Treatment with peginterferon-alpha2a and ribavirin may be individualized by genotype. Patients with HCV genotype 1 require treatment for 48 weeks and a standard dose of ribavirin; those with HCV genotypes 2 or 3 seem to be adequately treated with a low dose of ribavirin for 24 weeks.

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Background: The role of interferon in the prevention of hepatocellular carcinoma remains controversial. Aim: In this meta‐analysis we evaluated the hepatocellular carcinoma incidence in interferon‐treated and ‐untreated patients with hepatitis C virus‐related cirrhosis. Methods: Eleven studies with 2178 patients were found to fulfil our inclusion criteria. The pooled odds ratio (OR) and 95% confidence intervals (CI) were calculated from the raw study data. Results: Hepatocellular carcinoma development was significantly more frequent in untreated (21.5%) than in interferon‐treated patients (8.2%; OR: 3.0, 95% CI: 2.3–3.9). In the five studies reporting hepatocellular carcinoma incidence in patients with and without sustained response to interferon, hepatocellular carcinoma was detected at a much higher rate in patients without (9%) than with a sustained response (0.9%; OR: 3.7, 95% CI: 1.7–7.8). Moreover, hepatocellular carcinoma developed significantly more frequently in the untreated patients than in the non‐sustained responders (OR: 2.7, 95% CI: 1.9–3.9). The benefit from interferon on hepatocellular carcinoma incidence was not influenced by the study type (prospective or retrospective), the follow‐up duration, or the study origin. Conclusions: Interferon therapy significantly reduces the hepatocellular carcinoma risk in patients with hepatitis C virus cirrhosis. Hepatocellular carcinoma development becomes almost negligible among sustained responders, but a reduction in hepatocellular carcinoma incidence is also achieved even in the non‐sustained responders.

shimoto's disease, 1,2 as well as of thyroid autoantibodies and/ The prevalence of antithyroid peroxidase antibodies or thyroid dysfunction among patients with chronic hepatitis (ATPO) and/or of thyroid dysfunction was studied in 422 C. [3][4][5] However, the suggested link between hepatitis C and patients with chronic viral hepatitis C, B, and D. Baseline thyroid disease is still uncertain. Data in the literature are results were compared with those during and 6 months after few and differ widely among studies, depending on the charinterferon alfa (IFN-a) therapy. The overall prevalence of acteristics of the populations tested and the sensitivity of the ATPO among untreated patients was 14.1%, with no signifimethods used. [6][7][8] Moreover, in most reports, no comparison cant differences between chronic hepatitis C, B, or D, as well has been made between chronic hepatitis C and the other as between males and females. However, high ATPO titers known types of chronic viral hepatitis (B and D). (¢18 IU/mL) clustered significantly among females (8.7% vs.Therapy with interferon alfa (IFN-a), widely used in 3.4%; P Å .022), especially those with chronic hepatitis C chronic viral hepatitis B or C and in various malignant dis-(11.2% vs. 3.6%; P Å .036). Before treatment, 3.7% of the eases, has also been associated with a high prevalence of patients had thyroid dysfunction, mostly hypothyroidism autoantibodies, and rarely with the development of overt (3.5%), the latter increasing to 14.3% among patients with autoimmune diseases. Thyroid disease, with clinical manifes-ATPO titers ¢18 IU/mL. IFN-a treatment significantly intations of hypothyroidism or hyperthyroidism, has been recreased overall thyroid dysfunction (9.7%; P Å .001) and ported in 5% to 12% of patients who received IFN-a for hypothyroidism (7.8%; P Å .01), particularly among patients various diseases, 9-11 while antithyroid autoantibodies were with high baseline ATPO (38.5%; P Å .0002). Six months present in a high percentage. 11-14 Indeed, only a minority of after stopping IFN-a treatment, the prevalence of thyroid dyspatients with chronic viral hepatitis who are positive for function was 8.0%, still significantly higher than at baseline.antimicrosomal or antithyroid antibodies have thyroid dysBy multivariate analysis, the only predictor positively associfunction, which is usually subclinical. transcriptase polymerase chain reaction method (Amplicor, Roche

The incidence of HBsAg loss is about 0.8% in cirrhosis type B. Prognostic factors for clearance of HBsAg are initial HBeAg positivity and therapy with alpha interferon. Patients with cirrhosis type B, who lose HBsAg, have a low risk for liver cancer or liver-related death.

To evaluate hepatic expression of the nuclear proliferative marker Ki-67 and the p53 oncoprotein in hepatitis B virus (HBV)/HCV cirrhosis in relation to dysplastic liver cell changes and hepatocellular carcinoma (HCC). We studied needle liver biopsies from 107 patients with cirrhosis and no HCC (52 HBV, 55 HCV) who had been assessed for protocol studies, and 57 cirrhotic patients with HCC (40 HBV, 17 HCV). We evaluated small and large cell dysplastic changes along with the expression of Ki-67 and p53 by immunohistochemistry. The labelling index (LI) was defined as the proportion (%) of positive-stained nuclei of the 500 measured. Large and small cell dysplastic changes were observed in 12 and 9% of specimens respectively. Only small cell changes were associated with Ki-67 expression. Ki-67 LI was 5.50 +/- 5.7 in cirrhosis (13.90 +/- 3.84 in those with small cell dysplastic changes vs 4.64 +/- 4.98 in those without, P < 0.01), 10.2 +/- 5.95 in cirrhosis with HCC (P < 0.05) and 18.56 +/- 10 in HCC (P < 0.01). Neither the presence of small cell dysplastic changes nor the expression of Ki-67 was related to severity or aetiology of cirrhosis. Expression of p53 was observed in 30% of the non-tumorous and in 53% of the neoplastic tissue obtained from patients with HCC, with no differences between HCV and HBV. Ki-67 and p53 expression was associated with the tumour grade (P < 0.001). Our observations clearly demonstrate the association between the proliferation activity and the morphological changes in the cirrhotic liver from the non-dysplastic to dysplastic lesion to HCC. They also support the hypothesis that p53 alterations are a rather late event in carcinogenesis and related to HCC grade. And finally, they suggest that the final steps of hepatocarcinogenesis are common and independent of the aetiology of the chronic viral infection.

Chronic infection with hepatitis B virus (HBV) has been reported in two-thirds of cases of hepatocellular carcinoma (HCC) in Greece from 1973 to 1995, while chronic hepatitis C virus (HCV) infection in 10% of them. We studied the roles of HBV and HCV in HCC in Greece between 1996 and 2000 compared with the past, and possible differences in clinical and laboratory characteristics of HBV- and HCV-related HCC. Complete clinical and laboratory data from 306 patients with HCC, diagnosed from January 1996 to December 2000, were analyzed. Chronic HBV and HCV infection were detected in 52.3 and 21.6% of the patients, respectively. The ratio of HBV- to HCV-related HCC was 2.42. Compared with the data prior to 1996, there was a 101.8% increase in the relative frequency of HCV (P < 0.0001) and an 11.8% decrease in that of HBV (P = 0.033), with a -56.3% change in the ratio of HBV- to HCV-related HCC cases. Statistically significant differences in the male/female ratio, median age and frequency of multifocal lesions were found in HBV- vs HCV-related HCC. Although HBV still represents the major aetiological factor of HCC in Greece, its role has significantly decreased in the last 5 years, while a more significant increase has occurred in HCV-related HCC. The two aetiological types of HCC differ in Greece in demographic, epidemiological and other features.