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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Lymphocytic prolactin does not contribute to systemic lupus erythematosus hyperprolactinemia

Author(s):
Paraiba, D. B. [1] ; Soares, C. R. J. [2] ; Bartolini, P. [2] ; Arthuso, F. S. [2] ; Borba, E. F. [3] ; Bonfa, E. [3] ; Bronstein, M. D. [1]
Total Authors: 7
Affiliation:
[1] Univ Sao Paulo, Sch Med, Hosp Clin, Div Endocrinol & Metab, Neuroendocrine Unit, BR-01406100 Sao Paulo - Brazil
[2] IPEN CNEN SP, Dept Biotechnol, Sao Paulo - Brazil
[3] Univ Sao Paulo, Sch Med, Hosp Clin, Div Rheumatol, BR-01406100 Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: CLINICAL AND EXPERIMENTAL RHEUMATOLOGY; v. 28, n. 6, p. 866-872, NOV-DEC 2010.
Web of Science Citations: 8
Abstract

Introduction Lymphocytic prolactin (PRL) gene expression is detected in the majority of the immune cells and it is not known if this source contributes to hyperprolactinemia in systemic lupus erythematosus (SLE). We have therefore evaluated lymphocytic PRL secretion and gene expression in SLE and healthy controls. Methods Thirty SLE patients (ACR criteria) and 10 controls were selected for the study. Serum levels of PRL and macroprolactin were detected by immunofluorometric assay and gel filtration chromatography, respectively. The lymphocytic biological activity was determined by Nb2 cells bioassays. Lymphocytic PRL gene expression was evaluated by RT-PCR assay. Results The median serum PRL levels of the 30 SLE patients was higher than the control group (9.65 (1.9-38.9) vs. 6.40 (2.4-10.3) ng/mL, p=0.03). A significant difference was detected between median serum PRL levels of active SLE, inactive SLE and controls (10.85 (5-38.9) vs. 7.65 (1.9-15.5) vs. 6.40 (2.4-10.3) ng/mL), p=0.01). The higher frequency of mild hyperprolactinemia was detected among active SLE in comparison with inactive SLE and controls (7(38.9%) vs. 1 (8.3%) vs. 0(0%)), with statistical significance (p=0.02). Nb2 cells assay revealed uniformly low levels of lymphocytic PRL in active, inactive and control groups without statistical significance among them (24.2 (8-63) vs. 27 (13.6-82) vs. 29.5 (8-72) ng/mL), p=0.84). Furthermore, median lymphocytic PRL gene expression evaluated by RT-PCR assay was comparable in both active and inactive SLE groups (p=0.12). Conclusion This is the first study to exclude a lymphocytic source of PRL, pointing out a pituitary etiology for hyperprolactinemia in SLE. However, other sources from the immune system cannot be ruled out. (AU)