Oral contraceptive therapy and systemic lupus erythematosus

Abstract

The relationship between oral contraceptive therapy and systemic lupus erythematosus is not well defined. It has been reported that oral contraceptives may induce lupus: they may also exacerbate pre-existing disease. This report concerns a young woman in whom systemic lupus erythematosus developed three weeks after the commencement of oral contraceptive therapy, but who was shown to have had a chronic biological false positive serological test for syphilis for eight months prior to this. The significance of false positive serological tests for syphilis and the effect of female sex hormones on disease activity in systemic lupus erythematosus is discussed.

PIP: Oral contraceptive therapy has been reported to induce systemic lupus erythematosus (SLE) and rheumatic complaints with normal and abnormal serology. A case report is presented of a 23-year-old female in whom SLE developed 3 weeks after initiation of oral contraceptive (ethinyl estradiol 50 mg and norethisterone acetate 1 mg) usage, but who had experienced a chronic biological false positive (BFP) serological test for syphilis for 8 months prior to this. This implies that she had either a lupus diathesis or subclinical SLE which was unmasked by pill therapy rather than a de novo disease caused by this agent. A study of 134 patients with chronic BFP reactions found that 10 developed SLE, 4 developed discoid LE, and 6 developed a multiple sclerosis-like neuropathy probably due to SLE. BFP reaction is found in 10-20% of SLE patients. Other studies have found oral contraceptive therapy to exacerbate existing SLE and to induce serological markers (LE cells, antinuclear antibody, rheumatoid factor). In cases where SLE was exacerbated, the estrogen involved was either mestranol (0.5-1 mg) or ethinyloestradiol (0.5 mg). However, studies of women without symptoms have failed to show a significant association between oral contraceptive therapy, SLE serological markers, and rheumatic complaints. There is considerable evidence that female sex hormones play a role in determining SLE disease activity. There is a constant male:female ratio of 1:9, and the tendency to disease activity increases premenstrually, in pregnancy, and in the postpartum period.