TY - JOUR
T1 - Drug-Induced Vasculitis
T2 - New Insights and a Changing Lineup of Suspects
AU - Grau, Rafael G.
N1 - Publisher Copyright:
© 2015, Springer Science+Business Media New York.
PY - 2015/12/1
Y1 - 2015/12/1
N2 - 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.
AB - 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.
KW - Antineutrophil cytoplasmic antibodies
KW - Cocaine
KW - Drug-induced vasculitis
KW - Hydralazine
KW - Leukotrienes antagonists
KW - Levamisole
KW - Minocycline
KW - Monoclonal antibodies
KW - Propylthiouracil
KW - Rituximab
KW - Statins
KW - Tumor necrosis factor-alpha
KW - Vasculitis
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U2 - 10.1007/s11926-015-0545-9
DO - 10.1007/s11926-015-0545-9
M3 - Review article
C2 - 26503355
AN - SCOPUS:84945258431
SN - 1523-3774
VL - 17
JO - Current rheumatology reports
JF - Current rheumatology reports
IS - 12
M1 - 71
ER -