with both T and B cell markers, other complement factors, serum immunoglobulins and phytohaemagglutinin stimulation of lymphocytes. The total lymphocyte count in a further nineteen patients with measles who had died, studied retrospectively, was s i g n i f i c a n t l y lower than that in twenty-seven patients with measles who recovered. Children whose outcome was poor generally had absolute lymphocyte 3 counts below 2000 cells/mm whereas those who recovered had values above this level. (iv) Therefore children who w i l l die or develop chronic chest disease can be often distinguished, within two days of the appearance of the rash, from those who w i l l recover. In order to test the v a l i d i t y of this conclusion based on results obtained from a small sample the study was extended so as to increase the number of patients with measles who had severe lymphopenia (< 2000 cells/mm3). Seventy seven per cent of 30 children who had severe lymphopenia within 2 days of appearance of rash f a i l e d to recover: 30% died from pulmonary complications within a few days to two months of the onset of the exanthem while 47% developed chronic lung damage. This was s i g n i f i c a n t ly worse than the outcome in 30 children with lymphocyte counts above 2000 3 cells/mm , of whom 67% recovered, 33% developed chronic chest disease and none died. Persistence of severe lymphopenia (which was due to reduction 3 in both T and B cells) in those with i n i t i a l counts below 2000 cells/mm , for at least fifteen days after onset of rash, remained a good predictive index of morbidity and mortality. Reversal of immunoparesis in those with i n i t i a l severe lymphopenia was slower and less complete 42 days from the appearance of the rash in children who subsequently died or progressed to chronicity than in those who recovered. All patients who died f a i l ed to produce an adequate or sustained antibody response to measles. The results of these studies suggest that long term pulmonary and possibly neurological sequelae of measles are probably due to a transient widespread immunoparesis during early measles with persistent defects in specific immunity to measles and probably other viruses, whereas recovery is due to less severe effects of shorter duration. (v) In order to answer the question why some children do badly and others well after measles, studies on the HLA frequencies and measles antigen load have been undertaken in children with severe lymphopenia. Results of viral load are inconclusive and those of HLA suggest a trend towards histocompatibility linked genetic susceptibility to the development of severe lymphopenia in measles associated with HLA AW32. The therapeutic implication of these studies is that children with measles who are at risk for death and chronic disease can be identified early in the disease and intervention at this stage may reverse the severe immunosuppression which leads to rapid demise or modify the immunopathological changes progressing relentlessly in some cases to permanent lung and brain damage and occasionally to death.
Experimental diabetes in the baboon.
(1979) Naidoo, Dayananthan.; Asmal, A. C.
The object of the present study was to determine simultaneously aspects of hepatic and peripheral glucose metabolism in the intact baboon. Isotopic techniques were used to study glucose turnover rates, glucose recycling, glucose pool and space, and the forearm technique to study peripheral exchange of glucose. The results obtained in the normal animals acted as reference values for each animal. Thereafter diabetes mellitus was produced with streptozotocin, a drug causing destruction of the beta cells of the pancreatic islets. Experiments were then repeated in the acutely diabetic baboon and the nature and extent of the abnormalities in glucose metabolism documented. Lactate metabolism and peripheral lipid metabolism were included in the study in order to establish any interrelationships with glucose metabolism and to determine the abnormalities resulting from the production of diabetes. In the normal animal the turnover rate of lactate was greater than glucose although the lactate pool was much smaller than the glucose pool. After