Yin-Yi Chu1,2,3, Jur-Shan Cheng4,5, Ting-Shu Wu3,6, Chun-Wei Chen1,3, Ming-Yu Chang3,7,8, Hsin-Ping Ku2, Rong-Nan Chien3,9, Ming-Ling Chang3,9. 1. Division of Gastroenterology, Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Taoyuan 333423, Taiwan. 2. Department of Gastroenterology and Hepatology, New Taipei Municipal Tu Cheng Hospital, New Taipei City 236, Taiwan. 3. Department of Medicine, College of Medicine, Chang Gung University, Taoyuan 333323, Taiwan. 4. Clinical Informatics and Medical Statistics Research Center, College of Medicine, Chang Gung University, Taoyuan 333423, Taiwan. 5. Department of Emergency Medicine, Chang Gung Memorial Hospital, Keelung 20401, Taiwan. 6. Division of Infectious Diseases, Department of Internal Medicine, Linkou 333423, Taiwan. 7. Division of Pediatric Neurologic Medicine, Chang Gung Children's Hospital, Taoyuan 333423, Taiwan. 8. Division of Pediatrics, Chang Gung Memorial Hospital, Keelung 20401, Taiwan. 9. Division of Hepatology, Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Taoyuan 333423, Taiwan.
Abstract
Background: Hepatitis C virus (HCV) infection causes many extrahepatic cancers, and whether HCV infection is associated with esophageal cancer development remains inconclusive. Methods: A nationwide population-based cohort study of the Taiwan National Health Insurance Research Database (TNHIRD) was conducted. Results: From 2003 to 2012, of 11,895,993 patients, three 1:1:1 propensity score-matched cohorts, including HCV-treated (interferon-based therapy ≧6 months, n = 9047), HCV-untreated (n = 9047), and HCV-uninfected cohorts (n = 9047), were enrolled. The HCV-untreated cohort had the highest 9-year cumulative incidence of esophageal cancer among the three cohorts (0.174%; 95% confidence interval (CI): 0.068-0.395) (p = 0.0292). However, no difference in cumulative incidences was identified between the HCV-treated (0.019%; 0.002-0.109%) and HCV-uninfected cohorts (0.035%; 0.007-0.133%) (p = 0.5964). The multivariate analysis showed that HCV positivity (hazard ratio (HR): 5.1, 95% CI HR: 1.39-18.51) and male sex (HR: 8.897; 95% CI HR: 1.194-66.323) were independently associated with the development of esophageal cancer. Of the three cohorts, the HCV-untreated cohort had the highest cumulative incidence of overall mortality at 9 years (21.459%, 95% CI: 18.599-24.460) (p < 0.0001), and the HCV-treated (12.422%, 95% CI: 8.653-16.905%) and HCV-uninfected cohorts (5.545%, 95% CI: 4.225-7.108%) yielded indifferent cumulative mortality incidences (p = 0.1234). Conclusions: Although HCV positivity and male sex were independent factors associated with esophageal cancer development, whether HCV infection is the true culprit or a bystander for developing esophageal cancer remains to be further investigated. Interferon-based anti-HCV therapy might attenuate esophageal risk and decrease overall mortality in HCV-infected patients.
Background: Hepatitis C virus (HCV) infection causes many extrahepatic cancers, and whether HCV infection is associated with esophageal cancer development remains inconclusive. Methods: A nationwide population-based cohort study of the Taiwan National Health Insurance Research Database (TNHIRD) was conducted. Results: From 2003 to 2012, of 11,895,993 patients, three 1:1:1 propensity score-matched cohorts, including HCV-treated (interferon-based therapy ≧6 months, n = 9047), HCV-untreated (n = 9047), and HCV-uninfected cohorts (n = 9047), were enrolled. The HCV-untreated cohort had the highest 9-year cumulative incidence of esophageal cancer among the three cohorts (0.174%; 95% confidence interval (CI): 0.068-0.395) (p = 0.0292). However, no difference in cumulative incidences was identified between the HCV-treated (0.019%; 0.002-0.109%) and HCV-uninfected cohorts (0.035%; 0.007-0.133%) (p = 0.5964). The multivariate analysis showed that HCV positivity (hazard ratio (HR): 5.1, 95% CI HR: 1.39-18.51) and male sex (HR: 8.897; 95% CI HR: 1.194-66.323) were independently associated with the development of esophageal cancer. Of the three cohorts, the HCV-untreated cohort had the highest cumulative incidence of overall mortality at 9 years (21.459%, 95% CI: 18.599-24.460) (p < 0.0001), and the HCV-treated (12.422%, 95% CI: 8.653-16.905%) and HCV-uninfected cohorts (5.545%, 95% CI: 4.225-7.108%) yielded indifferent cumulative mortality incidences (p = 0.1234). Conclusions: Although HCV positivity and male sex were independent factors associated with esophageal cancer development, whether HCV infection is the true culprit or a bystander for developing esophageal cancer remains to be further investigated. Interferon-based anti-HCV therapy might attenuate esophageal risk and decrease overall mortality in HCV-infectedpatients.