Cystic disease of the liver following prenatal and perinatal exposure to aflatoxin B1 in rats.

Experiments were designed to elucidate the differences, if any, in the liver histology induced by aflatoxin B in newborn and adult animals. The transfer of toxic metabolites from pregnant rats to their litters was confirmed by thin layer chromatography of liver homogenates in the latter. Extensive cystic lesions of the biliary and hepatic type developed only in young animals. Multifocal hepatic necrosis, bile ductular proliferation, areas of altered hepatocytes, neoplastic nodules and hepatocellular carcinoma constituted the total spectrum in both adult and newborn animals. Increased susceptibility to the toxins early in life appears to be responsible for this intriguing phenomenon. These aspects may have a bearing on the genesis of childhood liver disease.

Role of macrophage-processed antigen in a Plasmodium berghei model.

The present study demonstrates that malarial parasite could be processed by macrophages in vitro to release 'super antigens'. These super antigens obtained from the peritoneal macrophages were more protective than those processed by the splenic adherent cells. BCG-stimulated macrophages were also able to process the antigens efficiently and these antigens were even superior to those obtained from the unstimulated macrophages. These modified antigens were potent inducers of DFPS to malarial antigens. It is thus concluded that parasite antigens, processed in vitro, carry specific immunogenic potential and are able to protect the recipients to parasite challenge.

Immune complexes in Indian kala-azar.

Patients with Indian kala-azar were investigated for the presence of circulating immune complexes by the platelet aggregation test, complement deviation test, and polyethylene glycol precipitation test. Circulating antibodies were tested by the conventional indirect immunofluorescence test using leptomonad forms of Leishmania donovani and Crithidia luciliae. The serum complement level (C3) was measured using the Mancini technique. The results indicate that a large number of patients with Indian kala-azar carry circulating immune complexes with a significant lowering of complement levels in their sera. These complexes may be intimately linked with the depressed cell-mediated immune responses that are commonly observed in these patients. The study warrants a detailed immunohistopathological examination of the kidneys for the presence of tissue-bound complexes in chronic patients. Further, it is revealed that Crithidia luciliae and Leishmania donovani share common antigens and the former can be used as a substitute for determining anti-leishmania antibody by the indirect fluorescence assay.

Hydatid disease associated with hepatic outflow tract obstruction.

Three unusual cases of hydatid disease associated with hepatic outflow tract obstruction are presented. One had Echinococcus multilocularis infection with complete obstruction of the inferior vena cava and the other two had E. granulosus infection with complete obstruction of the hepatic vein. The initial two were unsuspected clinically. The cases suggest that both outflow obstruction and hydatid disease may often be unrecognized. A high index of suspicion and appropriate investigation are essential for diagnosis and proper management.

Renal immune complexes in viral hepatitis.

Twenty-two patients dying of acute viral hepatitis were studied for the presence of renal immune complexes using direct immunofluorescence. A detailed light microscopic study of liver, kidney and other organs was also done and sera scanned for the presence of HBsAg. Results of light microscopy indicate that thirteen of twenty-two patients showed mild to moderate glomerular abnormalities. Immunofluorescence was positive in fifteen of twenty-two patients. IgA being positive in 28%. The incidence of HBsAg was low. It is suggested that both B and non-B type of hepatitis viruses are associated with a high incidence of renal immune complexes along with morphological alterations in the glomerulus.

The pathology of noncirrhotic portal fibrosis: a review of 32 autopsy cases.

A wide spectrum of clinical and morphologic changes in 32 autopsy cases of noncirrhotic portal fibrosis have been described. The disease frequently occurs in younger patients with a long history of splenomegaly, usually with a history of hematemesis. Females are affected almost equally as often as males in contrast to cirrhosis. The patients tolerate the bleeding episodes well. Death is usually due to massive hemorrhage. The diagnosis is achieved through a process of exclusion. A critical analysis of hemodynamic data, a splenoportogram, liver function tests (particularly Bromsulphalein retention) and angiographic data is mandatory. Needle biopsy of the liver appears to have limited value in making the diagnosis. The gross anatomic findings vary from a nearly normal liver to gross nodularity, seen particularly on the posteroinferior surface. In some cases these nodules are seen to physically impede the portal blood flow and contribute to portal hypertension. Phlebosclerosis of the smaller radicles of the portal vein and irregular scarring are the outstanding morphologic features of the disease. These changes are usually associated with irregular dilatation of some of the larger intrahepatic branches of the portal vein as well as fibroelastosis with or without occluding or organizing thrombi in both intra- and extrahepatic branches of the portal vein. The changes in hepatic venous radicles are characterized by irregular sclerosis, which seems to contribute significantly toward postsinusoidal block in advanced cases. The probable mode of evolution is discussed.