icon_folder.gif   Conference Reports for NATAP  
 
  AASLD ( American Association for the Study of Liver Diseases)
 
November 9-13, 2001, Dallas
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EFFECT OF INTERFERON THERAPY ON THE RISK OF HEPATOCELLULAR CARCINOMA AND MORTALITY IN PATIENTS WITH CHRONIC HEPATITIS C: A LARGE RETROSPECTIVE COHORT STUDY OF 3296 PATIENTS
 
Reported by Jules Levin
 
  This study is very interesting although it is a study limited to Japanese patients and does not address coinfected patients.
 
This data comes from the program abstract. The poster itself will be examined for any differences tomorrow. In brief, this study finds-
 
--a viral load reduction, even if its not an ETR or SVR response, may lead to better survival and less risk for liver cancer
 
--patients treated with interferon have significantly lower rates of liver cancer (HCC) than untreated patients
 
--the incidence of HCC in non-responders was no better than in untreated patients (although, it appears to me from the data in the abstract that there was a non-significant difference between non-responders and the control group --untreated) in multivariate analysis including biochemical response in looking at risk for death
 
--but, both sustained responders and those with transient viral response had significantly lower risk for HCC
 
--the overall cumulative survival rate and cumulative liver-specific survival rate were significantly higher in interferon treated patientsthan in untreated patients
 
--higher histological stage--more progressed disease--was an independent factor associated with death from liver-associated causes
 
--interferon decreased risk of death from all causes by 62%, and deaths from liver disease by 59%
 
--overall survival rate was better in interferon treated
 
EFFECT OF INTERFERON THERAPY ON THE RISK OF HEPATOCELLULAR CARCINOMA AND MORTALITY IN PATIENTS WITH CHRONIC HEPATITIS C: A LARGE RETROSPECTIVE COHORT STUDY OF 3296 PATIENTS
 
abstract 171
 
Yasuharu Imai, Ikeda Municipal Hosp, Ikeda Japan; Akinori Kasahara, Osaka Univ Hosp, Suita Japan; Takeshi Okanoue, Kyoto Prefectural Univ of Medicine, Kyoto Japan; Hirohito Tsubouchi, Miyazaki Med Coll, Miyazaki Japan; Sumio Kawata, Yamagata Univ Sch of Medicine, Yamagata Japan; Shinji Tamura, Osaka Univ Graduate Sch of Medicine, Suita Japan; Kentaro Yoshioka, Nagoya Univ Sch of Medicine, Nagoya Japan; Kendo Kiyosawa, Shinshu Univ Sch of Medicine, Matsumoto Japan; Shinichi Kakumu, Aichi Med Univ Sch of Medicine, Aichi Japan; Kiwamu Okita, Yamaguchi Univ Sch of Medicine, Ube Japan; Norio Hayashi, Osaka Univ Graduate Sch of Medicine, Suita Japan
 
Interferon therapy for chronic hepatitis C has been shown to reduce the risk of hepatocellular carcinoma, especially among virologic and biochemical responders. However, the effect of interferon therapy on mortality remains unclear. We studied the effect of interferon therapy on the development of hepatocellular carcinoma and mortality in patients with chronic hepatitis C. 3296 patients with histologically-proven chronic hepatitis C by the end of 1997 were enrolled. Of these 3025 patients received interferon therapy and 271 patients were untreated. Patients in the interferon treatment group received 4- to 12-month course of interferon. The degree of liver fibrosis was assessed by using the criteria of Desmet and colleagues (F0 to F4). Response to interferon was determined biochemically. The end point of follow-up was the date of the development of hepatocellular carcinoma diagnosed by periodic examination of abdominal ultrasongraphy or computed tomography, date of death or the closing date of the study. Effect of interferon therapy on the risk for hepatocellular carcinoma and mortality was analyzed by using Cox proportional hazard regression. The cumulative incidence of hepatocellular carcinoma was significantly lower in interferon-treated patients than in untreated patients (p = 0.0001). Cox proportional regression analysis revealed that interferon treatment significantly lowered the risk of developing hepatocellular carcinoma by 38% (p = 0.001). Although the cumulative incidence of hepatocellular carcinoma in non-responders and untreated patients did not differ, both sustained responders and transient responders had significantly lower cumulative risk of developing hepatocellular carcinoma (p = 0.0001). The risk ratios for development of hepatocellular carcinoma in patients with sustained response, transient response and no response were 0.16 (95%CI, 0.10 to 0.27), 0.54 (95%CI, 0.37 to 0.94) and 0.91 (95%CI, 0.68 to 1,23), respectively, compared with untreated patients. Both the overall cumulative survival rate and cumulative liver-specific survival rate were significantly higher in the interferon-treated patients than in the untreated patients (p = 0.0001 and p = 0.0001, respectively). In multivariate analysis, older age at diagnosis of chronic hepatitis (p = 0.0001 and p = 0.0001, respectively), male gender (p = 0.0001 and p = 0.0004, respectively) and higher histological stage (p = 0.0001 and p = 0.0001, respectively) were independent factors associated with death from all causes and from liver-specific disease. Interferon treatment significantly decreased the risk of death from all causes by 62% (p = 0.0001) and death from liver-specific disease by 59% (p = 0.0001). The cumulative overall survival rate as well as liver-specific survival rate in the sustained and transient responders was significantly higher than in the untreated patients (p = 0.0001 and p = 0.0001, respectively). Multivariate analysis performed including the factor of biochemical response to interferon demonstrated that the risk ratios of death from all causes and death from liver disease were 0.12 (95% CI, 0.06 to 0.25) and 0.02 (95%CI, 0.003 to 0.17), respectively, in sustained responders, 0.17 (95%CI, 0.09 to 0.33) and 0.13 (95%CI, 0.05 to 0.35), respectively, in transient responders and 062 (95%CI, 0.43 to 0.90) and 0.72 (95%CI, 0.46 to 1.13), respectively, in non-responders, compared with controls. In conclusion, interferon therapy for chronic hepatitis C not only reduces the risk of hepatocellular carcinoma but also improves the long-term survival, especially among biochemical responders.