Endocrine regulations最新文献

Cardiovascular diseases (CVD) and thyroid dysfunction are two of the most prevailing disorders in the world that are closely interlinked. Actions of thyroid hormones are mediated via thyroid receptors present in the myocardium and the vascular tissue. Primary mechanism that links thyroid dysfunction with CVD is the modification of cardiovascular risk factors (dyslipidemia, blood pressure, coagulation parameters, etc.) resulting in endothelial and left ventricular systolic and diastolic dysfunction. Both overt and subclinical hyperthyroidism and hypothyroidism may cause adverse alterations in cardiac function. Hyperthyroidism gives rise to palpitation, atrial fibrillation, systolic hypertension, and heart failure, whereas hypothyroidism increases diastolic hypertension, pericardial effusion, and the risk of ischemic heart disease via altering lipid and coagulation parameters. Early recognition and treatment of thyroid dysfunction may prevent adverse cardiovascular events in patients with or without pre-existing CVD. Certain cardiac conditions and medications can cause alterations in thyroid function that may predispose an individual to higher morbidity and mortality. In certain situations, thyroid dysfunction treatment may have cardiovascular benefits. This study deals with the interplay between cardiovascular and thyroid dysfunctions associated with clinical implications and management strategies.

Objective. The present study assessed the impact of type 2 diabetes mellitus (T2DM) duration on the serum asymmetric dimethylarginine (ADMA) and C-reactive protein (CRP) concentration in Bosnian patients. Methods. Participants for this cross-sectional study were randomly selected from the Family Medicine Clinic (Sarajevo, Bosnia and Herzegovina). Serum ADMA concentration was determined by ELISA. Serum high-sensitivity (hs-CRP) was determined by particle-enhanced immunonephelometry. ANOVA test followed by Scheffe post-hoc test or Kruskal-Wallis test followed by Man-Whitney test were used for statistical analysis. Results. The study included 38 patients in up to 10 years diabetes duration (≤10 years T2DM) group, 22 patients in greater than 10 years diabetes duration (>10 years T2DM) group, and 60 controls. Serum ADMA concentration in the >10 years T2DM group (1.81±0.15 μmol/L) was significantly higher compared to serum ADMA concentration in the ≤10 years T2DM group (1.38±0.41 μmol/L; p<0.001) and in controls (0.62±0.15 μmol/L; p<0.001). A significant difference in serum ADMA concentration was found between the <10 years T2DM group and the controls (p<0.001). The serum CRP concentration in the >10 years T2DM group [5.95 (4.20-9.12) mg/L] was significantly higher compared to serum CRP concentration in the <10 years T2DM group [2.35 (1.40-4.30) mg/L; p<0.001] and controls [0.85 (0.50-1.30) mg/L; p<0.001]. Significant difference in serum CRP concentration was observed between the <10 years T2DM group and controls (p<0.001). Conclusions. The present study showed an increase in the serum ADMA and CRP concentrations with the advancement of T2DM. These results suggest that ADMA and CRP may serve as indicators of endothelial dysfunction and chronic low-grade inflammation progression in patients with T2DM. Larger prospective studies are required to confirm the observed findings.

Several cross-sectional trials have revealed increased arterial stiffness connected with the cardiac autonomic neuropathy in types 2 and 1 diabetic patients. The pathophysiological relationship between arterial stiffness and autonomic dysfunction in diabetes mellitus is still underinvestigated and the question whether the presence of cardiac autonomic neuropathy leads to arterial stiffening or increased arterial stiffness induced autonomic nervous system impairment is still open. Both arterial stiffness and dysfunction of the autonomic nervous system have common pathogenetic pathways, counting state of the chronic hyperinsulinemia and hyperglycemia, increased formation of advanced glycation end products, activation of protein kinase C, development of endothelial dysfunction, and chronic low-grade inflammation. Baroreceptor dysfunction is thought to be one of the possible reasons for the arterial wall stiffening development and progression. On the contrary, violated autonomic nervous system function can affect the vascular tone and by this way alter the large arteries walls elastic properties. Another possible mechanism of attachment and/or development of arterial stiffness is the increased heart rate and autonomic dysfunction corresponding progression. This minireview analyzes the current state of the relationship between the diabetes mellitus and the arterial stiffness. Particular attention is paid to the analysis, interpretation, and application of the results obtained in patients with type 2 diabetes mellitus and diabetic cardiac autonomic neuropathy.

