Open AccessAssociation of autoantibodies to myeloperoxidase with different forms of vasculitis
Author(s) -
Tervaert J. W. Cohen,
Goldschmeding R.,
Elema J. D.,
Limburg P. C.,
van der Giessen M.,
Huitema M. G.,
Koolen M. I.,
Hené R. J.,
The T. H.,
van der Hem G. K.,
von dem Borne A. E. G. Kr.,
Kallenberg C. G. M.
Publication year - 1990
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780330829
Subject(s) - autoantibody , medicine , vasculitis , myeloperoxidase , polyarteritis nodosa , systemic vasculitis , glomerulonephritis , proteinase 3 , necrotizing vasculitis , pathology , immunology , anti neutrophil cytoplasmic antibody , gastroenterology , antibody , inflammation , kidney , disease
Abstract Antineutrophil cytoplasmic autoantibodies with specificity for myeloperoxidase (MPO) were found in 53 patient sera that were routinely submitted for antineutrophil cytoplasmic antibody determination. Based on clinical and histologic criteria, 15 of these 53 patients were classified as having systemic necrotizing vasculitis of the polyarteritis group, 11 patients were classified as having Wegener's granulomatosis (WG), and 14 were classified as having idiopathic crescentic glomerulonephritis. The remaining 13 patients did not fulfill the diagnostic criteria for these disorders, although most of these patients had clinical symptoms compatible with these disorders. While all patients with WG had renal involvement, only 4 of the 15 patients with systemic necrotizing vasculitis of the polyarteritis group had glomerulonephritis. The sensitivity of autoantibodies to MPO for either systemic necrotizing vasculitis of the polyarteritis group, WG, or idiopathic crescentic glomerulonephritis was further tested in all our patients with these disorders (n = 104). Twenty‐seven of 104 patients had autoantibodies to MPO. Furthermore, 69 of the remaining 77 patients had autoantibodies specific for the 29‐kd serine protease, which has been reported to be specifically associated with WG. Sera from 8 patients were negative for either of these antibodies (92% sensitivity of autoantibodies to MPO and/or the 29‐kd serine protease). The specificity of autoantibodies to MPO for either systemic necrotizing vasculitis of the polyarteritis group, WG, or idiopathic crescentic glomerulonephritis was also tested in selected groups of patients who had closely related diseases. Two of 144 patients had autoantibodies to MPO (specificity 99%). We conclude that these antibodies are not only associated with idiopathic and vasculitis‐associated crescentic glomerulonephritis, but also with classic polyarteritis nodosa, Churg‐Strauss syndrome, and the polyangiitis overlap syndrome without renal involvement. The presence of autoantibodies to MPO or the 29‐kd serine protease is highly sensitive and specific for systemic necrotizing vasculitis of the polyarteritis group, WG, and idiopathic crescentic glomerulonephritis.