Drug-Induced Vasculitis

New Insights and a Changing Lineup of Suspects

Research output: Contribution to journalArticle

26 Citations (Scopus)

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.

Original languageEnglish (US)
Article number71
JournalCurrent Rheumatology Reports
Volume17
Issue number12
DOIs
StatePublished - Dec 1 2015

Fingerprint

Vasculitis
Pharmaceutical Preparations
Antineutrophil Cytoplasmic Antibodies
Venules
Arterioles
Epigenomics
Early Diagnosis
Neutrophils
Arteries
Monoclonal Antibodies
Apoptosis

Keywords

  • Antineutrophil cytoplasmic antibodies
  • Cocaine
  • Drug-induced vasculitis
  • Hydralazine
  • Leukotrienes antagonists
  • Levamisole
  • Minocycline
  • Monoclonal antibodies
  • Propylthiouracil
  • Rituximab
  • Statins
  • Tumor necrosis factor-alpha
  • Vasculitis

ASJC Scopus subject areas

  • Rheumatology

Cite this

Drug-Induced Vasculitis : New Insights and a Changing Lineup of Suspects. / Grau, Rafael G.

In: Current Rheumatology Reports, Vol. 17, No. 12, 71, 01.12.2015.

Research output: Contribution to journalArticle

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