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Hepatitis C viral infection increases the risk of lymphoid‐neoplasms: A population‐based cohort study
Author(s) -
Su TungHung,
Liu ChunJen,
Tseng TaiChung,
Chou ShihWan,
Liu ChenHua,
Yang HungChih,
Wu ShangJu,
Chen PeiJer,
Chen DingShinn,
Chen ChiLing,
Kao JiaHorng
Publication year - 2016
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.28387
Subject(s) - medicine , cohort , hazard ratio , hepatitis c virus , population , hepatitis c , cohort study , lymphoma , immunology , proportional hazards model , confidence interval , virus , environmental health
Chronic hepatitis C viral (HCV) infection has been associated with non‐Hodgkin's lymphoma (NHL); however, the results are inconsistent among regions with different HCV prevalence rates. The temporal relationship, risk estimates, and association between HCV and lymphoid‐neoplasms remain unclear. This study investigated the temporal relationship between HCV infection and lymphoid‐neoplasms using a nationwide population‐based cohort. Patients with chronic HCV infection were retrieved from the Taiwan National Health Insurance Research Database during 2001‐2005 and designated as the HCV cohort. Those with prior malignancies or coinfected with hepatitis B or human immunodeficiency virus were excluded. The age, sex, and comorbidities, including rheumatological disorders and diabetes, were matched by propensity scores to another non‐HCV cohort. Both cohorts were followed longitudinally until 2009 for a new diagnosis of any lymphoid‐neoplasms or NHL. A total of 11,679 HCV and 46,716 non‐HCV patients were included and followed for 8 years. The incidence rates of any lymphoid‐neoplasms and NHL were significantly greater in the HCV cohort than the non‐HCV cohort (48.4 versus 22.1, and 37.0 versus 17.5 per 100,000 person‐years, respectively, both P < 0.001), even after we excluded lymphoid‐neoplasms developed within the first year of follow‐up. Cox proportional hazards regression analysis (after adjustment for age, sex, numbers of annual medical visits during follow‐up, and comorbidities) indicated that HCV infection was associated with an increased risk of either any lymphoid‐neoplasms (hazard ratio = 2.30, 95% confidence interval 1.55‐3.43, P < 0.0001) or NHL (hazard ratio = 2.00, 95% confidence interval 1.27‐3.16, P = 0.003). Conclusion: After adjustment for confounders and biases, chronic HCV infection is temporally associated with a two‐fold increased risk of lymphoid‐neoplasms, especially NHL, in Asian patients; additional large studies are needed to explore whether HCV eradication can reduce the incidence of lymphoid‐neoplasms. (H epatology 2016;63:721–730)