Effects of Prolactin on Autoantibody Titer and Differentiation of B lymphocyte Subsets in Patient with Hyperprolactinemia

Abstract Background: Hyperprolactinemia, marked by elevated serum prolactin levels, can result from pituitary adenomas, medications, or secondary causes like chronic kidney disease. In addition, it occurs physiologically during pregnancy and lactation. Prolactin, a multifunctional hormone, enhances antibody production and immune response by inhibiting the negative selection of autoreactive B-lymphocytes. It is implicated in the pathogenesis of autoimmune disorders such as systemic lupus erythematosus, rheumatoid arthritis, and Sjögren’s syndrome. Prolactin’s immunostimulatory effects are mediated through receptors on immune cells like T- and B-lymphocytes and macrophages. Investigating alterations in autoimmune markers in hyperprolactinemia patients without autoimmune symptoms is crucial for understanding its broader implications in autoimmunity. Materials and Methods: In this single-center, cross-sectional observational study, we have investigated B10 lymphocyte subsets in 30 patients with hyperprolactinemia and 24 controls. Included patients of age between 18 to 45 years and females with prolactin levels >50 ng/ml (treatment-naïve patients, not on dopamine agonists). Clinical variables included menstrual and drug history, and anthropometric measurements. Laboratory tests include a complete hemogram, liver and renal function tests, fasting and postprandial blood sugar, and endocrine markers (serum prolactin, thyroid function tests, and autoantibodies). Flow cytometry analyzed B-lymphocyte subsets, including CD-19 and CD-20 subpopulations. The exclusion Criteria includes Renal failure, Liver failure, Hypothyroidism, Chronic inflammatory diseases, Autoimmune disease, Lactating or using oral contraceptive, pregnant, menopausal, Diabetes mellitus, On medications such as dopamine agonist(e.g. cabergoline), and patients who are on steroids or immunosuppressant. Clinical variables included menstrual history, drug history, and anthropometric measurements. Laboratory tests encompassed a complete hemogram, liver and renal function tests, fasting and postprandial blood sugar, and endocrine markers (serum prolactin, thyroid function tests, and autoantibodies). Flow cytometry analyzed B-lymphocyte subsets, including CD-19 and CD-20 subpopulations. Results and Conclusion: Patients with hyperprolactinemia exhibit significantly lower levels of B-regulatory cells ( P = 0.029), significantly higher levels of plasmablasts ( P = 0.038), and elevated anticardiolipin immunoglobulin G levels ( P = 0.043) compared to those with normal prolactin level. Although the current study subjects did not have clinical autoimmune diseases, the findings suggest that hyperprolactinemia may contribute to the development of autoimmune disorders.