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Biomedical subjects

R G Hendrickse

Publications and source records attributed to R G Hendrickse.

At least 73 records · Page 4Linked to original sources

A case of paragonimiasis.

A 2 1/2-year-old girl recently arrived from eastern Nigeria presented with a soft tissue swelling of the infraclavicular region. Subsequent investigation revealed a cavity in the left lung associated with a small pleural effusion and leucocytosis with pronounced eosinophilia. Clinical and serological findings were compatible with the diagnosis of paragonimiasis. After a course of Bitin-S the chest x-ray returned to normal, the soft tissue changes disappeared, and the eosinophil count fell.

Child, Preschool↗

Dysentery.

Explore the source record for details and available documents.

Child↗

Aspects of tropical paediatrics.

Malnutrition interacting with infectious and parasitic diseases are the main causes of the appalling mortality in childhood in the tropics. The most important single safeguard against these in infancy is breast feeding and the trend now evident to abandon this is a disaster which demands urgent attention. Reasons for this trend are discussed. Efforts to control infectious diseases, other than smallpox, have had little success and the emergence and spread of dengue haemorrhagic fever in S.E. Asia have added new dimensions to the problem. Malaria is still widely prevalent in the tropics and falciparum malaria, holoendemic in much of Africa, remains a major cause of death with its most serious impact on pregnant women and children. The emergence and spread of drug resistant strains of this parasite in parts of the world is a cause for serious concern. Quartan malaria is also an insidious corruptor of health in childhood and commonly causes the nephrotic syndrome. Neonatal jaundice, often associated with G6PD deficiency, is increasing in frequency in urban areas of Africa and now constitutes a significant hazard to the newborn and requires urgent investigation. These problems in tropical paediatrics indicate the need for urgent reappraisal of our role as a profession in the affairs of the tropical developing world.

Adolescent↗

Differential protein clearances and response to treatment in Nigerian nephrotic children.

Remission followed prednisolone therapy in 9 out of 21 Nigerian children with the nephrotic syndrome who had highly selective proteinuria (CG/CA less than 15%). Of these, 5 patients have remained well off all treatment during a follow-up of nearly 5 years, 4 have relapsed more than once but have responded to further courses of prednisolone. 3 of 21 with less selective proteinuria also remitted but all relapsed and only one of these has responded again. The other two have relapsed and further courses of prednisolone have not totally abolished their proteinuria though they are asymptomatic and in good health. Toxicity (hypertension, sometimes with encephalopathy and infection) was commoner in the patients with less selective proteinuria treated with steroids than in those with highly selective proteinuria. 3 steroid-sensitive patients who had had repeated relapses became free from relapse off all treatment after a course of cyclophosphamide, given during steroid-maintained remission. All but 2 of the renal biopsies taken were regarded as abnormal. The lesions were less severe in those who responded than in those who did not. There is some evidence to suggest that Plasmodium malariae may be a cause of some of the steroid-sensitive disease, as well as the steroid-resistant.

Age Factors↗

The quartan malarial nephrotic syndrome.

A specific relationship between P. malariae and the nephrotic syndrome, originally postulated on epidemiologic evidence, has been substantiated by clinical, pathologic and immunologic observations. It would appear that quartan malaria causes an immune complex nephritis in some individuals that, once established, is sustained by mechanisms not yet fully explained but which may involve an autoimmune process. Evidence to support an immunologic pathogenesis of the renal lesions is provided by the presence of immunoglobulin, complement (C3) and quartan malarial antigen in biopsy specimens studied by immunofluorescence microscopy. In early cases in which some patients respond to treatment, fluorescence is coarsely granular but in late cases in which patients are unresponsive to treatment, fluorescence tends to be diffuse. Renal histology is distinctive and does not conform to any of the categories included in the conventional classification of the nephrotic syndrome in childhood. The basic lesion consists of thickening of glomerular capillary walls, leading to eventual obliteration of capillary lumina, and accompanying mesangial sclerosis leads ultimately to total glomerular sclerosis. A unique feature of electron microscopy is the presence of small lacunae scattered throughout the thickened capillary basement membrane. Histologic grading for severity of lesions shows positive correlation with response to treatment and immunofluorescence appearances. Prognosis is, in general, poor. The large majority of patients do not respond to treatment with prednisolone, azathioprine or cyclophosphamide, and prednisolone administration causes severe hypertension and other serious complications in a high proportion of patients.

Azathioprine↗

Intravenous feeding of young infants with persistent diarrhoea.

42 infants with persistent diarrhoea were fed intravenously using a simplified regime based on Intralipid and an aminoacid, Fructose and ethanol solution. Peripheral veins were used for up to 56 days, and with scalp veins complications were few and minor. The use of arm and leg veins caused more frequent local problems and is not advised. Central venous lines became necessary in 5 infants, and 3 developed septicaemia. The regime was well tolerated with adequate weight gain when intake was adjusted to the infants' needs. Rates of infusion of 1 g Intralipid/kg hourly over 2 hours and up to 1 g fructose/kg hourly over 14 hours did not cause persistent lipaemia (except transiently in 2 infants) nor metabolic acidosis. Infants must be fully rehydrated with correction of acidosis and electrolyte imbalance before starting intravenous feeding, or acidosis and dehydration from osmotic diuresis may occur. Intravenous feeding should be started gradually and cautiously in severely malnourished infants, and should not be used where liver function is abnormal.

Acidosis↗