producing diabetes glucose turnover rates increased threefold and correlated with the severity of hyperglycaemia. A significant increase in lactate turnover rates was noted but the increase was less than in the case of glucose turnover rates. The formation of glucose from lactate increased significantly but the fraction of the lactate turnover rate converted to glucose was unchanged. The glucose pool increased nearly threefold and correlated with the increase in glucose turnover rate. There was a significant but smaller increase in lactate pool which correlated with the increase in lactate turnover rate. Both glucose and lactate space decreased after diabetes but the decrease did not correlate with the severity of hyperglycaemia. In the majority of diabetic animals there was no glucose utilization in the forearm, and in fact glucose release was observed. Increased production of lactate occurred in the forearm of the diabetic baboon, despite decreased glucose utilization.Arterial levels of triglyceride and free fatty acid increased threefold after diabetes while the free glycerol level doubled. In the normal animal the general pattern of exchange in the forearm consisted of triglyceride and free fatty acid uptake and free glycerol release. In the diabetic animal triglyceride and free fatty acid release was observed, while the release of free glycerol was decreased. The pattern of forearm metabolism in the diabetic animals was variable and not as consistent as before the production of diabetes. Several interrelationships between glucose, lactate and lipid metabolism were noted. The baboons used in this study showed extreme sensitivity to the metabolic effects of Streptozotocin Diabetes. Hyperglycaemia increased in severity and ketoacidosis invariably developed in the second week. The animals were not treated with insulin and death from severe uncontrolled diabetes occurred in nearly all animals within two weeks. This study has demonstrated the severe abnormalities in hepatic and peripheral glucose metabolism in diabetes. The simultaneous pathogenesis of these abnormalities and their importance in the development of the acute diabetic syndrome have been defined. Associated abnormalities in lactate metabolism and lipid metabolism have also been documented.
The antenatal management of the twin fetus from 30 weeks gestation.
(1979) Houlton, M. C. C.; Philpott, R. Hugh.
The blood groups of the Natal Indian people.
(1980) Moores, Phyllis Patricia.; Bain, Peter G.
No abstract available.
A review of child health care in the Durban Metropolitan area.
(1981) Ramiah, Kowselia Ramaswami.
No abstract available.
Indicators of maternal child health.
(1981) O'Dowd, Patricia Bridget.
The introduction outlines the reasons for the priority of maternal and child health emphasizing the relatively simple resources required. The aims of such programmes must be identified and the results measured so that services can be monitored and evaluated. Categories of measurement are defined and indicators of maternal child health identified within these categories. A chapter is devoted to an outline of the principal non-medical determinants based on material from the Inter-American Investigation of Childhood Mortality. The significance of the principal indicators viz. the perinatal mortality rate, the infant mortality rate, the maternal mortality rate and growth and development data are compared. Chapter lV presents a report of a questionnaire study into local indices viz. Stillbirth rates, Caesarean Section rates and Maternal Mortality rates. The uptake of certain clinic services was also determined. Differences between groups and possible reasons for these are discussed. The final chapter points out the need for accurate birth and death registration and a reliable health information system and suggests methods for achieving this. Recommendations are made for upgrading the collection of data and for improving maternal and child health by research and peripheralization of services.
Challenges facing a community health physician in Bophuthatswana.
(1981) Matjila, Maila John.
No abstract available.
Nephrotic syndrome in African and Indian children in South Africa.
(1981) Adhikari, Miriam.
