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Nutritional vitamin D deficiency rickets was established in 41 Sudanese children aged from 3 months to 7 years by clinical, radiological and therapeutic response supported by biochemical investigations. There were 25 boys and 16 girls, of whom 42% were infants of less than 1 year. Forty-seven per cent of rachitic children were underweight. Six infants had early rickets with no bony swellings but had other clinical features and radiological evidence of rickets. One of them, aged 3 months, presented with hypocalcaemic convulsions. Three children had icthyosis. Serum alkaline phosphatase was raised in 75%, hypophosphataemia occurred in 68% and hypocalcaemia in 54% of patients. Anaemia, mostly hypochromic, was detected in 79%. Possible causes were poor socio-economic background, inadequate dietary intake in both mothers and children, prolonged breastfeeding, prematurity, limited sun exposure and type of residence. Nutritional vitamin D deficiency rickets should be looked for in Sudanese children, especially in preterms and in those living in flats.

One hundred and seventy nine children reporting to the paediatric cardiac clinic were studied consecutively over a 2 year period (1991-1993) using medical history, physical examination, chest x-ray, electrocardiography, echocardiography and complete haemogram. 100 (56%) of them had congenital heart disease, 70(39%) had rheumatic heart disease, four had cardiomyopathy and in five children no abnormality was detected. 58 of patients with congenital heart disease were females and 42 were males. Their age ranged between two weeks and 15 years and four months. Symptoms started in infancy in 89% of 94 symptomatic patients. The commonest symptoms were breathlessness, failure to thrive, repeated chest infections and cynosis. The other six patients were detected incidentally. Almost all types of defects were represented, the commonest being ventricular septal defect (VSD), Fallot's tetralogy, pulmonary stenosis, patent ductus arteriosus, atrioventricular septal defect and secondum atrial septal defect. Five patients with VSD were preterms. 91% of patients with VSD were symptomatic. VSD was small in one-third of patients. six patients with VSD aged 5-11 years had evidence of pulmonary hypertension, one of whom had Eisenmenger with cynosis and one found inoperable because of pulmonary vascular disease. Twenty patients had extracardiac malformations in 65% of whom more than one system was involved. 53% patients were anaemic. 47% of patients were underweight and 33% were marasmic while only 14% of controls were underweight and none of them was marasmic.

During the period April 1985 to November 1986 (18 months), 196 children (of age greater than 1 month) admitted to the Children's Emergency Hospital in Khartoum, Sudan, with clinical suspicion of meningitis/meningoencephalitis were followed up prospectively. Bacterial meningitis was diagnosed by culture, direct microscopy and/or antigen-detecting assays (co-agglutination and enzyme immunoassay) in 44 infants (25 Haemophilus influenzae type b, 8 Neisseria meningitidis, 7 Streptococcus pneumoniae, 3 enterobacteria and one mixed infection), aseptic meningitis in 52, cerebral malaria in 4 and febrile convulsions in 96. The majority of cases of bacterial meningitis were boys and 57% of those in whom H. influenzae was the commonest isolate were less than 1 year old. The presenting signs and symptoms are described as well as the transient and permanent short-term sequelae. The total mortality from bacterial meningitis was 19%, permanent neurological sequelae were seen in 26% of survivors. Prospective follow-up, including audiometry, of 35 children 1-2 months after discharge showed that 11% had hemiplegia and 20% had hearing impairment. The potential impact of vaccination against invasive H. influenzae infections is discussed.

One thousand, eight hundred and forty-six apparently healthy nursery and school children living in the Khartoum area and belonging to different socio-economic classes were studied. Nine hundred and thirty-seven were boys, 909 girls. Their ages ranged from three to 16 years. N-multistix strips were used to test for proteinuria and haematuria, the former being also checked by the sulphosalicylic acid test. Children with proteinuria of 1+ or more were further investigated by examining their urinary sediment for abnormal deposits and by testing for orthostatic proteinuria using day and night specimens of urine with specific gravity of 1.018 or more. Children who had no proteins on orthostatic testing were rescreened for proteinuria 10-14 days after the initial screening. The prevalence rate for proteinuria was 7.2% with no significant difference between boys and girls. In both sexes the prevalence rate increased significantly with age but was not influenced by the socio-economic status. Of the children with proteinuria, haematuria occurred in 27% and abnormal urinary deposits in 14.8%. Orthostatic testing showed a negative result for proteins in 44%, orthostatic proteinuria in 40%, of whom a third had either abnormal urinary sediments or haematuria, and continuous proteinuria in 15.6% of whom the majority had abnormal deposits.