Abstract
Prolactin, a peptide hormone, acts as a cytokine. It has been hypothesized that bromocriptine, a dopamine analog that suppresses pituitary secretion of prolactin, suppresses circulating prolactin and, through this mechanism, has the potential to suppress autoimmune disease. This rationale has been applied to the treatment of systemic lupus erythematosus (SLE), a prototype autoimmune illness that occurs spontaneously in animal models such as the F1 hybrid NZBxNZW mouse, and in humans. Treatment with bromocriptine was effective in treating some induced and spontaneous autoimmune disease in experimental models. Bromocriptine did slow the course of SLE in NZBxNZW mice when treatment was started before the appearance of clinical disease. In addition, bromocriptine was effective in treating established disease in this model. In three separate clinical trials, bromocriptine showed evidence that it had a therapeutic effect in treating human lupus. Bromocriptine is currently considered an unproven therapy for SLE. Its use is entirely experimental. The fact that bromocriptine was effective in treating NZBxNZW mice, the beneficial therapeutic effects in human trials, and the low toxicity of the drug form a solid rationale for undertaking further therapeutic trials.
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