Chronic Hepatitis: Aetiology and Current Management

The entity of chronic hepatitis has long been an enigma, and its treatment confusing. Recent studies have indicated the importance of excluding causes such as drugs, Wilson’s disease and α1-antitrypsin deficiency. After excluding such causes, there are 3 major groups — ‘autoimmune’, hepatitis B, and non-A, non-B (NANB) in all of which an immunological basis for pathogenesis exists. The autoimmune group has been subdivided into a milder type (chronic persistent hepatitis) and a more severe type (chronic active hepatitis) on histological grounds. Corticosteroids are indicated in chronic active hepatitis if cirrhosis or bridging necrosis is present. However, corticosteroids are contraindicated in disease due to the hepatitis B virus where chronic active hepatitis correlates with the presence of replicating virus (serum positive for e antigen, DNA polymerase and HBV-DNA), and in such cases antiviral agents and immunomodulation are being studied. Very little is known about NANB hepatitis in the absence of an assay and there may be more than a single agent. In hepatitis B, the development of serological markers, molecular probes (HBV-DNA), natural animal hepatitis with near-identical viruses, and δ antigen (a virus requiring coinfection with hepatitis B) have all extended our knowledge so dramatically that it is hoped that the enigma of chronic hepatitis will be solved when an assay for NANB hepatitis becomes available

Evaluation of the Crithidia Assay to Distinguish Between Autoimmune Chronic Active Hepatitis and Systemic Lupus-Erythematosus

The aim of this study was to determine if the Crithidia luciliae assay for auto‐antibodies to double‐stranded DNA, often positive in systemic lupus erythematosus, is always negative in auto‐immune chronic active hepatitis (CAH) as has recently been suggested. Twenty‐five patients were identified as having auto‐immune CAH. Mean duration of follow‐up was 10.5 years. Antinuclear antibodies were detected in 92%, smooth muscle antibodies in 76% and antimitochondrial antibodies in 16%. Antibodies to double‐stranded DNA were detected by the Crithidia assay in four patients (16%). Two of these patients had positive tests on only one occasion and no features of systemic lupus erythematosus. In the other two the assay was persistently positive. During follow‐up both developed arthritis and serositis but the liver lesion remained the dominant clinical feature. It was concluded that there is significant serological overlap between auto‐immune CAH and systemic lupus erythematosus making the Crithidia assay unreliable in distinguishing between them. Copyrigh