Objective. The aim of the present study was to investigate the expression of pyruvate dehydrogenase genes such as PDHA1, PDHB, DLAT, DLD, and PDHX in U87 glioma cells in response to glutamine and glucose deprivations in control glioma cells and endoplasmic reticulum to nucleus signaling 1 (ERN1) knockdown cells, the major endoplasmic reticulum (ER) stress signaling pathway, to find out whether there exists a possible dependence of these important regulatory genes expression on both glutamine and glucose supply as well as ERN1 signaling. Methods. The expression level of PDHA1, PDHB, DLAT, DLD, and PDHX genes was studied by real-time quantitative polymerase chain reaction in control U87 glioma cells (transfected by empty vector) and cells with inhibition of ERN1(transfected by dnERN1) after cells exposure to glucose and glutamine deprivations. Results. The data showed that the expression level of PDHA1, PDHB, DLAT, and DLD genes was down-regulated (more profound in PDHB gene) in control glioma cells treated with glutamine deprivation. At the same time, ERN1 knockdown modified the impact of glutamine deprivation on the expression level of all these genes in glioma cells: suppressed the sensitivity of PDHB and DLD genes expression and removed the impact of glutamine deprivation on the expression of PDHA1 and DLAT genes. Glucose deprivation did not significantly change the expression level of all studied genes in control glioma cells, but ERN1 knockdown is suppressed the impact of glucose deprivation on PDHX and DLD genes expression and significantly enhanced the expression of PDHA1 and PDHB genes. No significant changes were observed in the sensitivity of PDHX gene expression to glutamine deprivation neither in control nor ERN1 knock-down glioma cells. The knock-down of ERN1 removed the sensitivity of DLAT gene expression to glucose deprivation. Conclusion. The results of this investigation demonstrate that the exposure of control U87 glioma cells under glutamine deprivation significantly affected the expression of PDHA1, PDHB, DLAT, and DLD genes in a gene specific manner and that impact of glutamine deprivation was modified by inhibition of the ER stress signaling mediated by ERN1. At the same time, glucose deprivation affected the expression of PDHA1, PDHB, PDHX, and DLD genes in ERN1 knockdown glioma cells only. Thus, the expression of pyruvate dehydrogenase genes under glutamine and glucose deprivation conditions appears to be controlled by the ER stress signaling through ERN1.

Objective. This study was aimed to evaluate the prevalence of Cushing's syndrome and the diagnostic performance of the 1 mg dexamethasone suppression test in class 3 obese patients. Methods. Anthropometric measurements and other laboratory data, including 1 mg dexamethasone suppression test of 753 class 3 obese patients, who applied to the Endocrinology and Metabolism Outpatient Clinic for the pre-bariatric surgery evaluation between 2011 and 2020, were evaluated retrospectively. Results. An abnormal response to the 1 mg dexamethasone suppression test (cortisol ≥1.8 mcg/dl) was observed in 24 patients and the presence of Cushing's syndrome was confirmed by additional tests in 6 patients. The prevalence of abnormal dexamethasone suppression test was 3.18% and the prevalence of Cushing's syndrome 0.79%. The specificity value was determined as 97.5% for 1 mg dexamethasone suppression test with cortisol threshold value ≥1.8 mcg/dl. Conclusions. The prevalence of Cushing's syndrome was found to be low in class 3 obese patients and 1 mg of dexamethasone suppression test had a very sufficient performance for Cushing's syndrome screening in this patient group.

A 59-year-old woman presented with flushing attacks accompanied by tachycardia and hypotension, which lasted approximately 30 to 60 minutes, underwent 18 years ago a gastrointestinal tumor resection. The histologic examination revealed a poorly differentiated mixed neuroendocrine/adenocarcinoma located in the caecum with regional metastases. Postoperatively, the patient received combined chemotherapy of 5-fluorouracil with interferon for six months and since has remained asymptomatic. Her examination revealed positivity for chromogranin A (CgA) and a-Fetoprotein (aFP) (580 ng/24 h, normal range 27-94, and 10 IU/mL, normal range 0-6, respectively). Urinary 5-hydroxy indole acetic acid excretion was remarkably high (41.8 mg/24 h, normal range 2-10 mg/24 h). An abdominal Magnetic Resonance Imaging scan revealed multiple focal loci in the liver whose histological examination revealed a carcinoid tumor confirmed by an Octreoscan. Additional uptake was noted on the right shoulder and the right sternum-clavicle joint confirmed by Tc-99m MDP scan. The patient received somatostatin analogue therapy followed by long-acting release octreotide analogue therapy (30 mg/month) showing a partial improvement of relevant biomarkers. Two years later, carcinoid syndrome symptoms reappeared and due to the tumors expression of somatostatin receptors the patient received peptide receptor radionuclide therapy with 177Lu-DOTATATE that resulted in both clinical and biochemical improvements.

