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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
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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.
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