BACKGROUND. Recent data suggest that interferon therapy (IFN) can reduce the risk of progression to hepatocellular carcinoma (HCC) in patients with hepatitis C virus (HCV)-related cirrhosis. METHODS. A cohort of 189 patients with Child's Stage A cirrhosis of viral etiology followed prospectively were analyzed retrospectively to assess the effects of IFN on the clinical course and development of HCC. RESULTS. During a mean follow-up of 71.5 +/- 23.6 months, 7.9% of 88 treated and 21.8% of 101 untreated patients showed worsening of the Child's disease stage (P < 0.01); 5.6% of treated and 26.7% of untreated patients developed HCC (P < 0.001); and 3.4% of treated and 19.8% of untreated patients died of liver disease or underwent orthotopic liver transplantation (OLT) (P < 0.005). Using Cox's regression analysis, no treatment with IFN, high bilirubin and alkaline phosphatase (ALP) levels, and low leukocyte counts and prothrombin activity (PT) were associated significantly with worsening of Child's disease stage; no treatment with IFN, long term disease, low albumin and PT, and high gamma-glutamyl transpeptidase (GGT) were related significantly to HCC development; and no treatment with IFN, low albumin and PT, and high GGT and ALP were associated significantly with reduced survival. After adjustment for independent risk factors identified by multivariate analysis, the estimated cumulative probability of worsening of cirrhosis (P < 0.05), development of HCC (P < 0.001), and death or OLT (P < 0.006) was significantly lower in IFN-treated patients compared with untreated patients. This beneficial effect of therapy was statistically evident only in HCV positive patients. CONCLUSIONS. These results support the hypothesis that IFN improves clinical outcomes and reduces progression to HCC in patients with HCV-related cirrhosis. These conclusions, based on retrospective data, should be confirmed prospective.

Retrospective analysis of the effect of interferon therapy on the clinical outcome of patients with viral cirrhosis

FATTOVICH, Giovanna;
1998

Abstract

BACKGROUND. Recent data suggest that interferon therapy (IFN) can reduce the risk of progression to hepatocellular carcinoma (HCC) in patients with hepatitis C virus (HCV)-related cirrhosis. METHODS. A cohort of 189 patients with Child's Stage A cirrhosis of viral etiology followed prospectively were analyzed retrospectively to assess the effects of IFN on the clinical course and development of HCC. RESULTS. During a mean follow-up of 71.5 +/- 23.6 months, 7.9% of 88 treated and 21.8% of 101 untreated patients showed worsening of the Child's disease stage (P < 0.01); 5.6% of treated and 26.7% of untreated patients developed HCC (P < 0.001); and 3.4% of treated and 19.8% of untreated patients died of liver disease or underwent orthotopic liver transplantation (OLT) (P < 0.005). Using Cox's regression analysis, no treatment with IFN, high bilirubin and alkaline phosphatase (ALP) levels, and low leukocyte counts and prothrombin activity (PT) were associated significantly with worsening of Child's disease stage; no treatment with IFN, long term disease, low albumin and PT, and high gamma-glutamyl transpeptidase (GGT) were related significantly to HCC development; and no treatment with IFN, low albumin and PT, and high GGT and ALP were associated significantly with reduced survival. After adjustment for independent risk factors identified by multivariate analysis, the estimated cumulative probability of worsening of cirrhosis (P < 0.05), development of HCC (P < 0.001), and death or OLT (P < 0.006) was significantly lower in IFN-treated patients compared with untreated patients. This beneficial effect of therapy was statistically evident only in HCV positive patients. CONCLUSIONS. These results support the hypothesis that IFN improves clinical outcomes and reduces progression to HCC in patients with HCV-related cirrhosis. These conclusions, based on retrospective data, should be confirmed prospective.
cirrhosis type B; cirrhosis type C; clinical outcome; interferon therapy
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/2673
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