Atherosclerosis 174 (2004) 99–103 Hepatitis B and C virus infection and the risk of atherosclerosis in a general population Henry Völzke a,∗ , Christian Schwahn a , Birger Wolff b , Renate Mentel c , Daniel M. Robinson b , Volker Kleine b , Stephan B. Felix b , Ulrich John a a Institute of Epidemiology and Social Medicine, Ernst Moritz Arndt University, Walther Rathenau Street 48, D-17487, Greifswald, Germany b Department of Internal Medicine B, Ernst Moritz Arndt University, Greifswald, Germany c Institute of Microbiology, Ernst Moritz Arndt University, Greifswald, Germany Received 22 September 2003; received in revised form 22 December 2003; accepted 26 January 2004 Abstract Background: The development of atherosclerosis has an inflammatory component. Currently it is not clear, whether hepatitis B and C virus infections are associated with the risk of atherosclerosis. The aim of the present analysis was to investigate those relationships in a population sample. Methods and results: The study of health in Pomerania (SHIP) is a cross-sectional study of the adult population in the northeast of Germany. HBs antigen (HBsAg) and IgG antibodies against hepatitis B and C virus (anti-HBs and anti-HCV) were determined by enzyme linked immunosorbent assays. Fifteen subjects (0.4%) were positive for HBsAg, and 21 subjects (0.5%) were positive for anti-HCV. Among the persons who had no history of anti-hepatitis B vaccination, 213 individuals (5.0%) were found to be as positive for anti-HBs. These individuals and those with prevalent anti-HCV antibodies were regarded as cases (n = 233). The control group comprised of 4033 individuals. Multivariable analyses revealed that there was no independent association between anti-HBs and anti-HCV antibody seropositivity and atherosclerotic end-points such as prevalent myocardial infarction, stroke, carotid intima-media thickness (IMT), carotid plaques and stenoses. Conclusion: There is no association between serological markers for hepatitis B and C virus infection and the risk of atherosclerosis in this population sample. © 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Atherosclerosis; Hepatitis B; Hepatitis C; Study of health in Pomerania (SHIP) 1. Introduction Infections have been discussed to be associated with an in- creased risk of atherosclerosis. Infection induces an inflam- matory response and the pathogenesis of atherosclerosis has an inflammatory component. Activated inflammatory cells and mediators have prothrombotic and matrix-degrading effects which can influence the development of atheroscle- rosis. Currently, it is not clear, whether the general inflam- matory response to an infective agent is important for the development of atherosclerosis or whether there are spe- cific atherogenic microorganisms [1]. Such microorganisms which may directly cause or accelerate atherosclerosis in- ∗ Corresponding author. Tel.: +49-3834-867707; fax: +49-3834-866684. E-mail address: voelzke@uni-greifswald.de (H. Völzke). clude Chlamydia pneumoniae, Cytomegalovirus, Herpes simplex virus and Helicobacter pylori [2–6]. Among the hepatitis viruses which target the liver pri- marily and cause a characteristic inflammatory process, the hepatitis A, B and C viruses have been investigated for pos- sible atherogenic effects. Thus, the hepatitis A virus was reported to be associated with coronary artery disease [7]. However, the enterically transmitted hepatitis A virus infec- tion is self-limiting and does not cause a chronic inflamma- tion, whereas hepatitis B and C viruses have potential for chronicity. The results of two studies [8,9] suggest hepatitis B and C virus infection may be independent risk factors for carotid atherosclerosis. However, these findings have not al- ways been confirmed [10] and one study [11] even produced conflicting results with hepatitis virus infections being pro- tective against atherosclerosis. The aim of the present analysis was to investigate asso- ciations between hepatitis B and C virus infection and the 0021-9150/$ – see front matter © 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.atherosclerosis.2004.01.010