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  • Title: Correlation of prolactin serum concentrations with clinical activity and remission in patients with systemic lupus erythematosus. Effect of conventional treatment.
    Author: Vera-Lastra O, Mendez C, Jara LJ, Cisneros M, Medina G, Ariza R, Espinoza LR.
    Journal: J Rheumatol; 2003 Oct; 30(10):2140-6. PubMed ID: 14528507.
    Abstract:
    OBJECTIVE: The role of prolactin (PRL) in the pathogenesis of systemic lupus erythematosus (SLE) is controversial. The effect of conventional treatment (steroids, antimalarials, immunosuppressor drugs) on PRL concentrations is unclear. We investigated correlation of PRL levels with lupus activity in patients at entry and after 6 months of conventional treatment. METHODS: We studied 43 female patients with active SLE, who were divided in 2 groups; Group 1: 16 patients with minor organ involvement (cutaneous and articular involvement), and Group 2: 27 patients with major organ involvement (glomerulonephritis). Controls were 36 healthy individuals. PRL levels were determined by an immunoradiometric assay at entry and after 6 months of treatment. PRL levels were correlated with SLE Disease Activity Index (SLEDAI) score. RESULTS: Mild hyperprolactinemia (HPRL, 20-40 ng/ml) was found in 30/43 (69.7%) SLE patients. After 6 months of treatment a reduction in PRL levels was found in both groups: Group 1: 24.3 +/- 10.8 to 16.96 +/- 10.87 ng/ml (p < 0.001); and Group 2: 23.6 +/- 5.7 to 12.07 +/- 11.13 ng/ml (p < 0.001). The SLEDAI score also decreased after treatment: Group 1: 16.5 +/- 5.9 to 2.1 +/- 1.3 (p < 0.001); Group 2: 16.8 +/- 5.4 to 1.6 +/- 1.4 (p < 0.001). At entry and after treatment, a significant correlation between PRL levels and SLEDAI score was found in all patients (r = 0.4946, p = 0.0007, and r = 0.9086, p = 0.0001, respectively). CONCLUSION: HPRL was associated with SLE disease activity. Conventional immunosuppressive therapy decreased PRL levels in direct correlation with decreased SLE activity. This finding emphasizes that PRL may play a role in the pathogenesis and clinical expression of SLE.
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