Browsing by Author "Popović, Vera (35451450900)"

Background/Aim. Vitamin D deficiency is a well-established risk factor for bone disease, but emerging data suggest that altered vitamin D homeostasis may play a role in the development of type 2 diabetes mellitus (T2DM), dyslipidemia hypertension, and other cardiovascular diseases (CVD). The aim of this study was to investigate the prevalence of vitamin D deficiency in patients with T2DM with/without CVD, to correlate it with anthropometric and metabolic parameters and to determine the predictors of vitamin D deficiency. Methods. A total of 88 patients with T2DM (49 male/39 female, aged 61.0 ± 0.9 yrs, body mass index (BMI) 29.9 ± 0.4 kg/m2) and 67 patients (44 male/23 female, aged 63.6 ± 1.0 yrs, BMI 29.2 ± 0.5 kg/m2) with T2DM and CVD (myocardial infarction in 57 patients and angina pectoris in 10 patients) were included in this study. These patients were compared with 87 healthy subjects (35 male/52 female, aged 52.8 ± 1.4 yrs, BMI 27.2 ± 0.5 kg/m2). Weight, height, waist circumference and BMI were recorded in all patients. Also, total cholesterol, triglycerides, hemoglobin A1c (HbA1c) and 25-hydroxy-vitamin D [25(OH)D] levels were measured in all. According to 25(OH)D level, all subjects were divided into three categories: severe vitamin D deficiency (≤ 15 ng/mL), vitamin D insufficiency (15-20 ng/mL) and vitamin D sufficiency (20 ng/mL). We correlated vitamin D levels with anthropometric and metabolic status and determined the predictors of vitamin D deficiency. Results. Severe vitamin D deficiency was registered in 16.1% healthy subjects, in 21.6% patients with T2DM and in 26.9% patients with T2DM and CVD. Patients with T2DM who were vitamin D deficient had increased weight, waist circumference, cholesterol and triglyceride levels when compared with patients with T2DM who had sufficient vitamin D level. 25(OH)D levels correlated with BMI and waist circumference in all subjects, but did not correlate with metabolic parameters (lipids, HbA1c). The best predictors of vitamin D level in all subjects were weight, waist circumference and BMI. Conclusion. The high prevalence of vitamin D deficiency in patients with T2DM and particularly in patients with T2DM and CVD suggests that supplementation with vitamin D may be beneficial although there is still not sufficient evidence for recommending prescribing vitamin D.

Background/Aims: Exaggerated adrenocorticotropic hormone (ACTH) and cortisol responses to ghrelin in Cushing's disease (CD) have previously been reported, similarly to responses to corticotropin-releasing hormone (CRH). We assessed the ability of ghrelin to enhance ACTH and cortisol responses when added to CRH stimulation in CD patients. Methods: In 21 CD patients (18 females, 3 males; age 49.8 ± 10.2 years; BMI 29.8 ± 0.8) and 8 healthy subjects (7 females, 1 male; age 40.6 ± 5.3 years; BMI 29.9 ± 1.2), we administered (1) ghrelin 100 μg i.v. bolus, (2) CRH 100 μg i.v. bolus, and (3) ghrelin + CRH combination. ACTH and cortisol were analyzed by commercially available kits from samples taken at 0, 15, 30, 45, 60, 90 and 120 min. ACTH and cortisol responses were calculated as peak and area under the curve (AUC0-120 min). Results: ACTH and cortisol at baseline and stimulated with ghrelin and/or CRH (peak and AUC0-120 min) were significantly higher in CD patients compared to controls (p < 0.01). ACTH and cortisol responses to ghrelin or CRH were similar in CD patients. Combined ghrelin + CRH administration in CD patients produced the highest ACTH response (peak and AUC0-120 min) compared to ghrelin or CRH alone (p < 0.01). Cortisol responses after ghrelin + CRH were uncoupled with ACTH responses and similar to the response to ghrelin or CRH alone in both groups. ACTH and cortisol responses, during all three tests, were similar in CD patients with micro- or macroadenomas. Conclusion: Ghrelin administration causes exaggerated ACTH and cortisol responses in CD patients compared to healthy controls. In combination with CRH, it additionally enhances ACTH secretion without further additive effect on cortisol output. © 2016 S. Karger AG, Basel.

Background/Aims: Exaggerated adrenocorticotropic hormone (ACTH) and cortisol responses to ghrelin in Cushing's disease (CD) have previously been reported, similarly to responses to corticotropin-releasing hormone (CRH). We assessed the ability of ghrelin to enhance ACTH and cortisol responses when added to CRH stimulation in CD patients. Methods: In 21 CD patients (18 females, 3 males; age 49.8 ± 10.2 years; BMI 29.8 ± 0.8) and 8 healthy subjects (7 females, 1 male; age 40.6 ± 5.3 years; BMI 29.9 ± 1.2), we administered (1) ghrelin 100 μg i.v. bolus, (2) CRH 100 μg i.v. bolus, and (3) ghrelin + CRH combination. ACTH and cortisol were analyzed by commercially available kits from samples taken at 0, 15, 30, 45, 60, 90 and 120 min. ACTH and cortisol responses were calculated as peak and area under the curve (AUC0-120 min). Results: ACTH and cortisol at baseline and stimulated with ghrelin and/or CRH (peak and AUC0-120 min) were significantly higher in CD patients compared to controls (p < 0.01). ACTH and cortisol responses to ghrelin or CRH were similar in CD patients. Combined ghrelin + CRH administration in CD patients produced the highest ACTH response (peak and AUC0-120 min) compared to ghrelin or CRH alone (p < 0.01). Cortisol responses after ghrelin + CRH were uncoupled with ACTH responses and similar to the response to ghrelin or CRH alone in both groups. ACTH and cortisol responses, during all three tests, were similar in CD patients with micro- or macroadenomas. Conclusion: Ghrelin administration causes exaggerated ACTH and cortisol responses in CD patients compared to healthy controls. In combination with CRH, it additionally enhances ACTH secretion without further additive effect on cortisol output. © 2016 S. Karger AG, Basel.

