Vascular and glomerular manifestations of viral hepatitis B and C: a review.
Secondary vasculopathies have varied etiologies that include paraneoplastic processes (eg, migratory thrombophlebitis, urticarial vasculitis); direct invasion by tumors (eg, superior and inferior vena cava syndrome); metabolic diseases (eg, diabetes mellitus); and infections, among others. The infective causes of vasculitides could result from direct involvement of vessels by a vasculo-tropic agent (eg, mucor infection); adjacent inflammation nonspecifically affecting nearby vessels; or from infection-induced immune-mediated vasculitis. Viruses represent a major group in the development of the latter, and many human viruses have been reported to cause vasculitis. The vasculitic lesions secondary to hepatitis B and hepatitis C viruses largely fall within the spectrum of immune-mediated secondary vascular injury and are discussed in this review.
Adeyi
Oyedele A
OA
Department of Pathology, University Health Network/University of Toronto, 200 Elizabeth Street, Toronto, ON M5G 2C4, Canada. oyedele.adeyi@uhn.on.ca
D006509:Hepatitis B / Q000150:complications*; D006526:Hepatitis C / Q000150:complications*; D006801:Humans; D007678:Kidney Glomerulus / Q000473:pathology / Q000821:virology; D014657:Vasculitis / Q000473:pathology / Q000821:virology*