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.

Expression of prolactin receptors in the duodenum, kidneys and skeletal system during physiological and sulpiride-induced hyperprolactinaemia.

INTRODUCTION AND AIM: Hyperprolactinaemia in pregnancy leads to mild and reversible changes in the maternal skeletal system, and medicamentous hyperprolactinemia causes more detrimental effects. We conducted an experimental study to evaluate differences between Prlr gene expression in the duodenum, vertebrae and kidneys during physiological and medicamentous hyperprolactinaemia, which could influence calcium homeostasis. METHODS: Experimental animals (18 weeks old, Wistar female rats) were divided as follows: group P (nine rats that were 3 weeks pregnant), group M (ten rats that were intramuscularly administrated sulpiride (10 mg/kg) twice daily for 3 weeks), and the control group (C, ten age-matched nulliparous rats, 18-week-old). Laboratory investigations included measurements of serum ionized calcium, phosphorus, urinary calcium and phosphorus excretion, osteocalcin (OC), serum procollagen type 1 N-terminal propeptide (P1NP), vitamin D, parathyroid hormone (PTH) and prolactin (PRL). Relative quantification of gene expression for prolactin receptors in the duodenum, vertebrae and kidneys was determined using real-time PCR. RESULTS: Expression of the Prlr gene was significantly higher in the duodenum (p < 0.001) and lower in vertebrae (p < 0.001) and kidneys (p < 0.01) in rats with physiological hyperprolactinaemia (PHP) than in the control group. Significantly lower Prlr expression in the duodenum was verified (p < 0.001), along with increased Prlr gene expression in vertebrae (p < 0.001) and kidneys (p < 0.01), in rats with medicamentous hyperprolactinaemia (MHP) than in the C group. CONCLUSIONS: Downregulation of Prlr gene expression in the duodenum may explain the diminished intestinal calcium absorption in medicamentous hyperprolactinaemia. Prolactin takes calcium from the skeletal system following increased Prlr gene expression in the vertebrae to maintain calcium homeostasis, which increases the harmful effect on bone metabolism compared to that of physiological hyperprolactinaemia.

Localised Langerhans cell histiocytosis of the hypothalamic-pituitary region: case report and literature review.

INTRODUCTION: Langerhans cell histiocytosis (LCH) localised in the hypothalamic-pituitary region (HPR) is very rare, especially in adults. Diabetes insipidus (DI) is considered to be a hallmark of HPR LCH, while anterior pituitary abnormalities are usually seen as consequences of surgery, radiotherapy or chemotherapy. CASE DESCRIPTION: We present a patient with localised HPR LCH with dominant anterior pituitary dysfunction and tumour mass effects but without DI. Seven years after surgery and local radiotherapy, she is stable. Control MRI shows no residual tumour growth and thorough physical examination is still without any signs of disease spread. CONCLUSIONS: Anterior pituitary deficiency can appear without DI and not only as a consequence of LCH treatment. All patients with LCH should be screened for this endocrine abnormality so that appropriate substitution therapy may be provided.

Role of D-dimer in predicting mortality in patients with community-acquired pneumonia.

AIM: To determine whether D-dimer in patients with communityacquired pneumonia (CAP) can predict mortality risk better than standard biomarkers. METHODS: White blood cell (WBC), C-reactive protein (CRP) and D-dimer in 129 patients with CAP were analyzed. The recommended Pneumonia Severity Index (PSI) score was used to classify CAP patients into five groups according to the severity of disease (Group PSI I-V), and for predicting mortality. Additionally, the patients were divided in surviving and non-surviving group. RESULTS: White blood cell and CRP were not in correlation with the severity of CAP and the risk of mortality. The correlation between plasma D-dimer and severity of CAP was found (r=0.4993; p less than 0.001). The level of D-dimer was significantly higher in nonsurviving (2498.38 ± 1248.83 ng/mL) than in surviving patients (966.44 ± 968.73 ng/mL) (p less than 0.001). In predicting mortality risk, D-dimer showed sensitivity of 0.84 (cut of >1538 mg/mL), specificity 0.86 and AUC 0.859 (95%CI; 0.787-0.914). Pneumonia Severity Index in predicting of mortality risk for cut of > PSI III showed sensitivity of 0.92, specificity 0.62 and AUC 0.868 (95%CI; 0.797-0.921). There was no statistical difference between AUC of PSI and D-dimer (delta AUC= 0.00895) (p=0.9005). CONCLUSION: Coagulation abnormalities were presented in older patients with severe infections and comorbidity. Plasma D-dimer correlated better than standard inflammatory markers with severity of disease and risk of mortality in patients with CAP. In predicting mortality risk, D-dimer did not show difference among the PSI score.

[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.

Difficulties in establishing a timely diagnosis of pulmonary artery sarcoma misdiagnosed as chronic thrombo-embolic pulmonary disease: a case report.

INTRODUCTION: Pulmonary artery sarcomas are rare neoplasms that are often confused with chronic thrombo-embolic disease, as both can have similar clinical and imaging presentation. CASE PRESENTATION: In this report, we present a case of a 50-year-old man initially diagnosed with chronic thrombo-embolic pulmonary disease, but who was later found to have pulmonary artery sarcoma with poor survival prognosis. We review the clinical and imaging characteristics of the two diseases and discuss the difficulties in establishing a timely diagnosis. CONCLUSION: Similar clinical features and imaging presentation of pulmonary artery sarcoma and chronic thrombo-embolic pulmonary disease make definitive diagnosis difficult. This case report also illustrates and emphasizes that in any case with no predisposition factors for embolism, no evidence of deep venous thrombosis and pulmonary emboli, and inadequate relief of symptoms with anticoagulation, an alternative diagnosis of pulmonary artery sarcoma should be considered. If pulmonary artery sarcoma is diagnosed late in the course of the disease, there is usually a poor survival outcome.

Diagnostic value of CEA in pleural fluid for differential diagnosis of benign and malign pleural effusion.

UNLABELLED: The diagnostic value of tumor markers in pleural fluid is still the subject of debate. The aim of this work was to evaluate diagnostic value of carcinoembryonic antigen (CEA) in pleural fluid for differentiating malignant from non malign pleural effusion, and their additive value to cytological examination. DESIGN: Prospective, case control study. SETTING: Tertiary University hospital, Clinic for Lung Disease, Knez Selo. PATIENTS: Eighty two patients with pleural effusion, forty one with malignant, and forty one with non malignant pleural effusion. MEASUREMENTS AND RESULTS: Levels of CEA in pleural fluid was measured by IRMA CEA methods, INEP Belgrade. Patients with lung cancer were found to have significantly higher CEA levels than patients with non malign pleural effusion. Using cut off values of 2.4 ng/ml, the sensitivity of marker was 78%, and specificity 95.1% (CI 95%). The addition of CEA to cytology increase diagnostic rate from 68 to 85.3%. CONCLUSION: CEA may represent a helpful adjunct to cytology in order to include malignancy as probable diagnosis, thus guiding the selection of patients for more invasive procedures.