Lymphocytic prolactin does not contribute to systemic lupus erythematosus hyperprolactinemia

Autor(es)

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]

Afiliação do(s) autor(es)

^[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

• Tipo de documento: Artigo Científico
• Fonte: CLINICAL AND EXPERIMENTAL RHEUMATOLOGY; v. 28, n. 6, p. 866-872, NOV-DEC 2010.
• Citações Web of Science: 8

Resumo

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)

• Processo FAPESP: 05/51805-2 - Avaliação da prevalência de hiperprolactinemia e estudo da secreção e da atividade biológica da prolactina linfocitária em pacientes com lúpus eritematoso sistêmico (LES) em atividade e remissão de doença
• Beneficiário: Diane Belchior Paraiba
• Linha de fomento: Bolsas no Brasil - Doutorado Direto
• Processo FAPESP: 05/51806-9 - Avaliação in vivo da prevalência das isoformas de prolactina sérica em pacientes com doença autoimune (artrite reumatoide e lúpus eritematoso sistêmico) em atividade e remissão: comparação com a atividade in vitro da prolactina linfocitária em bioensaios com fibroblastos transfectados com receptor de prolactina humano
• Beneficiário: Marcello Delano Bronstein
• Linha de fomento: Auxílio à Pesquisa - Regular