Chronic non‐A, non‐B hepatitis: lack of correlation between biochemical and morphological activity, and effects of immunosuppressive therapy on disease progression

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Abstract
A study was made of 52 patients considered to probably have chronic non-A, non-B hepatitis who were seen during an eight-year period at Westmead Hospital, Sydney. The patients were followed for a median of 28 months to assess the natural history of the disease and, in a small number of patients, the effect of immunosuppressive therapy on disease progression was examined. In 94% of cases, infection appeared to have been acquired by a parenteral route; the remainder were sporadic infections. Fifty-six per cent of the patients had mild constitutional symptoms and the remainder were asymptomatic. Similarly, 54% of patients had no signs of chronic liver disease and none exhibited signs of hepatic decompensation. Liver biopsies were performed in 42 patients; chronic active heptitis with or without cirrhosis was present in 90%. However, neither the presence of symptoms nor the degree of biochemical abnormality were predictive of disease severity as determined histologically. Among eight patients treated with corticosteroids (with or without azathioprine), six underwent follow-up liver biopsy. Quantitative analysis of inflammatory and fibrotic changes indicated significant (p<0.01) progression of histological severity during a median 33 months (range 7-98 months) between biopsies with cirrhosis developing in four instances. In contrast, among the seven untreated patients rebiopsied after a median of 16.0 months (range 11-37 months) there was no overall change in histological severity and only one patient developed cirrhosis. It is concluded that histological assessment is required in all patients suspected of having chronic non-A, non-B hepatitis as other means of assessment are unreliable. At present, immunosuppressive therapy cannot be recommended for patients with this form of chronic viral hepatitis; as well as being unhelpful, such treatment may accelerate disease progression.

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