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NATURAL HISTORY OF ACTIVE CHRONIC HEPATITIS
Author(s) -
MISTILIS STEVEN P.,
SKYRING A. P.,
BLACKBURN C. R. B.
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.1968.17.3.214
Subject(s) - medicine , jaundice , hepatitis , natural history , incidence (geometry) , gastroenterology , anti nuclear antibody , endocrine system , physiology , antibody , immunology , pathology , autoantibody , hormone , physics , optics
Summary The aim of the present study was to outline the natural history of active chronic hepatitis. Data from 82 patients, suitably arranged for electronic data processing, relating to the onset, clinical course, liver function, morbidity, mortality, prevalence of endocrine changes and diseases in other organs, L.E. cell phenomenon and tissue antibody reactions, were analysed. Cumulative survival was calculated by the life table method. The criteria for the diagnosis of active chronic hepatitis are defined and features permitting differentiation from other closely related disorders emphasized. Most patients were females with a peak age incidence of 11 to 30 years. One‐third had an onset identical with viral hepatitis, and two‐thirds had an insidious onset with a variable clinical presentation. The presence or absence of jaundice, hyperglobulinæmia and L.E. cells, the particular age group or sex, multi‐organ involvement, endocrine changes, marked elevation of the SGOT level or abnormal tissue antibody reactions, made little difference to the over‐all clinical picture. Florid signs of hypercorticism were distinctly uncommon in the absence of steroid therapy. The serum bilirubin content was usually below 10 mg. per 100 ml., the SGOT level rarely exceeded 500 units per millilitre, and hyperglobulinæmia exceeding 7·0 grammes per 100 ml. was found in only nine cases. Hypersplenism was common, and antinuclear factors were frequently detected in patients who had no L.E. cells. Recurrent episodes of active liver disease, with or without liver failure, punctuated the course. Twenty per centum of patients had an anicteric disease. Hypersplenism was common, even in the absence of cirrhosis. Patients spent 6% to 30% of their time in hospital. The disease became inactive in 41%. In no case could reversibility of disease be documented. All patients eventually developed cirrhosis with or without portal hypertension. There were 21 deaths. Only six patients have so far survived for 10 years. Fifty per centum of deaths occurred in the first few years, when the disease was most active. Certain factors appear to influence the prognosis. Cumulative survival was only slightly better than that reported in other forms of cirrhosis.