[Rapid development of liver cirrhosis following acute non-A, non-B hepatitis].

Four cases of shortly developed liver cirrhosis as consequence of non-A-non-B-hepatitis are described. Liver cirrhosis was diagnosed by liver histology at days 254, 298, 651 and 891 after acute infection, respectively. For the first time a normal liver histology was documented in one case immediately before infection together with follow up biopsies of chronic hepatitis up to liver cirrhosis (day 891) after acute posttransfusion non-A-non-B-hepatitis.

[Prophylactic sclerosing of esophageal varices. Results of a prospective randomized 7-year longitudinal study].

Over a period of six years, esophageal varices (stage III or IV) were endoscopically diagnosed in 49 patients with confirmed liver cirrhosis and no previous bleeding. Prophylactic sclerotherapy of the esophageal varices was performed in 25 patients, while 24 were treated conservatively (control group). The groups were comparable as to duration, cause and severity of the cirrhosis, but differed in sex distribution.

[Nonalcoholic fatty liver hepatitis and fatty cirrhosis mimicking alcoholic liver diseases].

Non-alcoholic steatosis hepatitis and fatty cirrhosis represents an unfamiliar liver disease of yet unknown etiology, which is usually indistinguishable from alcoholic lesions by histological criteria. For the affected patients this means automatically the inappropriate assumption of hidden alcohol abuse. Out of 1467 liver biopsies during 1979 to 1982 we selected 25 patients (group I), who either denied alcohol intake or reported negligible consumption.

The renin-angiotensin-aldosterone system in fulminant hepatic failure.

The relationship of the renin-angiotensin-aldosterone system to blood pressure and sodium homeostasis and to renal function was investigated serially in 12 patients with fulminant hepatic failure. The plasma concentrations of renin, angiotensin II, and aldosterone were, in most instances, markedly increased. Systolic blood pressure, which was often very low, showed a significant inverse relationship to the plasma renin concentration, suggesting that the marked stimulation of the system is a homeostatic response to hypotension.