Wen-Cheng Li, Yi-Yen Lee, I-Chuan Chen, Cheng Sun, Feng-Hsiang Chiu, Chung-Hsun Chuang
Liver International. 2013;33(8):1194-1202.
Abstract and Introduction
Abstract
Background Hepatitis B/C viruses cause liver disease and metabolic disturbances.
Aims The purpose of this study was to evaluate the association between hepatitis B/C infection and metabolic syndrome (MS).
Methods In total, 26 305 subjects were included in this multicentre, cross-sectional study. Systolic and diastolic blood pressures, body mass index and waist circumference were measured. Total cholesterol, high- and low-density lipoprotein cholesterol, triglyceride, fasting blood glucose and uric acid were determined, and hepatitis B serum antigen (HBsAg) and anti-HCV antibodies were assayed using commercial kits.
Results MS was diagnosed in 2712 (23.0%) females, including 131 and 166 positive for HBsAg and anti-HCV respectively. In the men, 4594 (31.6%) were diagnosed with MS, including 326 positive for HBsAg and 131 positive for anti-HCV. No significant difference in the prevalence of MS was identified in any group, except men and women >45 years who were anti-HCV positive. Various metabolic alterations in both men and women >45 years were noted, including waist circumference, body mass index, fasting blood glucose and systolic and diastolic blood pressure. Notably, high- and low-density lipoproteins were significantly lower in positive subjects compared to those weakly positive and/or negative for anti-HCV.
Conclusions There were obvious metabolic derangements in patients coinflicted with MS and hepatitis C infections, particularly those >45 years of age. There is a pressing need to identify strategies to improve/resolve metabolic derangements to maximize sustained virological response rates in patients infected with HCV (and potentially HBV).
Introduction
Approximately 170 million (3% of the world's population) people are infected with the hepatitis C virus (HCV), and an overwhelming 2 billion people are currently infected with the hepatitis B virus (HBV) worldwide.[1–3] HBV and HCV are particularly prevalent in Asia and Taiwan. Over time, the hepatitis C and B viruses cause liver disease that often progresses from chronic hepatitis to fibrosis, cirrhosis and in some cases, hepatocellular carcinoma.[1, 2] In addition to being hepatotropic, the HCV is also known to cause metabolic disturbances, referred to as HCV-associated dysmetabolic syndrome (HCADS) characterized by steatosis, hypocholesterolaemia and insulin resistance (IR)/diabetes.[1]
The 'classic' metabolic syndrome (MS), which includes glucose abnormalities, central obesity, dyslipidaemia and hypertension, is increasingly common in Eastern countries, largely because of an obesity epidemic caused by the Westernization of many countries.[4] It is now widely accepted that patients with chronic HCV have a higher incidence of IR and type 2 diabetes mellitus than in patients with other liver diseases.[1] Further, several studies have suggested an association between chronic HCV and MS, reporting a prevalence of MS ranging from 4.1% to 44%.[5–7] It is also reported that insulin resistance, type 2 diabetes mellitus and HCADS negatively impact sustained virological responses (SVRs) to pegylated interferon- with ribavirin, and that MS is an independent predictor of a suboptimal SVR.[1] To date, the prevalence of full-blown MS (regardless of whether it is the classic form or the viral form, as described by Bugianesi et al.) among patients infected with HCV remains unknown.[8] Unlike HCV, the link between HBV and MS is not as well studied, despite the fact that infection with HBV is more common than HCV.
The purpose of this large, multi-centre, cross-sectional study was to evaluate the association between infection with either HBV or HCV and metabolic diseases, including MS and diabetes mellitus. The prevalence of both HBV and HCV infections, as well as type 2 diabetes, IR, obesity and MS, continue to increase at an alarming rate. There is therefore a pressing need to identify strategies for improving/resolving metabolic derangements to maximize SVR rates in patients infected with HCV (and potentially HBV). The findings of this study are anticipated to impact the prevention and long-term management of a multitude of HCV-positive individuals in the near future.
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