[Current problems in the diagnosis of biliary lithiasis].
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Biomedical subjects
Publications and source records attributed to R Oancea.
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The work deals with a group of 212 patients suffering from various forms of precirrhotic alcoholic liver disease and includes a period of 8.5 years (January 1981-June 1989). At least two liver biopsies were performed in all patients. according to the histological diagnosis, the patients were distributed into 6 subgroups: simple hepatic steatosis--24 cases (11.3%), hepatic fibrosis--40 cases (18.8%), hepatic steatofibrosis--69 cases (32.5%), acute alcoholic hepatitis--18 cases (8.5%), chronic active hepatitis--43 cases (20.3%) and chronic persisting hepatitis--18 cases (8.5%). The assessed histological parameters included: fatty transformation, hepatic fibrosis, inflammatory infiltrate within the lobules and in the portal spaces, hepatocellular necrosis, cholestasis, proliferation of the bile ductules and modification of the lobular architectonic. The work is aimed at pointing out the precirrhotic hepatic histological lesions induced by alcohol and fraught with an increased risk of progression towards liver cirrhosis. The histological sequential examination of alcoholic hepatic lesions confirm the possibility of progression and installation of the cirrhotic stage for a number of these lesions. Liver cirrhosis developed in 44 patients (20.7%) within a period of 3-7 years, on an average 5.5 years. The progression toward cirrhosis occurred in 12 patients (5.7%) with steatofibrosis, in 11 (5.2%) with hepatic fibrosis, in 14 (6.6%) with an intralobular inflammatory infiltrate, in 17 (8%) with hepatocellular necrosis, in 3 (1.4%) with cholestasis, in 5 (2.3%) with proliferation of the bile ductules and in 10 patients (4.7%) with a modification of the lobular architectonic. In addition, cirrhosis was detected in 8 patients (3.8%) with alcoholic hepatitis and in 13 patients (6.1%) with chronic active hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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The present paper reports on the recent possibilities of diagnosis in iatrogenic diseases of the liver. The iatrogenic diseases of the liver are diagnosed with difficulty since no clinical, biological and histological pathognomonic criteria are known. The hepatic lesions appearing after drug intake are extremely various, including: hepatocellular necrosis, cholestasis, hepatic granuloma, perisinusoid fibrosis, steatosis, pseudoalcoholic lesions, vascular lesions and hepatic tumours. Clinical criteria, very important for the diagnosis, are based on: appearance of the disease, regression of symptomatology when the treatment is interrupted and recurrence when it is administered again. The biological criteria are not specific but they may indicate the drug etiology of a liver disease. Increase in the serum concentration of aminotransferases might be the only biochemical disturbance and it might be overlooked if not systematically investigated. The immunological tests suggested for diagnosis of iatrogenic liver diseases are numerous but only a few of them are specific. Histological criteria cannot identify, for sure, the drug etiology of the lesions. They may suggest the possibility of a drug induced cause and may help in establishment of a correct diagnosis.
Drug-induced hepatitis still arouse many practical problems, as their pathogenesis has not been fully elucidated yet, given the absence of specific criteria. Drug-induced hepatitis are acute and chronic. Cytolytic hepatitis, cholestatic hepatitis and mixed hepatitis belong to the former category. Drug-induced hepatitis show various clinical and biological pictures, generally similar to those of viral hepatitis. In the most cases, the prognosis is good and their evolution favourable. Cytolytic hepatitis--the result of a wider hepatocytic necrosis--have a more severe prognosis. The most severe form is the fulminant acute hepatitis, a consequence of the substantial necrosis of the hepatic parenchyma. Chronic hepatitis appears after prolonged administration of some drugs with toxic action. Clinical and biological manifestations are not characteristic. Evolution towards cirrhosis is possible. Drug-induced hepatitis are treated by interruption of the drugs generating them. After removing the noxious agent, the disease resolution takes place in one or two weeks.
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