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.
Highlights
From a total of 19,298,735 individuals assessed between 1 January 2003 and 31 December 2012, 11,895,993 patients without baseline esophageal cancer were identified; 114,304 patients with Hepatitis C virus (HCV) infection and 11,781,689 patients without HCV infection were eligible for the study
The most compelling results of the current study were as follows: (1) The HCVuntreated cohort had the highest 9-year cumulative incidence of esophageal cancer among the three cohorts, while no difference in cumulative incidences was identified between the HCV-treated and HCV-uninfected cohorts; (2) HCV positivity and male sex were independent factors associated with esophageal cancer development; and (3) The HCVuntreated cohort had the highest cumulative incidence of overall mortality, while the HCV-treated and HCV-uninfected cohorts yielded nonsignificant mortality incidences
The findings that the HCV-treated cohort had a higher cirrhosis rate than the untreated cohort and that the HCV-infected cohort had higher cirrhosis and cardiometabolic complication rates but lower dyslipidemia rates than the HCV-uninfected cohorts were consistent with the ideas that only patients with significant fibrosis were reimbursed for interferon-based anti-HCV therapy by National Health Insurance (NHI), Taiwan [25], and HCV infection causes cirrhosis, cardiometabolic events, and hypolipidemia [8]
Summary
Esophageal cancer is the sixth leading cause of cancer death in males, with an estimated >500,000 new cases and >500,000 deaths annually, accounting for 3.2% of cancer creativecommons.org/licenses/by/ 4.0/). Cases and 5.37% of cancer deaths worldwide [1]. Asia are considered to have the highest incidence of esophageal cancer [2]. There are two main histological types of esophageal cancer: esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC). The risk factors for esophageal SCC include alcohol, smoking, betel nut chewing [4], and hypertension [5]. Metabolic syndrome (MetS) [6] and body mass index (BMI)/obesity [5,7] are related to a higher risk of EAC. A high BMI significantly decreases the risk of ESCC [5]
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