Drug-Induced Vasculitis: New Insights and a Changing Lineup of Suspects
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Abstract
An increasing number of therapeutic agents have been associated with a vasculitic syndrome. This usually involves small vessels, primarily capillaries, venules, and arterioles in leukocytoclastic vasculitis, small-vessel disease similar to an antineutrophil cytoplasmic antibody-related vasculitis, or mid-sized muscular arteries in a polyarteritis-like picture. Antineutrophil cytoplasmic antibodies are present in many cases of vasculitis regardless of the size of the vessel involved. Monoclonal antibodies used to treat many autoimmune disorders have become the most common agents associated with drug-induced vasculitis. Important advances in epigenetics, genetics, and neutrophil apoptosis are providing new insights into the pathogenesis of both drug-induced vasculitis and idiopathic vasculitis. Although management has not changed significantly in the past few years where withdrawal of the offending agent is the primary intervention, increasing awareness of drug-induced vasculitis can lead to earlier diagnosis and prevention of severe organ damage and fatalities.
Keywords
Antineutrophil cytoplasmic antibodies Cocaine Drug-induced vasculitis Hydralazine Leukotrienes antagonists Levamisole Minocycline Monoclonal antibodies Propylthiouracil Rituximab Statins Tumor necrosis factor-alpha VasculitisNotes
Acknowledgments
The author would like to gratefully acknowledge the assistance and patience extended to me by Dr. Ahlem A. Saleh, assistant librarian, at the Arizona Health Sciences Library.
Compliance with Ethical Standards
Conflict of Interest
The author declares that he has no competing interests.
Human and Animal Rights and Informed Consent
This article does not contain any information derived directly from human or animal subjects.
References
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