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NATURAL HISTORY OF ACTIVE CHRONIC HEPATITIS
Author(s) -
MISTILIS STEVEN P.
Publication year - 1968
Publication title -
australasian annals of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 0571-9283
DOI - 10.1111/imj.1968.17.4.277
Subject(s) - medicine , cirrhosis , hepatitis , natural history , biopsy , liver biopsy , alcoholic hepatitis , gastroenterology , pathology , alcoholic liver disease
SUMMARY This study was designed to clarify the natural history of active chronic hepatitis in terms of its pathology. One hundred and fifty liver biopsy sections were studied from 82 patients with the disorder. Attention was directed to the diagnostic changes in various stages of the disease, to the histogenesis of cirrhosis and to those changes important in predicting prognosis. The importance of a liver biopsy in diagnosis was assessed and the pathological changes were compared with findings in clinically related disorders such as persistent hepatitis, cryptogenic cirrhosis, primary biliary cirrhosis, acute infectious hepatitis and pericholangitis. An attempt was made to assess the relationship between clinical manifestations and severity of active chronic hepatitis on the one hand, and the type and severity of the histological change on the other. Biopsy changes in treated patients were compared with changes in those who did not receive corticosteroids, azathioprine or 6‐mercaptopurine. Active chronic hepatitis may be diagnosed from aspiration biopsy specimens, which show the changes of both acute and chronic perilobular hepatitis. The changes appear to be specific and biopsy often provides the only means of diagnosing the disorder. The course of the disease is highly variable and is characterized by repeated episodes of necrosis.·, Necrosis of entire consecutive lobules may account for clinical episodes of spontaneous hepatic coma. Patients with evidence of lobular or submassive necrosis have a subsequent poor prognosis. All patients eventually develop cirrhosis, but over half have histologically active disease during the entire course. In no case could reversibility of the process be demonstrated. There is no justification for previous terminology which divides the disease into sub‐groups, as these appear to be merely clinical variants of the same pathological process.