BACKGROUND/AIM: Hepatocellular carcinoma frequently develops during the advanced stages of chronic hepatitis C. We examined whether interferon prevents the development of hepatocellular carcinoma in chronic hepatitis C patients. METHODS: Japanese patients with chronic hepatitis C (n = 1.148; 117 with portal fibrous expansion (F1), 636 with bridging fibrosis (F2), 355 with bridging fibrosis and architectural distortion (F3)) and 40 cirrhotic (F4) patients were treated with interferon. These patients were followed from 1 to 7 years after interferon therapy. Blood tests and image analysis were serially performed to assess response to interferon and to detect hepatocellular carcinoma. Fifty-five cirrhotic type C patients (control F4) not receiving interferon were enrolled in this study. RESULTS: Sustained (SR: 27.5%) and transient (TR: 23.0%) responders totaled 50.5%, while 49.5% did not respond to interferon. SR showed an improvement in disease stage reflected by increased platelet counts. Fifty-two patients (9 F2, 36 F3, and 7 F4) developed hepatocellular carcinoma in the follow-up period; 3 SR, 8 TR, and 41 non-responders (NR). The cumulative incidence of hepatocellular carcinoma in F2 was significantly lower (p = 0.019) in SR compared with NR, but not in SR in F3 and F4 patients. However, the cumulative incidence of hepatocellular carcinoma was significantly decreased in all SR (p = 0.0001) and TR (p = 0.0397) compared with all NR. CONCLUSION: These results indicate that interferon therapy in chronic hepatitis C patients lowered the rate of progression of hepatocellular carcinoma in sensitive cases but not in patients in an advanced stage.
BACKGROUND/AIM: Hepatocellular carcinoma frequently develops during the advanced stages of chronic hepatitis C. We examined whether interferon prevents the development of hepatocellular carcinoma in chronic hepatitis Cpatients. METHODS: Japanese patients with chronic hepatitis C (n = 1.148; 117 with portal fibrous expansion (F1), 636 with bridging fibrosis (F2), 355 with bridging fibrosis and architectural distortion (F3)) and 40 cirrhotic (F4) patients were treated with interferon. These patients were followed from 1 to 7 years after interferon therapy. Blood tests and image analysis were serially performed to assess response to interferon and to detect hepatocellular carcinoma. Fifty-five cirrhotic type Cpatients (control F4) not receiving interferon were enrolled in this study. RESULTS: Sustained (SR: 27.5%) and transient (TR: 23.0%) responders totaled 50.5%, while 49.5% did not respond to interferon. SR showed an improvement in disease stage reflected by increased platelet counts. Fifty-two patients (9 F2, 36 F3, and 7 F4) developed hepatocellular carcinoma in the follow-up period; 3 SR, 8 TR, and 41 non-responders (NR). The cumulative incidence of hepatocellular carcinoma in F2 was significantly lower (p = 0.019) in SR compared with NR, but not in SR in F3 and F4 patients. However, the cumulative incidence of hepatocellular carcinoma was significantly decreased in all SR (p = 0.0001) and TR (p = 0.0397) compared with all NR. CONCLUSION: These results indicate that interferon therapy in chronic hepatitis Cpatients lowered the rate of progression of hepatocellular carcinoma in sensitive cases but not in patients in an advanced stage.
Authors: Jennifer L Steel; Kevin H Kim; Mary Amanda Dew; Mark L Unruh; Michael H Antoni; Marion C Olek; David A Geller; Brian I Carr; Lisa H Butterfield; T Clark Gamblin Journal: J Pain Symptom Manage Date: 2010-05 Impact factor: 3.612
Authors: C Rabe; T Pilz; C Klostermann; M Berna; H H Schild; T Sauerbruch; W H Caselmann Journal: World J Gastroenterol Date: 2001-04 Impact factor: 5.742