Clinical and immunological features of drug-induced and infection-induced proteinase 3-antineutrophil cytoplasmic antibodies and myeloperoxidase-antineutrophil cytoplasmic antibodies and vasculitis.
OBJECTIVE
Drugs and infections may induce antineutrophil cytoplasmic antibodies (ANCA) and vasculitic manifestations mimicking ANCA-associated vasculitides (AAV) and mechanisms relevant in their pathogenesis. This review summarizes the most recent findings in this field.


RESULTS
Drug-induced and infection-induced proteinase 3 (PR3)-ANCA and myeloperoxidase (MPO)-ANCA may be associated with a vasculitis clinically resembling AAV. Mechanisms relevant for the break of tolerance and induction of ANCA (e.g. danger signals, superantigens, neutrophil extracellular traps, protease-activated receptor-2, IL-17 cells) may be shared to some extent between drug-induced and infection-induced ANCA-positive vasculitis and AAV, especially with regard to the potential role of infection in Wegener's granulomatosis. Differences in immunopathology, clinical presentation, and functional aspects of ANCA help to distinguish drug-induced and infection-induced ANCA-positive vasculitis from AAV, and present new avenues for future research in this field.


CONCLUSIONS
Medications and infections, which induce PR3-ANCA and MPO-ANCA, have to be considered in the differential diagnosis of primary AAV. Moreover, there is clinical and experimental evidence for an association between certain drugs and infections with ANCA-production. Analysis of ANCA-induction in such conditions also sheds new light on our understanding of immune mechanisms relevant in the break of tolerance and ANCA-production in AAV.
Csernok
Elena
E
University of Lübeck, Department of Rheumatology, Vasculitis Center UKSH & Clinical Center Bad Bramstedt, Ratzeburger Allee 160, 23538 Lübeck, Germany. csernok@r-on-klinik.de
Lamprecht
Peter
P
Gross
Wolfgang L
WL
D056648:Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis / Q000139:chemically induced* / Q000382:microbiology* / Q000503:physiopathology; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000378:metabolism*; D001323:Autoantibodies / Q000032:analysis / Q000097:blood; D001424:Bacterial Infections / Q000150:complications / Q000276:immunology / Q000503:physiopathology; D019970:Cocaine-Related Disorders / Q000150:complications / Q000276:immunology / Q000503:physiopathology; D003937:Diagnosis, Differential; D006801:Humans; D007155:Immunologic Factors / Q000009:adverse effects; D053146:Myeloblastin / Q000276:immunology*; D009195:Peroxidase / Q000276:immunology*
D019268:Antibodies, Antineutrophil Cytoplasmic; D001323:Autoantibodies; D007155:Immunologic Factors; D009195:Peroxidase; D053146:Myeloblastin