title: Predisposing factors in sulphasalazine-induced systemic lupus erythematosus.
abstract: The aim of this study was to define predisposing factors in patients with sulphasalazine-induced systemic lupus erythematosus (SLE). Eleven patients with onset of SLE or SLE-like syndromes during sulphasalazine treatment are reported. Before the onset of SLE, five of the patients suffered from rheumatoid arthritis (RA), one from psoriatic arthropathy (PsoA), two from juvenile chronic arthritis (JCA) and three from ulcerative colitis (UC). At the time of diagnosis of drug-induced SLE, analysis of antinuclear antibodies (ANA), anti-double-stranded DNA antibodies (anti-dsDNA), anti-histone antibodies (anti-histones), acetylator status of the enzyme N-acetyltransferase 2 (NAT2) and HLA classification were performed. All patients were anti-DNA positive at disease onset and were determined to be slow acetylators. HLA A1 occurred in 4/10 patients, B8 in 5/10. HLA DR 3 was represented in one patient and DR 3(17) in five patients. The DQA1* 0501 allele was observed in 7/10 patients and DQB1 0201* in 6/10. Persistent SLE and development of nephritis were noted in patients with long duration of treatment and high cumulative dose of sulphasalazine (> 1000 g). In sulphasalazine-induced SLE, slow acetylator genotype and HLA haplotypes associated with idiopathic SLE seem to predict disease induction. Further, as the risk of developing persistent SLE and nephritis increases with long-standing sulphasalazine medication, it is of importance to monitor the patients with regard to signs of SLE during the entire treatment period.
authors.affiliation: Department of Rheumatology, Karolinska Hospital, Stockholm, Sweden.
authors.forename: I
authors.initials: I
authors.lastname: Gunnarsson
authors.forename: L
authors.initials: L
authors.lastname: Kanerud
authors.forename: E
authors.initials: E
authors.lastname: Pettersson
authors.forename: I
authors.initials: I
authors.lastname: Lundberg
authors.forename: S
authors.initials: S
authors.lastname: Lindblad
authors.forename: B
authors.initials: B
authors.lastname: Ringertz
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000974:Antibodies, Antinuclear / Q000032:analysis; D001171:Arthritis, Juvenile / Q000139:chemically induced / Q000150:complications / Q000276:immunology; D015535:Arthritis, Psoriatic / Q000139:chemically induced / Q000150:complications / Q000276:immunology; D001172:Arthritis, Rheumatoid / Q000139:chemically induced / Q000150:complications / Q000276:immunology; D001323:Autoantibodies / Q000032:analysis; D015984:Causality; D002648:Child; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000150:complications / Q000276:immunology; D004247:DNA / Q000032:analysis / Q000235:genetics / Q000276:immunology; D004305:Dose-Response Relationship, Drug; D005260:Female; D005838:Genotype; D006680:HLA Antigens / Q000032:analysis / Q000145:classification; D006657:Histones / Q000276:immunology; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000139:chemically induced* / Q000453:epidemiology* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009393:Nephritis / Q000139:chemically induced / Q000453:epidemiology / Q000276:immunology; D012217:Rheumatoid Factor / Q000032:analysis; D012460:Sulfasalazine / Q000009:adverse effects*; D013997:Time Factors
chemical_list: D000974:Antibodies, Antinuclear; D001323:Autoantibodies; D006680:HLA Antigens; D006657:Histones; D012460:Sulfasalazine; D004247:DNA; D012217:Rheumatoid Factor