There are comprehensive accounts of the nephrotic syndrome in childhood in temperate countries. Many of the important features of this disease have been known for close on to two decades. The causal link between malaria and nephrosis in tropical Africa has also been recognised and documented for a similar length of time. Very little was known of the nephrotic syndrome in the sub-tropical zones of Africa where malaria is not endemic. Anecdotal evidence in South Africa suggested that African children with this disease appeared to have steroid resistant nephrosis and a more protracted clinical course than expected from prevailing accounts in the literature and that Indian South African children generally responded to steroids. This thesis is the result of detailed investigations in to this disease in African and Indian children in Durban, South Africa. 2. Preliminary Study A preliminary study was undertaken in which 53 (12 African and 41 Indian) children with the nephrotic syndrome defined by clinical and biochemical criteria 1 ii were studied. Renal biopsies were not available on these patients. The results revealed that two thirds of the African children were over 5 years of age and 50% were males. Of the Indian children 50% were under 5 years of age and 50% were males. Nine African children were treated with steroids and 8 did not respond whereas 31 of the 39 Indian children treated clearly responded to steroid therapy. In addition 5 Indian patients were treated with cyclophosphamide and 3 responded. On follow-up 7 of the African children had persistent proteinuria, 2 experienced remissions and 3 were lost to follow-up. All the Indian patients experienced remissions. The differences between the 2 groups of nephrotic patients were quite striking and therefore a more detailed prospective study of this problem was undertaken. 3. Prospective Study of Primary Nephrotic Syndrome One hundred and seventy children of whom 104 were African and 66 Indian with primary nephrotic syndrome were studied. In both racial groups the male sex dominated, Indian children tended to present iii at a younger age group whereas African children presented at two peak ages, 5 years and between 5 - 10 years. 3.1 Histological Differences The histological types found on light microscopic examination of renal tissue were distinctly different between the African and the Indian children. The majority (85.6%) of the African children had 'obvious' glomerular lesions, the commonest being extramembranous nephropathy (29.8%). Although the proliferative group was the single largest group (40%) none of the subgroups exceeded the extramembranous type in their number. Minimal change accounted for only 14.4% of the African children with nephrotic syndrome. The majority of Indian children (72.7%) had minimal change on light microscopy, 9.1% focal glomerulosclerosis and 12.1% had proliferative changes. 3.2 Immunofluorescence Immunofluorescent studies also indicated differences between the two groups of patients. Generally, heavier deposits of immunoglobulins iv and complement components were identified on renal biopsy specimens of African children. This occurred even in MCNS where most African children had heavy IgG, light IgM, IgA and complement components whereas only a few of the Indian children had light IgM deposits. Similar differences were observed in diffuse mesangial proliferative glomerulonephritis and focal glomerulosclerosis where the numbers of patients were comparable. 3.3 Presenting Features Clinical features at presentation in the two groups were different, as expected from the nature of the histological findings in each group. In the African children (all histological groups) haematuria occurred in 35.5%, hypertension 16.3% and renal failure in 2.9%. The clinical features in the Indian children were not too different from MCNS elsewhere. Haematuria occurred in a small percentage (3%) of MCNS but was more frequent (10.7%) in other groups. Hypertension and renal failure occurred infrequently in histological categories other than MCNS where they did not occur at all. 3.4 Course and Outcome In view of the above it was not unexpected to find that the clinical course and outcome in the two groups were quite dissimilar. African patients in certain of the histological groups fared reasonably well, but none of the groups had the excellent prognosis of Indian MCNS. 3.4.1 Minimal Change One third of the African MCNS patients remitted and this was unrelated to steroids. The remainder who were followed for a reasonable duration of time remained proteinuric. None developed signs of serious renal impairment (azotaemia, hypertension). Indian MCNS experienced an excellent prognosis with 97.8% achieving remission and 81.6% being steroid sensitive. One third of these patients had a single episode of nephrosis while frequent relapses occurred in 28.2%. 3.4.2 Extramembranous Nephropathy Patients with extramembranous nephropathy, the largest group in the African patients, experienced hypertension more often (20%) vi and remission less often (30%) than do children in temperate climates. The clinical presentation, course and outcome in the majority of these patients were similar to adults with extramembranous nephropathy. 