Open AccessAutoantibodies against neutrophil cytoplasm components in systemic lupus erythematosus and in hydralazine‐induced lupus
Author(s) -
NÄSSBERGER L.,
SJÖHOLM A. G.,
JONSSON H.,
STURFELT G.,
ÅKESSON A.
Publication year - 1990
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1990.tb05342.x
Subject(s) - myeloperoxidase , autoantibody , medicine , immunology , elastase , antibody , systemic lupus erythematosus , neutrophil elastase , lupus erythematosus , proteinase 3 , hydralazine , anti neutrophil cytoplasmic antibody , vasculitis , biology , inflammation , enzyme , biochemistry , disease , blood pressure
SUMMARY Anti‐neutrophil cytoplasm antibody (ANCA) has been shown to be no marker of systemic lupus erythematosus (SLE) including lupus nephritis or of progressive systemic sclerosis (PSS). Antibodies against myeloperoxidase (anti‐MPO) and elastase, two granulocyte lysosomal enzymes, were found in patients with SLE but not in those with PSS, except for one patient who had anti‐MPO. Anti‐MPO was present in 21% of patients with SLE, and at low concentrations in about 80% of these cases. Anti‐elastase was found in four patients with SLE. In another group of six patients with a SLE‐like syndrome induced by anti‐hypertensive treatment with the anti‐hypertensive hydralazine, anti‐MPO antibodies occurred in all six, and anti‐elastase antibodies in five. Monitored during a 2‐year follow‐up period, anti‐MPO antibodies were found to persist, whereas anti‐elastase antibodies were rapidly eliminated, after withdrawal of the drug.