In order to evaluate the prognostic implications of the hepatitis B e system in patients with chronic persistent hepatitis (CPH), 53 consecutive patients were studied. Fourteen of 16 patients with HBsAg and HBeAg were followed from 12 to 120 months (mean, 38 months). Eleven of the 14 patients were persistently HBeAg positive and five of these developed chronic active hepatitis (CAH) or cirrhosis. A further nine patients were HBsAg positive but HBeAg negative at time of CPH diagnosis (mean follow-up, 47 months). One of these nine patients developed CAH during follow-up. The remaining 28 patients were all HBsAg negative, and only 2 or the 28 patients progressed to CAH or cirrhosis during the time of follow-up (mean, 43 months). It is concluded that the persistence of HBeAg in patients with CPH indicates a serious prognosis with a frequent transition to CAH or cirrhosis.

Adult↗

PubMedDate not supplied

Correlation between liver morphology and portal pressure in alcoholic liver disease.

In 14 alcoholic patients, the degree of hepatic architectural destruction was graded (preserved architecture; nodules alternating with preserved architecture; totally destroyed architecture) and related to portal pressure. A positive correlation was found between the degree of architectural destruction and both wedged hepatic vein pressure (r = 0.72, p less than 0.01) and wedged-to-free hepatic vein pressure (r = 0.67, p less than 0.02). Degree of fatty change, fibrosis, inflammation, necrosis and occurrence of Mallory bodies showed no correlation with portal pressure. After morphometrical evaluation of liver biopsies, no significant correlation was found between mean hepatocyte volume or relative sinusoidal vascular volume and portal pressure. To test whether an increase in hepatocyte volume compresses the vascular structures and causes portal hypertension, the ratio of relative sinusoidal vascular volume to mean hepatocyte volume, which expresses the compression of the vascular structures exerted by enlargement of hepatocytes, was related to portal pressure. No significant correlation was found. Further, mean hepatocyte volume was not significantly correlated to relative sinusoidal vascular volume. The present findings are in accordance with the hypothesis that elevated hepatic vascular resistance and portal pressure in alcoholic liver disease are in part determined by the severity of the hepatic architectural destruction and subsequent distorsion and compression of the efferent vein system. Parenchymal changes, including changes in hepatocyte volume, seem to be of minor importance.

Adult↗

PubMedDate not supplied

Alcoholic liver injury: defenestration in noncirrhotic livers--a scanning electron microscopic study.

The fenestration of hepatic sinusoidal endothelial cells in 15 needle biopsies obtained from chronic alcoholics without cirrhosis was studied by scanning electron microscopy. As compared to nonalcoholics, a significant reduction in the number of fenestrae and porosity of the sinusoidal lining wall (fractional area of fenestrae) was observed in acinar Zone 3, both in biopsies with and without Zone 3 fibrosis as judged by light microscopy. A significant reduction of porosity as shown in this study may influence the blood hepatocytic exchange and contribute to the alcohol-induced liver injury.

Biopsy, Needle↗