3.4.3 Proliferative Glomerulonephritis The patients in the proliferative group had a variable outcome depending on the subgroup to which they belonged. In diffuse mesangial proliferation, African patients had a higher incidence of hypertension and fewer remissions and fared less well than Indian patients. The diffuse endocapillary glomerulonephritis, membranoproliferative and focal proliferative nephritis groups of patients suffered severe disease with a failure to remit and progression to death. In the diffuse exudative group, remissions occurred or proteinuria persisted but severe relapse and death did not occur. The worst prognosis was in the focal proliferative group with the highest incidence of persistent relapse. 3.4.4 Focal Glomerular Sclerosis Focal glomerular sclerosis was an unusual vii histological diagnosis in the African child (3.9%) with a poorer prognosis (persistent proteinuria or death) when compared to Indian children in whom one third remitted and the rest had persistent proteinuria. 3.4.5 Tropical Nephropathies It is difficult to comment on the course of the tropical nephropathy (not related to malaria) and tropical extramembranous groups as the numbers are small. However, in tropical extramembranous, none remitted (all African children) and in tropical nephropathy one Indian child remitted but one of 2 African children died and the other had persistent proteinuria. 3.5 Response to Therapy Perhaps the most important practical aspect of the nephrotic syndrome in the African child was the response to steroid therapy. Thirty two African children were given steroid therapy. Thirty (93.7%) did not respond. Five children deteriorated or died during steroid therapy. Very few patients (4) were given cyclophosphamide and none responded. viii Generally intravenous albumen, diuretics and a high protein diet were not very effective in those patients with severe, clinical disease but were of benefit in milder disease. Indian children taken as a whole, responded well to steroid therapy. Seventy-eight percent of the whole group responded to steroids and 21.4% developed cushingoid features. Of the 19 Indian children (all MCNS) treated with cyclophosphamide 63.2% responded of whom about a quarter got toxic side effects (alopecia, darkened nails and leucopenia). Chlorambucil therapy in 4 children (all MCNS) was successful in all. 3.6 Complications Serious infections (septicaemia, peritonitis, urinary tract infection, meningitis, arthritis, osteitis, measles, chicken pox) occurred in 8.7% of the African patients. Eighteen percent had less severe infections. Just over a quarter of the Indian children suffered severe infections. The majority of these patients were MCNS and about 50% were on steroids or cyclophosphamide at the ix time of their infection. Renal biopsy complications were minor, these being abdominal pain and tenderness or transient haematuria. A few patients developed renal haematomas which were detected or monitored by ultrasonography. The single serious complication was the development of a renal abscess at the biopsy site requiring partial nephrectomy. 3.7 Mortality The overall mortality was 5.8%. Seven of the 10 deaths were African children in the Proliferative Group and 3 of the 10 deaths were Indian children. 4. Secondary Nephrotic Syndrome The secondary nephrotics formed an interesting group of patients. Of the 22 patients classified as secondary nephrotics 11 (50%) were related to streptococcal infection either as rapidly progressive glomerulonephritis or transient NS following APSGN. HBsAg was detected in the blood of 8.6% of the African patients. However the HB sAg carrier rate in this age group is 7.4%.The incidence in these patients probably reflects the high incidence in this population group. Collagen vascular disease occurred in 2 patients, both Indian. 5. Conclusions and Recommendations The results of this study demonstrates the strikingly different incidences of the various histological categories in the two race groups studied with a less favourable prognosis and fewer remission rates being achieved in African children. Indian children had more serious infections more often than African children. Steroid and immunosuppressive agents were of no value and probably hazardous in the African child. Some patients deteriorated on these drugs. Indian children who had an excellent response to these drugs were however at significant risk of developing serious infections. Why African children in Durban develop obvious glomerular lesions has not been established. Known or possible aetiological agents such as malaria, schistosomiasis, streptococcal infections and collagen diseases have been excluded. The answer to the above question may in fact lie in genetic predisposition,host factors and environmental influences, either singly or in combination, predisposing to the development of obvious x i glomerular lesions. These require more intensive investigation and judging from the yield of similar studies in other areas of the world expectations have to be guarded.
An overview of occupational health in the Durban Metropolitan area.
(1981) Jinabhai, Champaklal Chhaganlal.
No abstract available.
A study of diabetes mellitus in young Africans and Indians (age of onset under 35) in Natal.
(1982) Mahomed, Abdool Khalek Omar.
No abstract available.
