Elevated bioactive prolactin levels in systemic lupus erythematosus--association with disease activity

• Published in: Journal of rheumatology Vol. 28; no. 10; p. 2216
• Main Authors: Pacilio, M, Migliaresi, S, Meli, R, Ambrosone, L, Bigliardo, B, Di Carlo, R
• Format: Journal Article
• Language: English
• Published: Canada 01.10.2001
• Subjects: Adolescent; Adult; Aged; Animals; Biological Assay; Female; Humans; Hyperprolactinemia - blood; Hyperprolactinemia - epidemiology; Hyperprolactinemia - immunology; Immunoradiometric Assay; Lupus Erythematosus, Systemic - blood; Lupus Erythematosus, Systemic - epidemiology; Lupus Erythematosus, Systemic - immunology; Lymphoma; Male; Middle Aged; Prevalence; Prolactin - blood; Prolactin - immunology; Rats; Severity of Illness Index; Tumor Cells, Cultured
• ISSN: 0315-162X

To assess the possibility that prolactin (PRL) is involved in the pathogenesis of systemic lupus erythematosus (SLE). We determined serum PRL levels in 122 serum samples from 78 unselected patients with SLE (73 women, 5 men, age range 16-71 yrs). Disease activity was defined according to Lupus Activity Criteria Count (LACC) and scored by Systemic Lupus Disease Activity Index (SLEDAI). Serum PRL concentrations were determined by immunoradiometric assay (IRMA) and by biological assay (BA) that evaluates Nb2 lymphoma cell proliferation. Hyperprolactinemia (> 20 ng/ml) was found in 21 patients (26.9%) by IRMA and in 31 (39.7%) by BA. A significant correlation between IRMA and BA PRL levels was found (rs 0.46, p < 0.001). According to LACC, SLE was active in 29 patients and inactive in 49. In those with active disease median PRL levels were higher both by IRMA (18.5 ng/ml, range 2.2-51.2 vs 10.6 ng/ml, range 3.9-29.6; p < 0.001) and BA (21.0 ng/ml, range 12.4-84 vs 14.9 ng/ml, range 4.2-46.1; p < 0.001). Hyperprolactinemia was associated with active disease in 13/21 patients (61.9%) by IRMA and in 18/31 (58.1%) by BA (p < 0.01). SLEDAI scores correlated with PRL levels both by IRMA (rs 0.5, p < 0.001) and BA (rs 0.41, p < 0.02). A followup analysis on serum samples from 44 patients seen again after 6-8 mo confirmed the above results. There was no difference in the rate of different clinical manifestations in hyperprolactinemic and normoprolactinemic subjects, apart from the increased prevalence of malar rash and central nervous system manifestations in the patients with hyperprolactinemia (p < 0.03 and p < 0.01, respectively). Hyperprolactinemia was frequently detected in patients with SLE by IRMA and by BA and was associated with disease activity. Our findings suggest that PRL may play a role in the pathogenesis of SLE.