Journal of Clinical and Translational Hepatology

Journal of Clinical and Translational Hepatology

Saturday, 10 / 16 / 2021

Abstract

Thrombosis Associated with Viral Hepatitis

Luca Galli1,2, Victor E.A. Gerdes2, Luigina Guasti1 and Alessandro Squizzato*1

1Research Center on Thromboembolic Disorders and Antithrombotic Therapies, Department of Clinical and Experimental Medicine, University of Insubria, Varese, Italy; 2Department of Medicine, Slotervaart Hospital, Amsterdam, The Netherlands

Abstract

Viral hepatitis may promote the development of venous thromboembolism (VTE) and, more specifically, portal veinthrombosis (PVT). In this narrative review, we summarize the clinical data and discuss the possible pathogenetic roles of cytomegalovirus (CMV), Epstein-Barr virus (EBV), and hepatitis A, B, and C viruses (HAV, HBV, HCV) in the occurrence of VTE. CMV is the first qualified candidate to enter the list of VTE minor risk factors, and in the rare case of fulminant infection, both EBV and CMV, like any severe infection or inflammatory disease, increase risk for thrombosis. In chronic hepatitis B and C, it remains controversial whether antiphospholipid antibodies are important for thrombotic complications or merely an epiphenomenon. Retinal vein occlusion described in chronic hepatitis C is usually attributed to the treatment with interferon. Eltrombopag, used for HCV related thrombocytopenia, has been associated with increased thrombotic risk. The imbalance between procoagulantand anticoagulant factors associated with chronic liver disease may have clinical implications. This may help to explain why these patients are not protected from clinical events such as VTE, PVT, and the progression of liver fibrosis.

Doi: 10.14218/JCTH.2014.00031
Journal of Clinical and Translational Hepatology 2014 vol. 2 Pages: 234-239
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