Interleukin-1 production in acute viral hepatitis.

The in vitro production of interleukin-1 in 15 children with acute hepatitis A and five children with acute hepatitis B was determined by measuring lymphocyte activating factor secreted by peripheral blood monocytes in a thymocyte proliferation assay. Aluminium hydroxide induced production of lymphocyte activating factor was significantly lower in patients with acute hepatitis A as well as patients with hepatitis B as compared with healthy control subjects. In both forms of acute viral hepatitis production of lymphocyte activating factor was severely depressed during the first week, increased gradually during the further course of the illness, but did not reach normal concentrations within the first three weeks after onset of the acute symptoms of the disease. No correlation could be found between in vitro production of lymphocyte activating factor and the severity of liver disease as estimated by the rise of serum concentrations of transaminases, bilirubin, or several parameters of acute phase reaction (alpha 1 antitrypsin, C reactive protein, erythrocyte sedimentation rate). The reduced production of interleukin-1, as assessed by determination of lymphocyte activating factor, could explain the only moderate acute phase reaction seen during acute viral hepatitis.     

The stomach in malnutrition.

Basal gastric acid output was reduced in 9 out of 14 infants and young children with malnutrition compared with 21 age-matched controls. In all the patients the response of the gastric mucosa to stimulation by pentagastrin was impaired, and gastritis of variable severity was present in 8 out of the 9 patients in who biopsies were performed. Impaired gastric acid secretion probably contributes towards bacterial overgrowth and diarrhoeal diseases in malnourished children.     

Food antibodies in malnutrition.

Antibodies to several food proteins were detected in the serum of 13 out of 20 malnourished children. Antibody activity was found mainly in the IgG and IgA classes. On ingestion of food items to which antibodies were demonstrated, no untoward symptom occurred nor was complement activation observed in vivo. It is suggested that food antibodies in malnourished children result from atrophied gut mucosa and reduced secretory immune response, which permit passage of intact or incompletely digested protein molecules, and impaired phagocytic function of hepatic reticuloendothelial system. Such antibodies do not appear to play any immediate immunopathological role.     

Secretory IgA in protein-calorie malnutrition.

The secretory IgA system was investigated in children with protein-calorie malnutrition (PCM). The results of the study indicated that in children suffering from kwashiorkor and marasmus the concentration of IgA in duodenal fluid, saliva, nasal secretions, and tears was significantly reduced on admission and returned to normal 4 weeks after treatment. However, the concentration of secretory IgA in children with mild to moderate PCM was similar to that of normal children. Secretory IgA deficiency may be an important factor in promoting bacterial growth and this may account for the increased incidence and severity of mucosal infections in children with severe PCM.     

Indicators of malnutrition in leukaemic children.

In 24 children with acute leukaemia a low serum albumin concentration (31 g/l or less) and a median weight:height ratio of less than 0.95 on admission were indicators of severe weight loss.     

Defective Candida killing in childhood malnutrition.

This study shows that malnourished children have impaired candidacidal activity of leucocytes, a finding which runs parallel to the higher rates of isolation of Candida sp. from throat secretions. In well nournished subjects the mean candidacidal ability was 44.5% in the moderately undernourished group it was 17.6%, and in the severely malnourished group it was 13.7%. This impaired candidacidal capacity may be important in the establishment of large numbers of Candida sp. which are commonly found in the upper intestine and in the pathogenesis of diarrhoea in children with malnutrition.     

Serum complement and immunoconglutinin in malnutrition.

Serum haemolytic complement activity and C3 were significantly decreased in 35 malnourished children. The changes were more pronounced in those with infection. Electrophoretically altered forms of complement C were detected in 14. There was an inverse correlation between C3 levels and immunoconglutinin titres. Nutritional rehabilitation and eradication of infection reversed the abnormalities. It is suggested that reduced complement function in malnutrition is the combined result of impaired synthesis, complement activation in vivo, and changes in plasma volume, and that it may contribute to an increased susceptibility to infection in undernourished individuals.