Abstract
ObjectiveThe association between Sjögren’s syndrome (SS) and chronic hepatitis virus infection is inconclusive. Hepatitis B (HBV) and hepatitis C virus (HCV) infections are highly prevalent in Taiwan. We used a population-based case-control study to evaluate the associations between SS and HBV and HCV infections.Materials and MethodsWe identified 9,629 SS patients without other concomitant autoimmune diseases and 38,516 sex- and age-matched controls without SS from the Taiwan National Health Insurance claims data between 2000 and 2011. We utilized multivariate logistic regression to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) of the associations between SS and HBV and HCV infections. Sex- and age-specific (<55 and ≥55 years) risks of SS were evaluated.ResultsThe risk of SS was higher in patients with HCV than in those without chronic viral hepatitis (OR = 2.49, 95% CI = 2.16–2.86). Conversely, HBV infection was not associated with SS (OR = 1.10, 95% CI = 0.98–1.24). Younger HCV patients were at a higher risk for SS (<55 years: OR = 3.37, 95% CI = 2.62–4.35; ≥55 years: OR = 2.20, 95% CI = 1.84–2.62). Men with HCV were at a greater risk for SS (women: OR = 2.26, 95% CI = 1.94–2.63; men: OR = 4.22, 95% CI = 2.90–6.16). Only men with chronic HBV exhibited a higher risk of SS (OR = 1.61, 95% CI = 1.21–2.14).ConclusionHCV infection was associated with SS; however, HBV only associated with SS in men.
Highlights
Sjögren’s syndrome (SS) is a chronic autoimmune disorder which results in the lymphocytic infiltration of the exocrine glands and polyclonal B-cell activation [1]
The risk of SS was higher in patients with hepatitis C virus (HCV) than in those without chronic viral hepatitis (OR = 2.49, 95% confidence intervals (CIs) = 2.16–2.86)
hepatitis B virus (HBV) infection was not associated with SS (OR = 1.10, 95% CI = 0.98–1.24)
Summary
Sjögren’s syndrome (SS) is a chronic autoimmune disorder which results in the lymphocytic infiltration of the exocrine glands and polyclonal B-cell activation [1]. The etiology of SS is thought to arise from a specific combination of individual environmental and genetically predisposed factors. Viruses such as hepatitis C virus (HCV) are considered to be exogenous risk factors for developing the disease [7]. Since the earliest report in 1992 by Haddad et al, numerous authors have reported a relationship between SS and HCV in the past two decades [6,8,9,10,11,12,13]. The pathogenesis of HCV-associated SS is not well established
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