Imad W Uthman1, Azzudin E Gharavi. 1. Department of Internal Medicine, Faculty of Medicine, American University of Beirut, Beirut, Lebanon. iuthman@aub.edu.lb
Abstract
OBJECTIVE: To study the relationship between viral infections and the induction of antiphospholipid (aPL) antibodies. METHODS: We reviewed the medical literature from 1968 until 2000 using MEDLINE and the key words virus, infection, antiphospholipid, and anticardiolipin. RESULTS: Anticardiolipin antibodies and/or lupus anticoagulant were associated with a number of viral infections, including hepatitis C virus, human immunodeficiency virus, cytomegalovirus, varicella zoster, Epstein-Barr virus, adenovirus, and parvovirus B. In many instances, the presence of these antibodies was associated with thrombosis. CONCLUSION: The clinical significance of finding aPL antibodies in patients with viral infections remains unknown. In some patients, these antibodies may be transient and disappear within 2 or 3 months. In other susceptible individuals, they may persist and raise the question of whether infections may trigger the development of aPL antibodies in autoimmune diseases. Copyright 2002, Elsevier Science (USA). All rights reserved.
OBJECTIVE: To study the relationship between viral infections and the induction of antiphospholipid (aPL) antibodies. METHODS: We reviewed the medical literature from 1968 until 2000 using MEDLINE and the key words virus, infection, antiphospholipid, and anticardiolipin. RESULTS: Anticardiolipin antibodies and/or lupus anticoagulant were associated with a number of viral infections, including hepatitis C virus, human immunodeficiency virus, cytomegalovirus, varicella zoster, Epstein-Barr virus, adenovirus, and parvovirus B. In many instances, the presence of these antibodies was associated with thrombosis. CONCLUSION: The clinical significance of finding aPL antibodies in patients with viral infections remains unknown. In some patients, these antibodies may be transient and disappear within 2 or 3 months. In other susceptible individuals, they may persist and raise the question of whether infections may trigger the development of aPL antibodies in autoimmune diseases. Copyright 2002, Elsevier Science (USA). All rights reserved.
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