Search

Out of 200 children suffering from Indian childhood cirrhosis studied during a five-year period, histologic confirmation of the disease was available in 141. Two out of 2l siblings also had ICC. In a pair of the twins while one had ICC, the other had fatty change and focal necrosis in the liver. The disease appears to be universally fatal. The hepatic lesion essentially consists of severe and continuing parenchyma! injury, progressive interstitial fibrosis leading rapidly to architectural disorganization, inflammatory reaction and poor hepatocytic regeneration, Intracellular hyaline forms a prominent feature and is often of diagnostic and prognostic value. Initial lesion in the disease is unknown though the 2 cases available with us and one of the twins showed non-specific changes unlike viral hepatitis. Even the established lesion is different from hepatic alteration in viral hepatitis. There seems to be at present no definite clue to the etiopathogenesis of the disease. Many aspects of the disease point against a viral or nutritional etiology. The role of toxins is to be explored. The liver cells of children suffering from ICC fail in certain respects to attain maturity. This and the role of heredity, viruses and toxins needs further study. [ABSTRACT FROM AUTHOR]

This paper reinforces the idea of integrating more closely the social and medical sciences with an emphasis on people. The nexus between health and development is examined together with national research capability building as part of essential national health research progress. Suggestions are made identifying the most urgent requirements for further action.

Millions of people suffer and many die from lack of minute traces of nutrients. Methods of prevention are cheap and simple. Their universal application could yield health and economic benefits comparable to those achieved by smallpox eradication.

The influence of protein deficiency on the hepatotoxicity of carbon tetrachloride (CCl4) was investigated in a group of rhesus monkeys. Animals fed a protein-rich diet served as controls. The results indicate that protein-deficiency protects the liver against acute hepatotoxicity of this drug. The protective effect is abolished if the animals are administered phenobarbital prior to the administration of CCl4. The protective action is due to a reduction, in protein deficiency, of the endoplasmic reticulum associated enzymes involved in hepatotoxicity of CCl4. Repeated administration of CCl4, which induces hepatic regeneration, resulted in disappearance of fat from periportal cells in protein-deficient animals. The regenerating cells (because of their better enzyme system) acquire "nutritional autonomy" and are thus able to synthesize adequate amounts of lipoproteins for mobilization of liver triglycerides.

In view of the depressed immunity in protein malnutrition, an assessment of the lymphoproliferative activity of the constantly stimulated mesenteric lymph node of the guinea pig was undertaken. A significant reduction of this activity was observed in protein deficiency. a) The germinal centers were reduced in number and size; new formation in the medulla was rarely seen. Lymphoid cells showed lowering of mitotic index and mitotic rate and prolongation of mitotic duration and turnover time. Nuclear labeling with (3)H-thymidine was focal and localized to the peripheral zone. b) Mitotic activity and nuclear labeling were less pronounced in the outer cortex and medulla and least in the paracortical area. Specific uptake of (3)H-thymidine paralleled the low labeling index. c) No appreciable reduction in the number of plasma cells in the medulla was observed. Serum gamma-globulin levels were not significantly altered, but albumin levels were consistently reduced. This was suggestive of preferential preservation of plasma cell activity in the malnourished host. d) There were significant lymphopenia and neutropenia with relative increase of neutrophils in the peripheral blood. This might indicate more severe involvement of lymphopoiesis than myelopoiesis in protein malnutrition.

It is estimated that 4 million children die each year of vaccine-preventable diseases and that another 4 million are permanently disabled. Although vaccination is the most cost-effective health technology, there is a gap between what we know and what we apply. We seem to be succeeding more in attaining new knowledge than in applying what we know. It takes more than a string of discoveries to provide the benefits of science to the people. Appropriate application of the vaccines presently available against diseases such as measles, poliomyelitis, neonatal tetanus, and pertussis could result in a significant reduction in mortality and morbidity among infants and children attributable to these diseases; continued development and deployment of newer vaccines against some dominant components of the diarrhea-dysentery-pneumonia complex of illnesses could result in further reduction. Improved management practices; more heat-stable, less-expensive, and safer vaccines; and vaccines that require fewer doses are critical for success in future immunization programs.

An epidemic of liver disease, characterized by onset with high fever, rapidly progressive jaundice, and ascites occurred in a rural area of India. Several hundred people were affected and mortality was high. The epidemic was heralded by the appearance of similar features in the village dogs. Liver biopsy specimens from eight cases and autopsy material from one human case and two dogs were studied. Characteristic features were centrizonal scarring, hepatic venous occlusion, ductular proliferation and cholestasis, focal syncytial giant-cell tr-nsformation of hepatocytes, and pericellular fibrosis. Toxic quantities of aflatoxin B1 were found in samples of corn, the staple food grain of the people, that was obtained from the domestic food stores. The etiology of the disease could not be unequivocally established, but aflatoxins, perhaps in combination with other factors, may have been the cause.