Endocrine Abstracts

Background/aim: This study was conducted to determine hyperprolactinemia significance in starting and maintaining sterile inflammation in breast tissue.

Methods: We observed 50 patients with nipple discharge syndrome. Patients were divided into clinical group (27 patients with hyperprolactinemia and nipple discharge) and first control group (23 patients with normal serum prolactin and nipple discharge). The second control group included patients from clinical group after treatment of hyperprolactinemia and achieving normalized serum prolactin levels. Cytologic evaluation of samples, taken from all patients with mammary secretion, was done using standard staining techniques haemathoxilin–eozine and May-Grünwald/Giemsa.

Results: Our results showed significantly higher presence of lipid and protein material in clinical group in comparison to first control group (P<0.01). Our data also demonstrated significantly higher number of ductal epithelial cells (P<0.05) and ductal histiocities (P<0.001) in clinical group patients compared to first control group. Inflammatory cells frequency was similar in clinical (22.22%) and first control group (26.09%), but completely withdrawn in second control group. Macrophagies frequency was proportionally higher in clinical group (44.44%) compared to first control group (17.39%). Erythrocites were significantly lower in the clinical group patients (P<0.001) than in the first control group. Significantly decreased mammary secretion (P<0.01), lower lipid (P<0.01) and protein synthesis (P<0.01) and less presence of all cellular categories (P<0.01) were obtained after normalization of serum prolactin levels. Bacteriological analysis of mammary secretion revealed pathogens bacteria only in two clinical group patients.

Conclusion: The most expressive role hyperprolactinemia demonstrated in domain of mammary ductal secretory activity, making mammary secretion reach in lipid and protein material and simultaneously increasing number of ductal epithelial cells, ductal histiocytes, inflammatory cells and ‘foam cells’-macrophages. This cytological findings indicate that hyperprolactinemia promote periductal and intraductal sterile inflammation which is withdrawing after serum prolactin normalization.