Non-insulin-dependent diabetes in young Indians : a clinical and biochemical study.
(1982) Jialal, Ishwarlal.
One of the earliest recorded references to polyuria is found in the Papyrus Ebers (1500 BC) and much later the occurrence of "honey urine" was noted by an ancient Hindu physician, Sushrutha, in old Indian Sanskrit (400 BC). However, the first good clinical description of the disease is ascribed to Celsus, although the name "diabetes" was introduced by Aretaeus of Cappadocia. The body of knowledge which has accumulated since these early recordings to the present state of the art reflects a most impressive sojourn, punctuated by many milestones, each adding impetus to future attempts in a relentless endeavour to unravel the aetiopathogenesis of this common malady. However, this "sweet evil" (diabetes) remains an enigma in many ways. There is little doubt today that there are 2 major types of diabetes: juvenile onset diabetes, presently known as insulin-dependent diabetes mellitus (IDDM) and maturity onset diabetes, referred to as non-insulin dependent diabetes mellitus (NIDDM). In NIDDM aggregation of HLA types, evidence of cell mediated immunity and the presence of circulating islet cell antibodies, which are characteristically associated with IDDM, are not found. There is also a vast difference in concordance of diabetes in the co-twins between the two types of diabetes suggesting that a different mixture of genetic and environmental factors is operative in the pathogenesis of these two types of diabetes. In I960, Fajans and Conn drew attention to the existence of a form of diabetes with an onset before the age of 35 years. Their patients showed a substantial improvement in glucose tolerance when treated with an oral hypoglycaemic agent, tolbutamide. Subsequent to this report numerous studies from various parts of the world confirmed this entity of non-insulin dependent diabetes in the young (NIDDY) in White Caucasians. There are, however, several different syndromes presenting as mild carbohydrate intolerance in the first two to three decades of life. The classical form of NIDDY is a mild non-insulin requiring form of diabetes in which the disorder is inherited as a dominant trait; there is little progression of glucose intolerance, if any, with time, and the diabetes is rarely accompanied by vascular complications. This subtype of diabetes is referred to as MODY (maturity onset diabetes in the young) and thus constitutes a subset under the broad umbrella of NIDDY. However, recently compelling evidence for heterogeneity within MODY has been presented. This evidence is based on the prevalence of certain HLA antigens, insulin responses to oral glucose, occurrence of vascular complications, progression of hyperglycaemia to the stage of insulin requirement and failure to demonstrate autosomal dominant inheritance in some families studied. In the South African Indian population which has a high prevalence of diabetes, Campbell was the first to draw attention to NIDDY in Indians more than two decades ago. Since this initial report, nobody has really studied NIDDY in any depth in South Africa and certainly not in the Indian population. NIDDY in the local Indian population is of particular interest for the obvious reason that diagnostic and management problems arise daily in a population with a high prevalence of non-insulin dependent diabetes. It is vital that the clinical features, endocrine and associated biochemical aberrations be known in detail if this condition is to be managed appropriately and adequately. A study of these aspects therefore became the primary task of this thesis. To pre-empt any challenge that patients were not really diabetic, the strict criteria of the W.H.O. for the diagnosis of diabetes were chosen. It should therefore be borne in mind throughout this study that a group of rather severe diabetics were selected by design. The patients studied represent the rather extreme end of the spectrum. But, in the event, this selection proved advantageous in that it covered an unstudied part of the spectrum and some light could be shed on the natural history of the disorder. In the long term the purpose was to prepare the ground for what must become the thrust of future studies, namely the biochemical pathogenesis of NIDDM. If it is true that some forms of NIDDY are inherited dominantly, existing techniques should make it possible to identify a gene(s) locus and if this is done the biochemical basis of this disorder must be identifiable. In the present study direct examination of these aspects were not undertaken, but an attempt was certainly made to pinpoint those biochemical abnormalities which are perhaps primary or central to the whole disorder.

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