RISK-FACTORS FOR HEPATOCELLULAR-CARCINOMA AND ITS INCIDENCE AFTER INTERFERON TREATMENT IN PATIENTS WITH CHRONIC HEPATITIS-C

Citation
A. Kasahara et al., RISK-FACTORS FOR HEPATOCELLULAR-CARCINOMA AND ITS INCIDENCE AFTER INTERFERON TREATMENT IN PATIENTS WITH CHRONIC HEPATITIS-C, Hepatology, 27(5), 1998, pp. 1394-1402
Citations number
46
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
27
Issue
5
Year of publication
1998
Pages
1394 - 1402
Database
ISI
SICI code
0270-9139(1998)27:5<1394:RFHAII>2.0.ZU;2-I
Abstract
To elucidate the risk factors for liver carcinogenesis and to examine the incidence of hepatocellular carcinoma (HCC) after interferon thera py, 1,022 chronic hepatitis C patients treated with interferon were fo llowed by ultrasonography for 13 to 97 months (median 36 months). Sust ained response with prolonged alanine aminotransferase normalization w as found in 313 patients, transient response with alanine aminotransfe rase relapse after therapy in 304, and no response in 405, Forty-six d eveloped HCC, of whom 5 were sustained responders, 9 were transient re sponders, and 32 were nonresponders. The cumulative incidence of HCC i n transient responders was almost equal to that in sustained responder s, and it was significantly higher in nonresponders than in sustained and transient responders (P = .0009), The seventh-year cumulative inci dence rates of HCC in sustained responders, transient responders, and nonresponders mere estimated to be 4.3%, 4.7%, and 26.1%, respectively . However, there was no significant difference in the cumulative incid ence of HCC between patients with HCV subtype 1 and 2 (P = .14). Cox r egression analysis showed that the risk of HCC development was not ele vated in transient responders compared with sustained responders, but that the risk was 7.90-fold higher in nonresponders than in sustained responders (P = .008), Patients greater than or equal to 55 years of a ge had a significantly higher risk ratio (4.65) than did those under 5 5 years of age (P = .006). The risk of HCC development in men was 4.35 times higher than the risk in women (P = .02). However, the degree of fibrosis was not a significant risk factor for the development of HCC (risk ratio, 3.16; P = .052). These results suggest that patients in the high-risk group of HCC after interferon therapy were those who sho wed no response, those who were older, and those who were male, and th at such patients should be carefully followed using ultrasonography.