[Autoimmune hepatitis and/or hepatitis C]. / Autoimunski hepatitis i/ili hepatitis "C".

UNLABELLED: 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. PATIENTS AND METHODS: 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. RESULTS: 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. DISCUSSION: 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

[Diagnostic and prognostic criteria in acute non-A, non-B viral hepatitis with a prolonged course]. / Dijagnosticki i prognosticki kriterijumi u akutnom virusnom hepatitisu "ni-A-ni-Be" produzenog toka.

In a prospective three-year-long study of Non-A, Non-B infections carried out in the Institute of Infectious and Tropical Diseases in Belgrade, by a method of exclusion and in about 30% of patients' liver biopsies, 75 cases of acute viral hepatitis Non-A, Non-B were discovered. It makes only 2.29% of all cases of acute viral hepatitis diagnosed and treated in the same period in this institution. In prolonged forms of the disease (24 cases) the chronicity was shown by epidemiological data (posttransfusion hepatitis), fluctuation of transaminase and rise of gamma globulins in acute phase of the disease. Liver biopsies performed in the first four months of the disease were of no prognostic value.

[Malacoplakia of the kidney]. / Malakoplakia bubrega.

Malakoplakia is a rare disease expressed as a special type of inflammatory reaction to infection with various bacteria and fungi. This unusual response is based on defective function of the macrophage system. In malakoplakia infiltrates, most cells are macrophages mixed with lymphocytes, plasma cells and fibroblasts. The macrophages (von Hansemann's histiocytes) with intracytoplasmatic inclusions defined as Micaelis-Guttmann bodies are pathognomonic histological findings. The clinical manifestation of the disease depends on the localisation of lesions, most often in the urinary bladder and the kidney. The authors present a case of renal malakoplakia of in a 32-year-old female patient. The symptoms were not enough characteristic for making the true diagnosis. The diagnosis of malakoplakia was established during autopsy. The histopathological examination revealed von Hansemann's histiocytes and Michaelis-Guttmann bodies in malakoplakia infiltrates.