ACTA ENDOCRINOLOGICA (BUC)

Objective. We hypothesized that vitamin D-deficient diabetic patients might demonstrate cognitive deficits and therefore investigated this association in patients with diabetes mellitus (DM). Methods. This study comprised 236 patients with type 2 DM (118 with vitamin D deficiency (less than 20 ng/ mL) and 118 without vitamin D deficiency as the control group). All patients were outpatients in the endocrinology clinics of Baskent University, Turkey from 1 October 2013 to 31 January 2014 and, chosen in a randomized manner according to their application time. The serum vitamin D levels were measured and cognitive functions were evaluated using the Mini Mental Status Examination (MMSE). Results. The mean age in the study and control group was 57.02±7.30 and 58.92±7.58 years, respectively (p=0.051). The male:female ratio in the study and control group was 1.00:1.46 and 1.00:2.11, respectively. The study group was further divided into three subgroups: patients with mild, moderate, and severe vitamin D deficiency. The study outcomes revealed no significant relationship between the vitamin D deficiency level and the total score or subscores of the MMSE (p<0.05). Conclusions. These study results do not confirm the hypothesis that vitamin D deficiency unfavorably affects cognitive functions in patients with type 2 DM.

Parathyroid cysts are a rare medical condition, that is why they represent a diagnostic and therapeutic challenge for the practitioner. We report a case of nonfunctional symptomatic parathyroid cyst in a 36-year old woman revealed by an anterior cervical swelling. There was a high concentration of parathormone (PTH) within the cyst fluid extracted before surgery (PTH 426 pg/mL).

Pituitary adenomas are fully characterized only by immunohistochemistry. The technical limitations, gaps and peculiarities influence the pathology diagnosis. More and more data shows that clinically nonfunctioning pituitary adenomas could synthesize or secrete hormones or their subunits. The tumor pathology is monomorphous or polymorphous, difficult to differentiate from normal adjacent tissue. Light microscopy (LM) qualitative analysis using basic or special stains can differentiate between tumor and normal tissue and allows elimination of artifacts. Electron microscopy (EM) completes the diagnosis in selected cases. Pituitary adenomas immunohistochemistry was done by LM in 120 cases (84 ? clinically nonfunctioning adenomas ? NFA and 36 acromegalics with or without PRL secreting adenomas - ACM) using the avidine-biotin complex method. In 26 cases we determined by EM the immunoreactive cells (17 NFA and 9 ACM) using the immunogold method. We observed high tumor immunoreactivity (mono or plurihormonal) in 43/84 (51%) NFA, 13/36 (36%) ACM respectively. Serum excess hormones and tissue immunoreactivity were significantly concordant for prolactin in NFA cases and for GH, in ACM cases (p<0.05). Mute pituitary adenomas have no clinical expression of hormonal products either they produce biologically inactive components or they synthesize but do not secrete hormones in sufficient amounts to increase serum level and to determine a systemic response. A concordance between LM and EM immunoreactivity was observed only for GH in ACM patients group (p<0.05). The differences could be due to dimensions of the samples or the number of granules inside of the cells (sparsely granulated adenomas are negative or low immunoreactive at the LM level). EM evaluation of NFA identified 2 oncocytomas and 4 null cell adenomas. The complete evaluation of pituitary adenomas includ a qualitative and quantitative analysis at the LM level using special methods, validated at the EM level in order to identify clinically mute immunoreactive cells ? a possible target for specific drugs therapies in the future.

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Objective. Osteoporosis is a complex disease and its development is influenced by genetic, epigenetic, metabolic, and environmental factors. However, specific genetic factors associated with osteoporosis are not fully understood. The aim of this study was to identify genetic risk factors for osteoporosis. Methods. This study included 86 females with osteoporosis and 47 healthy females. We analyzed rs1800587, rs16944, rs1799814, rs4988321, rs2228570, and rs35211496 variations in IL1A, IL1B, CYP1A1, LRP5, VDR, and RANK, respectively, using polymerase chain reaction-restriction fragment length polymorphism (PCRRFLP) analysis. Results. Our analysis revealed that the CT and TT genotype for rs1800587 in IL1A was associated with higher bone mineral density in the lumbar spine, trochanter, Ward's triangle, and femoral neck (p=0.020, p=0.021, p=0.015, and p=0.013, respectively). The rs1800587 variation in IL1A was associated with a reduced risk of osteoporosis in both dominant and codominant inheritance models (CC vs. CT, p=0.016 and CC vs. CT/TT, p=0.035, respectively). However, we did not identify any statistically significant differences in either genotype or allele frequencies between the control group and the patients with osteoporosis for the other genetic variations examined. Conclusion. Our findings suggest that the rs1800587 variation in IL1A gene is associated with a significantly decreased risk of osteoporosis in the Turkish population.

