[Autoimmune hepatitis and/or hepatitis C]

Hepatitis C virus (HCV) was identified in 1989 as a primary aetiologic agent of parenterally transmitted non-A non-B hepatitis and a major cause of acute and chronic hepatitis worldwide [1, 2]. Extrahepatic manifestations that are associated with chronic HCV infection include: type II cryoglobulinaemia, membranoproliferative glomerulonephritis, porphyria cutanea tarda, Sjogren syndrome, autoimmune thyroiditis, lichen planus, etc. [3, 4]. Likewise, there is a very interesting link between HCV and autoimmune hepatitis type I [5-7]. The second generation of immunoassays confirmed positive anti HCV in a relatively low percent of patients (0-5%) with autoimmune hepatitis type I [5-7]. This fact suggests that HCV infection is not an important factor in the pathogenesis of autoimmune hepatitis, but it is not excluded. The examination of autoimmune markers is highly significant for the proper decision of the therapy: interferon therapy leads to exacerbation of autoimmune hepatitis, while corticosteroids enhance virus replication in patients with HCV infection. There is a percentage of patients suffering from both diseases, and in this case the therapeutic strategy is the treatment of predominant disease. The aim of the study was to establish the proper diagnose and make an adequate therapeutic decision in HCV infection combined with positive autoantibody findings.

In our study forty nine patients with HCV infection of autoimmune markers are described. Diagnosis of HCV infection was confirmed by clinical, biochemical, serological and histological examinations. ANA, AMA, and ASMA as non-specific autoimmune markers have been studied. Significant titre of ANA is 1:80, AMA 1:40 and ASMA 1:20 or higher. The patients included in the study were HBsAg negative, anti-HCV positive (at least six months) and had no sign of any other chronic disease, such as Morbus Wilson, alpha-1-antitrypsin deficiency or haemochromatosis.

The relevant data on patients are shown in Table 1. It is evident that 45% of patients had no known risk factors. The results of autoantibody are shown in Table 2. Eleven patients (22%) had autoantibodies, of whom one had 1:40 titre of ANA, while three had 1:80 titre of ASMA. Positive titre of AMA 1:40 was found in two patients. The distribution of relative autoantibody concentrations showed insignificant titres. The interferon therapy was used in five HCV RNA positive cases without progression.

Pathologic immune responses are sometimes the primary cause of autoimmune disorder, and sometimes the second one. The best studied factors that produce autoimmune disorder, are viruses. Probably the best evidence of virus aetiology of autoimmune hepatitis is the presence of anti-HCV antibody in some patients with autoimmune hepatitis type 1. Our clinical trial revealed the presence of autoantibodies in 22% of patients who suffered from HCV infection. These results are very similar to those of other authors [3, 5, 6, 16]. From the clinical point of view all patients can be divided into three groups: 1) The first group consists of patients with false positive results of anti-HCV and "true" autoimmune hepatitis type 1. Corticosteroid treatment is recommended. 2) The second group consists of patients with HCV infection and low percent of autoantibodies titres. These patients should be treated with alpha-interferon. 3) The third group consists of patients suffering from both diseases: chronic hepatitis C and autoimmune hepatitis. In this case, the initial treatment should start with corticosteroids (as low risk therapy) but if the progression is still on, corticosteroids should be substituted by interferon therapy. Our patients belonged to the second group, because of nonspecific titres of relative autoantibody concentrations. Our conclusion was that none of these patients had autoimmune hepatitis but certain autoimmune phenomena. The interferon therapy was used in five HCV RNA positive cases without