BACKGROUND: the aim of this study was to determine whether hepatitis C virus (HCV) is an underlying cause of the increase in the incidence of hepatocellular carcinoma (HCC) in the United States. STUDY: the medical records of all patients who had received a pathologic diagnosis of HCC at the University of Texas M.D. Anderson Cancer Center, Houston, Texas, U.S.A., during 1993 through 1998 were reviewed. Only patients residing in the United States were analyzed. All patients were tested for HCV and hepatitis B virus serologic markers. RESULTS: the number of patients with HCC referred to M.D. Anderson Cancer Center increased from 143 in 1993 through 1995 to 216 in 1996 through 1998. Twenty-six patients (18%) and 66 patients (31%) with anti-HCV antibodies were diagnosed with HCC from 1993 to 1995 and from 1996 to 1998, respectively, thus constituting a significant increase ( = 0.01). Although the age distribution of these patients did not differ significantly between 1993 to 1995 and 1996 to 1998, the increase in HCV-associated HCC was greatest among patients 40 to 49 years old. Hepatitis B surface antigens (HBsAg) or anti-hepatitis B core antigens were found in 37 patients (26%) with HCC during 1993 to 1995 and in 37 patients (17%) with HCC during 1996 to 1998 ( = 0.06). Moreover, a significant decrease in the prevalence of HBsAg from 1996 to 1998 (21 patients; 10%) compared with 1993 to 1995 (25 patients; 18%) was observed ( = 0.03). CONCLUSION: hepatitis C infection is the major viral factor contributing to the increase in HCC incidence observed in this large-scale, single-center United States-based experience.
BACKGROUND: the aim of this study was to determine whether hepatitis C virus (HCV) is an underlying cause of the increase in the incidence of hepatocellular carcinoma (HCC) in the United States. STUDY: the medical records of all patients who had received a pathologic diagnosis of HCC at the University of Texas M.D. Anderson Cancer Center, Houston, Texas, U.S.A., during 1993 through 1998 were reviewed. Only patients residing in the United States were analyzed. All patients were tested for HCV and hepatitis B virus serologic markers. RESULTS: the number of patients with HCC referred to M.D. Anderson Cancer Center increased from 143 in 1993 through 1995 to 216 in 1996 through 1998. Twenty-six patients (18%) and 66 patients (31%) with anti-HCV antibodies were diagnosed with HCC from 1993 to 1995 and from 1996 to 1998, respectively, thus constituting a significant increase ( = 0.01). Although the age distribution of these patients did not differ significantly between 1993 to 1995 and 1996 to 1998, the increase in HCV-associated HCC was greatest among patients 40 to 49 years old. Hepatitis B surface antigens (HBsAg) or anti-hepatitis B core antigens were found in 37 patients (26%) with HCC during 1993 to 1995 and in 37 patients (17%) with HCC during 1996 to 1998 ( = 0.06). Moreover, a significant decrease in the prevalence of HBsAg from 1996 to 1998 (21 patients; 10%) compared with 1993 to 1995 (25 patients; 18%) was observed ( = 0.03). CONCLUSION:hepatitis C infection is the major viral factor contributing to the increase in HCC incidence observed in this large-scale, single-center United States-based experience.
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