Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic lupus erythematosus (SLE) induced by drugs, primarily hydralazine and procainamide, is reviewed and compared with idiopathic SLE, and the use of these drugs in patients with idiopathic SLE is discussed. The etiology of SLE is unclear, but genetic predisposition is an important factor. Although more than 25 drugs have been suggested as causes of SLE, the majority of confirmed cases of drug-induced SLE involve hydralazine or procainamide. Parts of these chemical compounds apparently interact with nucleoproteins, causing stimulation of antinuclear antibody (ANA) production. The average age of patients with drug-induced SLE is nearly twice that of patients with idiopathic SLE. Approximately half the patients with drug-induced SLE are women, compared with 92% of patients with idiopathic SLE. For SLE induced by hydralazine or procainamide, musculoskeletal symptoms (especially arthritis in the hands and wrists) are the most common clinical manifestation. In patients with SLE induced by these drugs, ANAs and LE cells are present, erythrocyte sedimentation rate is often elevated, and a false-positive serologic test for syphilis is seen more frequently than in idiopathic SLE. Baseline ANA status should be determined before therapy with these drugs, and patients should be observed carefully for signs and symptoms of SLE. Hydralazine-induced SLE may be dose related; limiting the daily dose to 200 mg is recommended. Some drugs have been shown to exacerbate idiopathic SLE; these include estrogen-containing oral contraceptives and ibuprofen. Hydralazine and procainamide are probably safe for use in patients with idiopathic SLE, but alternative therapy should be considered. The clinical and laboratory manifestations of drug-induced SLE are similar to those of idiopathic SLE, but central nervous system and renal involvement are rare in drug-induced SLE.
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PMID:Drug-induced systemic lupus erythematosus. 286 63

The clinical features, autoantibody changes, acetylator and HLA-DR phenotype of 20 patients with hydralazine-induced systemic lupus erythematosus are described. Four cases of particular interest are discussed in greater detail. Hydralazine sensitivity is more common in women, slow acetylators and the HLA-DR4 phenotype. Symptoms can occur even after many years of treatment and clinical awareness must be maintained for all patients to detect sensitivity at an early stage; there is no timely safe dose even in rapid acetylators. Joint symptoms predominate and full resolution is usual on discontinuing hydralazine. Failure of resolution should raise the suspicion of an underlying cause for the arthritis.
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PMID:Hydralazine sensitivity: clinical features, autoantibody changes and HLA-DR phenotype. 332 39

Twenty-seven hypertensive patients (23 blacks, 4 whites) treated with hydralazine had frequent serologic evidence of autoimmunity. However, only 1 patient developed a lupus syndrome. Acetylator phenotype influenced the autoimmune response; slow acetylators had a higher incidence and titers of autoantibodies. The lupus patient not only had high titers of autoantibodies but they were predominantly IgG in contrast to the predominant IgM antibodies found in other slow acetylators. Hydralazine treatment did not alter cell-mediated immune responses and hydralazine antibodies were not detected. However, half the patients tested who received hydralazine had positive lymphoproliferative responses to the drug.
Arthritis Rheum 1981 Aug
PMID:Immunologic effects of hydralazine in hypertensive patients. 697 54

Patients with drug-related lupus erythematosus produce antibodies to nuclear histones which can be detected by a three-step indirect immunofluorescence technique. Procainamide-related antinuclear antibodies were detected by this technique, but hydralazine-related antinuclear antibodies were not. Certain evidence suggests that antibodies induced by the two drugs are reactive with different subclasses of histones. Hydralazine was shown to interact with a soluble DNA-histone complex, and the resulting interaction rendered the histone moiety resistant to trypsin digestion. This mechanism may help to maintain DNA-histone complexes in a potentially immunogenic form and result in the production of autoantibodies.
Arthritis Rheum 1981 Aug
PMID:The role of histones as nuclear autoantigens in drug-related lupus erythematosus. 702 42