This material is based upon work supported by the Office of Research and Development, Medical Research Service, Department of Veterans Affairs; the Department of Internal Medicine, University of Missouri, Columbia, Missouri; the Lupus Foundation of America, the Kansas City, Kansas and Charlotte, North Carolina chapters of the Lupus Foundation of America; and the Missouri Agricultural Experimental Station Project MO-137.
Effects of Prolactin in Stimulating Disease Activity in Systemic Lupus Erythematosusa
Version of Record online: 7 FEB 2006
Annals of the New York Academy of Sciences
Volume 840, NEUROIMMUNOMODULATION: MOLECULAR ASPECTS, INTEGRATIVE SYSTEMS, AND CLINICAL ADVANCES pages 762–772, May 1998
How to Cite
WALKER, S. E., MCMURRAY, R. W., HOURI, J. M., ALLEN, S. H., KEISLER, D., SHARP, G. C. and SCHLECHTE, J. A. (1998), Effects of Prolactin in Stimulating Disease Activity in Systemic Lupus Erythematosus. Annals of the New York Academy of Sciences, 840: 762–772. doi: 10.1111/j.1749-6632.1998.tb09615.x
- Issue online: 7 FEB 2006
- Version of Record online: 7 FEB 2006
Abstract: Systemic lupus erythematosus (SLE), a chronic autoimmune illness, is influenced by hormones. High prolactin concentrations were associated with early death from autoimmune renal disease in NZB/NZW mice, an animal model of severe SLE. NZB/NZW mice that delivered and nursed pups and those that underwent pseudopregnancy had changes in serum IgG and autoantibodies. NZB/NZW mice treated with the prolactin-suppressing drug bromocriptine had prolonged lives. Elevated serum prolactin concentrations are reported in SLE patients of both sexes. We found four women with long-standing hyperprolactinemia who developed SLE. A survey of premenopausal women whose sera were submitted for autoantibody testing showed that 20% with anti-ds-DNA antibodies also had high prolactin levels. Many hyperprolactinemic patients whose sera were referred to an endocrinology laboratory had positive FANA tests (women 33%, men 53%) but did not have SLE. Disease activity was suppressed in six of seven SLE patients treated with bromocriptine. All had elevated disease activity and five became unexpectedly hyperprolactinemic after treatment stopped. Manipulating serum prolactin affords a means of treating clinical SLE activity.