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Adult giant cell hepatitis (AGCH) is a rare event and only about 100 cases have been reported within the last 20 years. The AGCH has been observed in association with viral infection, drug reactions or autoimmune disorders but in many cases its etiology remains unclear. AGCH manifests clinically as severe form of hepatitis histologically characterized by diffuse giant cell transformation of hepatocytes. We report the case of a 39-yr-old man with acute community-acquired hepatitis without previous pathology of the liver. Laboratory data revealed slight hypergammaglobulinemia and high titer of anti-smooth-muscle antibody with negative serology of hepatotropic viruses and absence of other known causes of hepatitis. Preliminary diagnosis of autoimmune hepatitis was established, additionally confirmed by excellent clinical and biochemical improvement during corticosteroid treatment. A liver biopsy showed the typical findings of panlobular syncytial giant cell hepatitis and positive HCV-RNA both in serum and liver. The above verified the diagnosis of acute type C hepatitis manifested histologically as adult giant cell hepatitis. After three months of treatment we withdrew corticosteroids as spontaneous clearance of HCV occurred and the lack of autoantibodies in serum as well as significant improvement of liver histology was ascertained. Within 30 months of the follow-up we have not observed biochemical and immunological abnormalities and control liver biopsy has shown no signs of hepatitis.

The natural history of chronic hepatitis C (CHC) is characterized by gradual progression of hepatic fibrosis, which can lead to cirrhosis. The aim of our study is to examine the influence of ineffective antiviral therapy on progress of the liver disease in CHC patients.Seventy-seven treated and non-treated CHC patients with two liver biopsies: baseline (BLB) and control (CLB) performed at least 12 months after treatment and at least 18 months from BLB in non-treated patients were studied. Twenty-eight CHC patients (age: 40.3 +/- 9.2 yrs; 22M), non-responding to interferon therapy (all with pretreatment fibrosis), were compared with non-treated patients divided into subgroups NT1 (21 patients [age: 45.1 +/- 11.2 yrs; 10M] with fibrosis in BLB) and NT2 (28 patients [age: 34.7 +/- 12.6; 17M] without fibrosis in BLB). The baseline clinical data between study groups as well as activity grade and fibrosis staging scores of the paired biopsy samples were compared.All three groups were comparable in terms of mean duration of the disease and interval between biopsies. There were no significant differences of clinical features in T and NT1 groups. In CLB, the patients from NT1 group presented non-significant worsening of staging and grading and in NT2 group a slight but statistically significant increase in grading was observed. In contrast, the treated patients had a slight, but significant improvement in liver histology.Antiviral treatment stopped the progression of liver disease in CHC despite the lack of biochemical and virological response. In non-treated patients a slight tendency to worsening of morphological parameters was observed.

We presented the results of treatment in patients with AHC and compared these findings with natural outcome of AHC in untreated patients.Ten treated AHC patients (5F/5M, mean age: 35.5 yrs; all HCV-RNA-positive including 9 anti-HCV-positive). Antiviral treatment was started within 3 to 18 (median 9) weeks after the onset of acute hepatitis including eight patients with monotherapy of IFN and two patients with combined (IFN + ribavirin) therapy.Fifty consecutive untreated AHC patients (26F/24M, mean age: 40.8 yrs; all HCV-RNA-positive, including 29 anti-HCV-positive) without contraindications to treatment with IFN.Only one treated patient presented no response and the other 9 patients presented rapid normalization of serum ALT levels in 4th-6th week of the therapy. In two patients, ALT increased in the course of therapy and after adding ribavirin the treatment was continued up to 48 weeks in total. At the end of treatment point, nine patients showed biochemical and virological response, but one relapsed both in biochemical and virological respect and virological relapse was observed in another one. Finally, sustained response was observed in 7 of 10 (70%) of treated compared with 22 of 50 (44%) untreated patients (p = n.s.). The beneficial effect of antiviral treatment was observed among patients with early anti-HCV seroconversion: 7 of 9 treated patients recovered persistently compared with 8 of 29 untreated (p = 0.021).The antiviral therapy in AHC seems to be effective and should be widely used, especially for individuals with early anti-HCV seroconversion. Ribavirin seems to be helpful for patients, who have not responded to interferon monotherapy.

Combined interferon-alpha (IFN) plus ribavirin therapy is recommended as first-line regimen treatment of chronic hepatitis C (CHC) patients. The aim of the study was to evaluate the selected clinical factors in the prediction of response to IFN with ribavirin for initial therapy and retreatment of CHC.Ninety eight consecutive CHC patients who completed the combined IFN with ribavirin therapy (24 or 48 weeks), including 79 naive patients (age: 41.0 +/- 10.9 yrs; 51M; NAIVE group) and 19 nonsustained responders to prior IFN monotherapy (age: 40.8 +/- 10.2 yrs; 10M; RETHERAPY group). Sustained Response (SR) was defined as persistent normalization of ALT and loss of serum HCV-RNA 6 months after the end of treatment; all other patients were defined as nonresponders (NR). Age, gender, pretreatment histology (assessed according to Ishak's scoring system) and baseline ALT, gamma-GTP and iron serum levels were compared in SR and NR patients, separately in NAIVE and RETHERAPY groups.The baseline clinical characteristics of NAIVE and RETHERAPY group did not differ significantly. 28 of 79 (35.4%) NAIVE patients and 9 of 19 (47.4%) RE-THERAPY patients achieved SR to the therapy. NAIVE sustained responders presented significantly lower staging scores and gamma-GTP levels in comparison with nonresponders. Multivariate logistic regression analysis showed that only fibrotic score lower than 3 was independently (p = 0.04) associated with SR. In RETHERAPY group, only female gender was positively correlated with SR. The other analyzed parameters did not significantly differ between responders and nonresponders.The results of the present study suggest that sustained response to combined therapy in naive CHC patients is associated with absence or minimal hepatic fibrosis prior to the therapy. Among retherapy patients, females are more likely to achieve sustained response, irrespective of fibrosis stage.

Patients with on-going HBV viral replication often present with clinical features of active chronic hepatitis. Until the recent introduction of nucleoside analogues, interferon-alpha was the only approved drug for these patients. One of the former drugs, lamivudine, has been shown in clinical trials in the US and Asia to effectively inhibit the viral polymerase of HBV. Our study was undertaken to assess the efficacy and safety of lamivudine therapy in Polish patients with chronic hepatitis B.Forty-five patients with chronic hepatitis B (HBeAg positive, anti-e negative, HBV-DNA positive by hybridization assay) were enrolled in the study. The patients received 100mg of lamivudine orally, once daily for 12 months. They returned for routine clinical and laboratory control every two weeks during the first months of treatment, and later at 3-month intervals while receiving lamivudine.At the end of treatment, serum HBeAg was not detected in 21 patients (48.8%), and anti-HBe appeared in the serum of 19 patients. 37.2% of the patients in the study group showed sustained suppression of serum HBV DNA at the end of treatment. Lamivudine therapy was well tolerated, with the rate of occurrence of adverse events similar to that observed in other clinical studies.12-month lamivudine therapy in this Polish population of patients with chronic hepatitis B induced a high rate of HBeAg seroconversion, accompanied by reduction of HBV-DNA and the normalization of alanine aminotransferase activities.