title: Elevated serum prolactin or elevated prolactin/cortisol ratio are associated with autoimmune processes in systemic lupus erythematosus and other connective tissue diseases.
abstract: OBJECTIVE
  . We investigated whether serum prolactin (Prl) alone or an increased Prl/cortisol ratio correlated with the autoimmune processes in systemic lupus erythematosus (SLE) and other connective tissue diseases (CTD).
  
  
  METHODS
  Serum Prl, cortisol, cytokines, and autoantibodies were measured in 29 patients with SLE and 29 patients with other CTD by ELISA. The patients were clinically assessed.
  
  
  RESULTS
  Serum Prl was elevated in both SLE (p < 0.05) and other CTD (p < 0.01). Some patients with SLE had reduced serum cortisol levels. In SLE only, the Prl and cortisol levels were correlated (p <0.05), suggesting a parallel activation of the different neuroendocrine pathways. Both groups of patients showed significantly increased Prl/cortisol ratios (p < 0.01 in SLE and p < 0.05 in other CTD). In CTD other than SLE, increased tumor necrosis factor-alpha correlated with the elevated Pri/cortisol ratio (p < 0.05). In SLE, other CTD and control sera, elevated levels of IgG anti-cardiolipin antibody (aCL) were accompanied by increased Prl (0.01 <p < 0.05). In other CTD, the production of IgM aCL and IgG antithyroglobulin was associated with increased levels of either Prl or cortisol, respectively (p < 0.05 for both). In SLE, the production of IgA rheumatoid factor was increased with an elevated Prl/cortisol ratio (p <0.05). Moreover, in SLE only, strongly enhanced synthesis of IgG anti-double stranded DNA, as well as IgG antithyroid microsomal antibodies were accompanied by elevated Prl (p <0.05 for both).
  
  
  CONCLUSIONS
  In SLE and other CTD, increased Prl favored the autoimmune processes, which are reflected by the presence of higher titers of autoantibodies. In many cases, increased PrI was accompanied by elevated cortisol.
authors.affiliation: Department of Rheumatology, University Hospital, Zurich, Switzerland.
authors.forename: M
authors.initials: M
authors.lastname: Neidhart
mesh_terms: D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000097:blood; D000974:Antibodies, Antinuclear / Q000097:blood; D001323:Autoantibodies / Q000097:blood; D004247:DNA / Q000276:immunology; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000276:immunology*; D006966:Hyperprolactinemia / Q000097:blood / Q000276:immunology*; D007030:Hypothalamo-Hypophyseal System / Q000276:immunology; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D007371:Interferon-gamma / Q000097:blood; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000276:immunology; D008875:Middle Aged; D010913:Pituitary-Adrenal System / Q000276:immunology; D012217:Rheumatoid Factor / Q000097:blood / Q000276:immunology; D012795:Sialoglycoproteins / Q000097:blood; D013745:Tetanus Toxoid / Q000276:immunology; D013954:Thyroglobulin / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D017153:Antibodies, Anticardiolipin; D000974:Antibodies, Antinuclear; D001323:Autoantibodies; C507763:IL1RN protein, human; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D012795:Sialoglycoproteins; D013745:Tetanus Toxoid; D014409:Tumor Necrosis Factor-alpha; C056626:thyroid microsomal antibodies; D007371:Interferon-gamma; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D004247:DNA; D012217:Rheumatoid Factor; D013954:Thyroglobulin; D006854:Hydrocortisone