The British Journal of Rheumatology, Vol 36, 1089-1094, Copyright © 1997 by British Society for Rheumatology
I Gunnarsson, L Kanerud, E Pettersson, I Lundberg, S Lindblad and B Ringertz
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.
ORIGINAL PAPERS
Predisposing factors in sulphasalazine-induced systemic lupus erythematosus
Department of Rheumatology, Karolinska Hospital, Stockholm, Sweden.
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