Significance of Duodenal Prolactin Receptor Modulation by Calcium and Vitamin D in Sulpiride-Induced Hyperprolactinemia.

Background and Objectives: Hyperprolactinemia, as a potential side-effect of some antipsychotic medications, is associated with decreased bone density and an increased risk of fractures. This study investigates whether calcium and vitamin D supplementation affects prolactin receptor (Prlr) gene expression in the duodenum, vertebrae, and kidneys of female rats with sulpiride-induced hyperprolactinemia. Materials and Methods: Twenty-one-week-old female Wistar rats were assigned to three groups: Group S consisted of ten rats who received sulpiride injections (10 mg/kg) twice daily for 6 weeks; Group D (10 rats) received daily supplementation of 50 mg calcium and 500 IU vitamin D along with sulpiride for the last 3 weeks; and Group C consisting of seven age-matched nulliparous rats serving as a control group. Real-time PCR was used to assess Prlr gene expression in the duodenum, vertebrae, and kidneys. Results: In Group S, Prlr gene expression was notably decreased in the duodenum (p < 0.01) but elevated in the vertebrae and kidneys compared to Group C. Conversely, Group D exhibited significantly increased Prlr expression in the duodenum (p < 0.01) alongside elevated expression in the vertebrae and kidneys. Conclusions: In sulpiride-induced hyperprolactinemia, decreased Prlr gene expression in the duodenum may lead to reduced intestinal calcium absorption. Consequently, prolactin may draw calcium from the skeletal system to maintain calcium balance, facilitated by increased Prlr gene expression in the vertebrae. However, vitamin D supplementation in sulpiride-induced hyperprolactinemia notably enhances Prlr gene expression in the duodenum, potentially ameliorating intestinal calcium absorption and mitigating adverse effects on bone health.

[Significance of hyperprolactinemia for cytomorphologic features of breast secretions].

BACKGROUND/AIM: Nipple discharge syndrome is a clinical entity capable of presenting various disorders such is mammary infection (nonpuerperal and puerperal mastitis), intraductal papillomas, fibrodenoma, breast cancer and hyperprolactinemia syndrome. The aim of the study was to determine differences in cytological features of mammary secretion in patients with hyperprolactinemia and those with normal serum prolactin levels and to define the role of growth hormone, follicle-stimulating hormone, luteinizing hormone and thyroid-stimulating hormone in creating cellular profile of breast secretion. METHODS: The study included 50 patients with nipple discharge syndrome. The patients were devided into the clinical group (27 patients with hyperprolactinemia and nipple discharge) and the control group I (23 patients with normal serum prolactin and nipple discharge). The control group II included the patients of the clinical group achieving normalised serum prolactin levels after the treatment of hyperprolactinemia. Serum prolactin, follicle-stimulating hormone and luteinizing hormone levels were assessed by RIA using commercial kits IRMA hPRL, hLH and hFSH, (INEP, Zemun, Serbia) while serum growth hormone and thyroid-stimulating hormone levels were assessed by RIA using commercial kits LKB-wallac. Cytologic evaluation of samples, taken from all the patients with mammary secretion, was done using standard techniques of staining Haemathoxilin-eozine and May-Grünwald/Giemsa. RESULTS: Our results showed a significantly higher presence of lipid and protein material in clinical group, in comparison with the control group I (p < 0.01). Also, our data demonstrated significantly higher number of ductal epithelial cells (p < 0.05) and ductal histiocities (p < 0.001) in the clinical group, compared with the control group I. Macrophagies frequency was proportionally higher in clinical group (44.44%) compared the control group I (17.39%). Erythrocites were significantly lower in the clinical group (p < 0.001) than in the control group I. 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. CONCLUSION: Growth hormone, follicle-stimulating hormone, luteinizing hormone and thyroid-stimulating hormone did not show significant influence on creating cytological features of mammary secretion. The most expressive role, hyperprolactinemia demonstrated in the 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 and "foam cells"--macrophages. These cytological findings indicate that hyperprolactinemia promote periductal and intraductal steril inflammation which withdraws after serum prolactin normalization.