GH secretion after growth hormone-releasing hormone (GHRH), growth hormone releasing peptide-6 (GHRP-6) and after combined administration of both peptides was studied in a patient with lactotrope and thyrotrope hyperplasia due to primary hypothyroidism. Pituitary pseudotumor disappeared after thyroid hormone replacement; this was evidenced by magnetic resonance imaging (NMR). There was no difference between areas under the curve (AUC(0-120min)) during GHRH test before and after thyroid hormone replacement (136.5 vs 129.0 μg/l min). Maximal GH increases over basal values (ΔGH) did not change (1.5 and 1.9 μg/l) GH secretion induced by GHRP-6 increased after treatment (AUC(0-120min) 197.2 vs 650.4 μg/l min). ΔGH increments were 4.0 and 18.3 μg/l before and after therapy respectively, When the peptides were administered together a synergistic effect on GH secretion was observed but GH release was much more powerful after pituitary pseudotumor disappearance (AUC(0-120min) 1043.2 vs 2046.7 μg/l min). This was accompanied by increased ΔGH (22.7 vs 35.5 μg/l). The synergic action of peptides normalized in euthyroid condition and after the resolution of pituitary pseudotumor mainly due to improved GB[ response to GHRP-6. Blunted response of GH to GHRP-6 and GHRP-6 plus GHRH were in part due to known effects of hypothyroidism on GH secretion. Hypothalamopituitary disconnection and/or decrease in the synthesis of an unknown factor in the hypothalamus which mediates the effects of GHRP-6 may have participated in the GH responsiveness of this patient, This case adds to in vivo evidence that GHRP-6 operates through a non-GHRH dependent mechanism.

GH secretion after growth hormone-releasing hormone (GHRH), growth hormone releasing peptide-6 (GHRP-6) and after combined administration of both peptides was studied in a patient with lactotrope and thyrotrope hyperplasia due to primary hypothyroidism. Pituitary pseudotumor disappeared after thyroid hormone replacement; this was evidenced by magnetic resonance imaging (NMR). There was no difference between areas under the curve (AUC(0-120min)) during GHRH test before and after thyroid hormone replacement (136.5 vs 129.0 μg/l min). Maximal GH increases over basal values (ΔGH) did not change (1.5 and 1.9 μg/l) GH secretion induced by GHRP-6 increased after treatment (AUC(0-120min) 197.2 vs 650.4 μg/l min). ΔGH increments were 4.0 and 18.3 μg/l before and after therapy respectively, When the peptides were administered together a synergistic effect on GH secretion was observed but GH release was much more powerful after pituitary pseudotumor disappearance (AUC(0-120min) 1043.2 vs 2046.7 μg/l min). This was accompanied by increased ΔGH (22.7 vs 35.5 μg/l). The synergic action of peptides normalized in euthyroid condition and after the resolution of pituitary pseudotumor mainly due to improved GB[ response to GHRP-6. Blunted response of GH to GHRP-6 and GHRP-6 plus GHRH were in part due to known effects of hypothyroidism on GH secretion. Hypothalamopituitary disconnection and/or decrease in the synthesis of an unknown factor in the hypothalamus which mediates the effects of GHRP-6 may have participated in the GH responsiveness of this patient, This case adds to in vivo evidence that GHRP-6 operates through a non-GHRH dependent mechanism.

Introduction Currently there is little information on the effects of prolactin (PRL) on the coagulation and fibrinolytic systems. Objective The aim of this study was to evaluate the effects of hypeprolactinemia on the parameters of the hemostatic system and activation of the coagulation system. Methods We studied PRL levels, body mass index (BMI), values of activated partial thromboplastin time (aPTT), prothrombin time (PT), thrombin time (TT), D-dimer level, von Willebrand factor antigen (vWFAg) and fibrinogen in 15 young female patients with microprolactinomas before and after therapy and in 15 healthy female controls. Results As expected, pretreatment PRL levels were significantly higher in patients than in controls (140.90±42.87 vs. 12.53±4.05 ng/ml; p<0.001). PT, although still in the normal range, was prolonged in patients with hyperprolactinemia as compared to the control group (13.53±1.39 vs. 12.65±0.53 s; p=0.03) and normalized after therapy (12.69±0.65 vs. 12.65±0.53 s; p=0.88). TT, although in normal range, was significantly shorter in the hypeprolactinemic patients than in the controls (14.34±4.52 vs. 17.21 ±1.35 s; p<0.025) and after treatment remained significantly shorter than in the controls (15.17±1.55 vs. 17.21±1.35 s; p<0.0001). D-dimer values before treatment in the patients with hyperproplactinemia were above the normal range (239.47±107.93 vs. 131.27±50.64 ng/ml, p=0.002) and decreased to normal values after therapy (239.47±107.93 vs. 146.60±39.15 ng/ml; p<0.001). D-dimer levels correlated with PRL (r=0.30) and the change in serum D-dimer values significantly correlated with the change in PRL levels during therapy (r=0.62). aPTT, vWFAg and fibrinogen were similar in patients and controls. Conclusion In our study, increased thrombin generation that resulted in elevated D-dimer levels may be one of the contributing factors to the prethrombotic state in patients with hyperprolactinemia. © 2014, Serbia Medical Society. All rights reserved.