The androgen dehydroepiandrosterone (DHEA) belongs to the group of steroid hormones that are produced by the adrenal cortex. In vitro, T lymphocytes, on exposure with DHEA, have been shown to produce increased amounts of Th1 cytokines such as IFN-y and IL-2, whereas the production of Th2 cytokines such as IL-4 was decreased (Daynes et al. 1990). Moreover, DHEA and DHEA-sulphate serum levels were found to be decreased in patients with SLE unrelated to disease activity or treatment (Jungers et al. 1982). In an animal model of lupus (female NZB/NZW mice), treatment with androgens resulted in an improvement in disease activity. The ability of androgens to promote an immunodeviation toward Th1 as well as their efficacy in lupus mice prompted studies in humans (Melez et al. 1980). Accordingly, patients with lupus nephritis or severe cytopenias were treated with DHEA, 200 mg/d. As a result of this treatment, no difference in SLE disease indices compared with placebo was noted. Only the loss of bone mineral density was lower in DHEA-treated patients (Solsky and Wallace 2002). Three pivotal trials involving nearly 500 patients with mild to moderate disease activity suggest that DHEA (200mg/day) has favorable effects in SLE, including steroid-sparing properties, improvement of bone mineralization, increase in patient visual assessment scores, and a decrease in SLEDAI and SLAM indices (Chang et al. 2000, Mease et al. 2000). Therefore, DHEA is currently being proposed as an adjunct to antimalarials that may be particularly effective in improving cognitive function and fatigue (Ferrario et al. 2000, Hallegua et al. 2000). However, in women, virilization has to be considered as a possible side effect of DHEA therapy.

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