Background. Arecoline, a plant alkaloid of betel nut, is consumed by millions of people, for increased capacity of work. It causes immunosuppression, hepatotoxicity, and disturbance in antioxidant production, but it stimulates HPA axis and induces thyroid dysfunction.\r\nAim. To investigate the role of arecoline on adrenal activity, glycemia and glycogen profile in mice.\r\nMaterials and methods. Arecoline was injected intraperitoneally at a dose of 10 mg/kg body wt for 20-60 min for acute administration. In chronic administration the same dose was used daily for 15 days. Corticosterone, epinephrine, norepinephrine, blood glucose and liver glycogen profiles were measured after 20, 40 and 60 min, in acute administration and after 15 days in chronic administration.\r\nResults. Arecoline in acute administration increased corticosterone, norepinephrine and epinephrine levels and induced hyperglycemia with depletions of liver glycogen. But\r\nchronic arecoline administration with the same dose for 15 days caused ultrastructural degenerations of adrenal cortex and medulla with the elevation of corticosterone, and\r\ndepletions of norepinephrine and epinephrine levels. Arecoline also caused hypoglycemia and elevated liver glycogen. Atropine (arecoline receptor antagonist) prevented arecoline action on adrenal activity or blood glucose ? liver glycogen interaction.\r\nConclusion. The findings indicate that arecoline initially stimulates adrenal activity, but subsequently inhibits it with alterations of glycemic and glycogen profiles. Arecoline action is mediated by arecoline receptor in mice. Arecoline may have immunological action via adrenal hormonal suppression in mice.

Hypoparathyroidism is a disease characterized by low serum calcium and inappropriate low parathyroid hormone (PTH) levels. Common therapy for chronic hypoparathyroidism usually includes oral calcium and activated vitamin D supplementation (calcitriol), hypoparathyroidism being the one of few endocrine disorders not replaced by the missing hormone. In January 2015, FDA approved PTH (1-84) for the treatment of hypoparathyroidism in patients who cannot be well-controlled on calcium and active forms of vitamin D alone and for whom the potential benefits are considered to outweigh this potential risk. Until now, there are 4 phase 3 clinical trials investigating the role of human recombinant PTH (1-84) for the treatment of hyopoparathyroidism: Replace, Race, Relay, and Repeat. These studies demonstrated a more than 50% reduction in calcium and active vitamin D requirements. Future strategies for the treatment of hypoparathyroidism could be stem cell therapy recombinant with PTH and viral or nonviral factors or parathyroid gland transplantation.

Introduction. Genetic disorders associated with the development of the pituitary gland and cranial bones may cause a genetic tendency toward Sheehan’s syndrome (SS). Our aim in this study was to investigate expression disorders in the genes responsible for the development of the pituitary gland and cranial bones in patients with SS. Materials and Methods. Forty-four patients who were previously diagnosed with SS and 43 healthy women were compared in terms of the mean expression values of genes including the prophet of PIT-1 (PROP1), HESX homeobox 1 (HESX1), POU class 1 homeobox 1 (POU1F1), LIM homeobox 3 (LHX3), LHX4, glioma-associated oncogene homolog 2 (GLI2), orthodenticle homeobox 2 (OTX2), SIX homeobox 3 (SIX3), SIX6, T-box transcription factor 19 (TBX19), transducin-like enhancer protein 1 (TLE1), TLE3, distal-less homeobox 2 (DLX2), DLX5, MSH homeobox 2 (MSX2), and paired box 3 (PAX3). Results. The mean expression values of the HESX1, TLE1, TLE3, and MSX2 genes were significantly different in the SS group from the healthy control group, while the mean expression values of the remaining genes were similar. Conclusion. The present study concludes that abnormal expressions of HESX1, TLE1, TLE3, and MSX2 genes may cause a genetic predisposition to the development of SS.