Idiopathic, cryptogenic, or tropical splenomegaly, as it is variously termed, is often encountered at the Mulago Hospital in Kampala. Trowell (1950) reported several cases in which no good reason could be found for gross splenomegaly, and discussed the current theories of aetiology. Leather (1961) made the important observation that many cases had a mild portal hypertension in the absence of any evidence of cirrhosis on liver biopsy. Of the 41 cases he investigated 29 showed sinusoidal infiltrates by lymphocytes, histiocytes, and plasma cells, an appearance that had been noted elsewhere in the tropics by Fawdry (1955) from Aden, and by Chaudhuri et al. (1956) from India.The present report describes a series of cases of marked splenomegaly admitted to the New Mulago Hospital, Kampala, in which combined clinical, haematological, parasitological, and pathological investigations were carried out to assess the cause and effect of the large spleens. Materials and MethodsOver a period of eight months 64 patients with marked splenomegaly were investigated in the New Mulago Hospital, Kampala.Routine haematological investigations were prepared by standard techniques (Dacie, 1956). In five patients the red-cell survival and splenic uptake were estimated, using 5Cr-tagged red cells (Mollison and Veall, 1955), and the sites of red-cell destruction were assessed by the method of Hughes Jones and Szur (1957 BudtzOlsen, 1952;Atkinson and Sherlock, 1954). Splenic puncture specimens were examined for malaria parasites and leishmaniae. Initially, random peripheral thick blood was examined for malaria parasites and trypanosomes, but in the latter part of the study a minimum of 10 consecutive daily blood films were examined for malaria parasites by two observers.Stools were examined by the formol-ether-concentration technique (Ridley and Hawgood, 1956) for ova, cysts, and parasites. Rectal snips were examined for schistosome ova.Sera from 40 patients were examined by a fluorescent antibody technique (Voller, 1964) for the presence of malarial antibodies. Control sera from patients without splenomegaly were also examined. The antigen used was Plasmodium bastianellii.

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SYNOPSIS In 1964 as part of a population study, the blood cholesterols of 1,292 school children in the town of Busselton in Western Australia were examined. A gradual rise in the median value throughout school life was demonstrated in both boys and girls, with a pre‐adolescent rise comparable with similar studies elsewhere. In 1969 the cholesterol levels of the children with the highest, middle and lowest 5% levels in 1967 were repeated and showed a highly significant correlation, thus indicating that a single cholesterol estimation in childhood is of considerable predictive value, at least over a 2 year period. Comparison of cholesterol levels of 929 children with those of their parents revealed a significant correlation between parents and children throughout the whole cholesterol range. It has not been possible to demonstrate whether the cause is dietary or genetic, except in a few cases of genetic hyperlipidaemia, but it is likely that, at least in those children with a cholesterol higher than 250 mgm% of the cause is genetic. The mother's cholesterol is more closely related than the father's to that of the children. This might be due to both a genetic contribution to the children and her role in controlling the diet of the family, this control being greatest on the young children.

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