Objective. Prolactinoma, as a common endocrine disorder and the most frequent type of pituitary tumor, acts primarily as a suppressor on the gonadal functions. It is generally successfully treated with dopamine agonists; however, treatment resistance still remains in an unneglectable ratio. In this study, we aimed to identify factors, which may play a role in the treatment response. Methods. Seventy-six patients with prolactinoma, who have been routinely followed between 2018 and 2022 in Istanbul Research and Educational Hospital Endocrinology Outpatient Clinic, were included into the study. Initial prolactin level, adenoma size, baseline weight, body mass index (BMI), glucose, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and triglyceride levels were obtained from the patient's medical records. The patients were divided into two groups: treatment respondent and non-respondent (refractory) ones, according to treatment response in the duration as suggested by the guidelines. The treatment respondent and non-respondent groups were compared according to the initial and the 3rd month prolactin levels, adenoma size, weight, BMI, and metabolic values. Results. The initial tumor diameter was 15.27±10.62 mm in the refractory and 7.42±4.42 mm in the treatment respondent groups (p=0.01). The refractory group had higher prolactin baseline level 269.96±275.78 µg/l vs. 124.55±67.35 µg/l of the respondent group (p=0.01). The refractory group had higher the 3rd month prolactin level 50.97±52.55 µg/l vs. 29.70±27.31 µg/l of the respondent group (p=0.04). The refractory group had higher frequency of cystic/hemorrhagic adenoma (47.6%, n=11/21) (p=0.01), baseline pituitary failure (33.3%, n=7/21) (p=0.01), and baseline cavernous sinus invasion (25.8, n=5/21) (p=0.01). The treatment respondent group had lower initial body weight (69.54±17.51 kg vs. 83.29±16.21 kg) (p<0.01), and lower BMI (25.98±5.47 kg/m² vs. 27.69±6.42 kg/m²) (p=0.02). Conclusions. In this study, initial tumor size, male gender, weight, BMI, the 3rd month prolactin level, initial pituitary deficiency, and cystic/hemorrhagic component in pituitary imaging in patients with prolactinoma were associated with a lower treatment response.

Postmenopausal women are at great risk of mental health deterioration, which may lead to morbidity and mortality. The decrement of mental health with aging is attributed to hormonal changes, lowered physical activity, sleep disturbances, economic factors, as well as modifiable variables such as smoking and obesity. Studies have shown controversial results on the association between obesity and mental health in postmenopausal women. This study is a systematic review of the evidence available on the association between obesity and mental health in postmenopausal women with the aim to identify the most reliable obesity measure that has been shown in association with mental health as well as the effective measures that have been practiced for improving mental health in postmenopausal obese women. CINAHL, Scopus, Science Direct and PubMed including Medline databases were searched. Out of 3,766 articles, 23 studies of average to good quality were included, out of which 17 were cross-sectional and 6 interventional. Out of the 17 studies, 12 showed a positive association between obesity and deterioration of mental health, 3 showed a negative association and two showed no association. From the interventional studies, 4 showed positive and two not significant impact of the intervention used on obesity and mental health. In conclusion, more studies showed a positive association between obesity, especially visceral obesity, and mental health issues particularly depression, anxiety, and sleep disorders. Combination of caloric restriction and exercise seems to have a better impact on the mental health of the postmenopausal in comparison with other interventions.

Mitochondria, the cell powerhouse, are membrane-bound organelles present in the cytoplasm of almost all the eukaryotic cells. Their main function is to generate energy in the form of adenosine triphosphate (ATP). In addition, mitochondria store calcium for the cell signaling activities, generate heat, harbor pathways of intermediate metabolism and mediate cell growth and death. Primary mitochondrial diseases (MDs) form a clinically as well as genetically heterogeneous group of inherited disorders that result from the mitochondrial energetic metabolism malfunctions. The lifetime risk of the MDs development is estimated at 1:1470 of newborns, which makes them one of the most recurrent groups of inherited disorders with an important burden for society. MDs are progressive with wide range of symptoms of variable severity that can emerge congenitally or anytime during the life. MD can be caused by mutations in the mitochondrial DNA (mtDNA) or nuclear DNA genes. Mutations inducing impairment of mitochondrial function have been found in more than 400 genes. Furthermore, more than 1200 nuclear genes, which could play a role in the MDs' genetic etiology, are involved in the mitochondrial activities. However, the knowledge regarding the mechanism of the mitochondrial pathogenicity appears to be most essential for the development of effective patient's treatment suffering from the mitochondrial disease. This is an overview update focused on the mitochondrial biology and the mitochondrial diseases associated genes.

Paraneoplastic syndromes, induced by an immunological cross-reaction or hormone/peptide secretion, are an atypical presentation of tumors. Some tumors, such as small cell lung cancer and bronchial carcinoid, can be adrenocorticotropic hormone (ACTH) secreting tumors. Less commonly, parotid acinic cell carcinoma can be ACTH-secreting tumor leading to Cushing's syndrome. Few literature cases have described ACTH related paraneoplastic syndrome of parotid adenocarcinoma. Because of the rarity of the condition, little is known about the management and prognosis of this phenomenon. In this report, we highlighted the case of a 59-year-old male with a past medical history of parotid adenocarcinoma treated with surgery, chemotherapy, and radiation therapy presented with clinical and biochemical signs of hyperaldosteronism. Abdominal ultra-sound, computed tomography, and magnetic resonance imaging showed hepatic mass. Liver biopsy with immunohistochemistry confirmed the presence of parotid adenocarcinoma secreting ACTH. He is on paclitaxel and carboplatin medication with good clinical response.