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Twenty-five cases of rapidly developing ascites occurring in an epidemic form were observed in a tribal district in Central India during August 1972-May 1973. Eleven of the patients died. Six patients were brought to hospital and studied for periods of two to 17 months. Necropsy was performed on one patient who died. The clinical features suggested an outflow tract obstruction such as a Budd-Chiari-like syndrome or venoocclusive disease. Radiographic and haemodynamic studies demonstrated a combination of post and perisinusoidal blocks. Liver dysfunction was indicated by the presence of a marked bromsulphthalein retention and mild to moderate hypoalbuminaemia. Histological examination of the liver biopsies showed changes that ranged from centrizonal haemorrhagic necrosis to an extensive centrilobular fibrosis associated with central vein occlusion. The disease was apparently caused by a food toxin, and the possible nature of this is discussed. [ABSTRACT FROM PUBLISHER]

Sixty-three unselected cases of giardiasis, with no evidence of other systemic disease, were screened for evidence of steatorrhoea. No patient had any evidence of protein-energy malnutrition. Seventeen (27%) of the cases had steatorrhoea; three (17-8%) of the 17 patients having steatorrhoea also had D-xylose malabsorption. Vitamin B12 absorption was normal in all. Bacterial culture and qualitative analysis of bile salt in jejunal fluid was carried out in all the 17 cases having steatorrhoea as well as 13 cases with normal absorptive parameters (eight cases of irritable bowel syndrome and five cases of giardia infection) who served as controls. All the patients showing bacterial overgrowth had free bile acids in their duodenal aspirate. Free bile acids could also be detected in jejunal aspirates of five of the seven patients having no bacterial overgrowth. Two control cases of giardia infection with normal small bowel function and sterile duodenal aspirate showed evidence of bile salt deconjugation. The significance of these findings is discussed in relation to the pathogenesis of steatorrhoea in patients with giardiasis. The possible role of giardia in bile salt deconjugation is suggested. [ABSTRACT FROM PUBLISHER]

ABSTRACT- We studied the risk of post-transfusion hepatitis (PTH) in recipients of blood collected from voluntary donors screened for HBsAg. Two hundred and fifty patients without any previous history of liver disease or transfusion were followed up for 12 months subsequent to cardiac surgery. Thirty-five of them had closed-heart surgery without receiving transfusion and served as controls. The remaining 215 patients received single-point transfusions (mean 4 ± 2.4 units). None of the controls and 15 (6.9%) blood recipients developed PTH. Three (20%) patients had hepatitis-B-virus-induced hepatitis while the remainder (80%) had non A, non B (NANB) hepatitis. The number of units of blood transfused and surrogate markers for development of PTH (donor alanine aminotransferase, anti-HBc and anti-HBs antibody) were not associated with the occurrence of PTH (p>0.05). Nine (60%) of the 15 patients developing PTH were asymptomatic. All the patients recovered from the PTH, except one who died of fulminant hepatitis. At the end of 1 year of follow-up, none of the patients had evidence of chronic hepatitis. Only three (25%) of the patients with NANB-PTH developed anti-hepatitis C virus (HCV) antibody during the follow-up. We conclude that the incidence of PTH in India is similar to other parts of the world and NANB virus was the major cause of the PTH. The absence of chronicity and lack of seroconversion to anti-HCV antibody in the majority of the patients after 1 year of follow-up may suggest the possibility of a NANB virus other than HCV as the major cause of PTH in India. [ABSTRACT FROM AUTHOR]

ABSTRACT- An enzyme-linked immunosorbent assay has been developed by using IgM antibodies from the acute stage as a source to capture the antigen in stools of patients with epidemic non-A, non-B (NANB) viral hepatitis. 29/69 (42.3%) of the patients and 3/9 (33.3%) contacts were positive for a suspected NANB viral antigen. However, only 1/27 (3.7%) of the negative controls drawn from amongst the patients with amoebiasis, giardiasis, hepatitis due to virus A and healthy individuals was positive for NANB antigen in the stool. The suspected NANB viral antigen was more frequently detected in stools collected between the 14th and 18th day of icteric hepatitis. The study suggests that IgM antibodies from patients with acute viral NANB hepatitis react with an antigen present in the stools of a high proportion of patients with epidemic NANB viral hepatitis. This serological test may be useful to establish the etiological diagnosis of non-A, non-B (fecal-oral) viral hepatitis. ELISA-positive stools contained 27 nm viral particles. [ABSTRACT FROM AUTHOR]

ABSTRACT- Nine patients with acute liver failure due to Plasmodium falciparum liver injury admitted to the Rajgarhia Liver Unit of the All-India Institute of Medical Sciences during 1982-84 are presented. The liver was palpable in all the patients, and eight had splenomegaly. Investigations revealed mild to moderate abnormality in liver function tests. All were negative for the markers of acute infection due to hepatitis A and B viruses. Blood film examination showed P. falciparum alone in seven and along with P. vivax in the remaining two patients. Liver histology, which was identical in all eight patients where liver biopsy was done, showed centrizonal necrosis and hyperplastic Kupffer cells loaded with malarial pigment. All the patients recovered with specific anti-malarial and supportive treatment. Our observations suggest that malaria due to P. falciparum may present as jaundice and encephalopathy which stimulates acute hepatic failure due to fulminant hepatitis. [ABSTRACT FROM AUTHOR]

ABSTRACT- In this study the morphological changes in the livers of marmosets inoculated with stool extracts from epidemic non-A, non-B hepatitis patients in India were examined. The histologic changes of epidemic non-A, non-B hepatitis in marmosets consisted mainly of round cell infiltration in the portal tracts, spotty liver cell necrosis, sinusoidal lymphocyte infiltration, and Kupffer cell mobilization. By electron microscopy, liver cells from infected marmosets showed cisternal dilation of the endoplasmic reticulum, irregularly-shaped nucleus, and disorganization of the mitochondrial cristae. In some areas interaction of lymphocytes with hepatocytes was observed. Similar observations have been made in type B hepatitis infection, presumably due to liver cell damage mediated by immune mechanisms. The result of our study is also compatible with the interpretation that the liver cell damage in this experimental model may be mediated by immune mechanisms. [ABSTRACT FROM AUTHOR]

ABSTRACT- Bridging necrosis was recorded in 14% of 361 patients with acute viral hepatitis on examination of the liver biopsy. The clinical and biochemical features of acute viral hepatitis with bridging necrosis were compared with acute viral hepatitis with no bridging necrosis (NBN). It was noted that fever of more than 8 days' duration in the pre-icteric phase, the presence of mild ascites and pedal edema during the icteric phase, increasing or persistently high levels of serum bilirubin even 4 weeks after the onset of the icteric phase and positive hepatitis-B surface antigen were significantly more common in acute viral hepatitis with bridging necrosis. Hepatitis-B surface antigen clearance was slow in this group. The long-term complication of chronic hepatitis was more frequent in patients with acute viral hepatitis with bridging necrosis. [ABSTRACT FROM AUTHOR]