To examine the effects of interferon (IFN) therapy on clinical, biochemical, and histological features in patients with compensated hepatitis C virus (HCV)-related cirrhosis, we have conducted a randomized, controlled trial of IFN therapy versus observation. Eight centers included a total of 99 patients with biopsy-proven cirrhosis. IFN-␣2b, 3 million units three times per week, or no antiviral therapy was given for 48 weeks. Twenty-three patients dropped out. End-of-treatment biochemical response was not observed in any of the 39 controls but was observed in 6 of the 47 treated patients (P F .02); sustained biochemical response was obtained in only 2 treated patients. Controls and treated patients did not significantly differ with regard to the changes in serum level of albumin, bilirubin, ␣-fetoprotein, in plasma prothrombin, in histological activity, or liver collagen content. During trial or follow-up (160 ؎ 57 weeks), hepatocellular carcinoma developed in 9 controls and 5 treated patients (NS); decompensation of cirrhosis occurred in 5 controls and 7 treated patients. Seven controls and 10 treated patients died. In conclusion, in patients with compensated HCV-related cirrhosis, a 48-week course of IFN therapy is safe and is able to induce end-of-treatment biochemical response in a significant proportion of patients. However, a 48-week course of IFN therapy usually fails to achieve sustained response and, within the limit of this study, did not significantly improve the 3-year outcome. Therefore, a longer course of IFN therapy or combination therapy with ribavirin should be evaluated in patients with HCV-related cirrhosis. (HEPATOLOGY 1999;29:1870-1875.)Cirrhosis is a common complication of chronic hepatitis C, affecting approximately 20% of patients followed up for more than 10 years. 1 Currently identified risk factors for cirrhosis in hepatitis C virus (HCV)-infected patients are age at contamination, duration of infection, degree of histological activity, and alcohol consumption. 2,3 Natural history of HCVrelated cirrhosis is jeopardized by a high incidence of hepatocellular carcinoma (up to 5% per year) 4-7 and hepatic decompensation (up to 25% at 4 years). 4,6,7 Mortality rate is about 15% to 20% at 4 years. HCV-related cirrhosis accounts for 30% of liver transplantation in adults. 1 A treatment able to halt the progression of liver disease once cirrhosis is established but not yet complicated would be of great interest. Current data on the efficacy of interferon (IFN) therapy in patients with HCV-related cirrhosis are conflicting. Cirrhosis is a marker of a poor response to IFN therapy. 8 However, when genotype and serum viral load are taken into account, it is unclear that cirrhosis has any independent value in predicting a poor response to IFN therapy. 8 It has been recently suggested that IFN therapy can prevent the subsequent development of hepatocellular carcinoma, 9 but this contention is not supported by all studies. [5][6][7] In addition, the effects of IFN therapy on mortality rate and probab...

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This multidisciplinary study summarising published data and current practices produced a therapeutic algorithm, which should facilitate the standardised, optimised management of skin toxicity associated with EGFR inhibitors in France.

Because 70% to 75% of patients with chronic hepatitis C either do not respond to or relapse after interferon (IFN) therapy, and because ursodeoxycholic acid (UDCA) has been shown to reduce aminotransferase levels in patients with chronic hepatitis, we undertook a prospective controlled randomized trial of IFN (group I) versus IFN plus UDCA (group II) in 80 patients with chronic hepatitis C. IFN was administered in both groups for 6 months (3 to 5 million units [MU] three times a week), and in group II UDCA (10 mg/kg/d) was administered with IFN and then alone for 3 additional months. Response to therapy was defined as the normalization of alanine transaminase (ALT) levels. The results showed that 6 months after cessation of IFN, 59% of responders had relapsed in group I but only 27% had relapsed in group II (P = .03). There was no difference between the two groups for the initial (month 6) and the late (months 15 and 18) response rates to IFN. There was no virological effect or significant histological improvement attributable to the addition of UDCA to IFN treatment. In conclusion, the results of this study show that the addition of UDCA to IFN therapy significantly prolongs the period for which serum ALT remain, within the normal range after discontinuation of IFN. Further studies would be required to determine whether UDCA has any potential for long-term amelioration of the histological severity of liver disease caused by hepatitis C virus (HCV) infection, and, therefore, whether it could be advocated as an adjunct to antiviral therapy.