10 results match your criteria: "Department of Endocrinology and MetabolismAcademic Medical Center[Affiliation]"
Eur J Endocrinol
June 2018
Department of Endocrinology and MetabolismOdense University Hospital, University of Southern Denmark, Odense, Denmark.
Objective: To construct a predictive score for the development or progression of Graves' orbitopathy (GO) in Graves' hyperthyroidism (GH).
Design: Prospective observational study in patients with newly diagnosed GH, treated with antithyroid drugs (ATD) for 18 months at ten participating centers from EUGOGO in 8 European countries.
Methods: 348 patients were included with untreated GH but without obvious GO.
Eur J Endocrinol
May 2018
Departments of EndocrinologyUniversity of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Background: A substantial proportion of all pheochromocytomas is currently detected during the evaluation of an adrenal incidentaloma. Recently, it has been suggested that biochemical testing to rule out pheochromocytoma is unnecessary in case of an adrenal incidentaloma with an unenhanced attenuation value ≤10 Hounsfield Units (HU) at computed tomography (CT).
Objectives: We aimed to determine the sensitivity of the 10 HU threshold value to exclude a pheochromocytoma.
J Mol Endocrinol
April 2018
Department of Endocrinology and MetabolismAcademic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
Acute or chronic exposure to stress can increase the risk to develop major depressive disorder, a severe, recurrent and common psychiatric condition. Depression places an enormous social and financial burden on modern society. Although many depressed patients are treated with antidepressants, their efficacy is only modest, underscoring the necessity to develop clinically effective pharmaceutical or behavioral treatments.
View Article and Find Full Text PDFEndocr Connect
February 2018
Department of Internal MedicineMedical Center Slotervaart, Amsterdam, the Netherlands.
Introduction: Abnormal coagulation tests have been observed in patients with primary hyperparathyroidism (HPT) suggesting a prothrombotic effect of parathyroid hormone (PTH). Vitamin D deficiency (VIDD) is the most frequent cause of secondary HPT. Aim of our study was to investigate the influence of HPT secondary to moderate-to-severe VIDD and vitamin D replacement on the coagulation and fibrinolysis system.
View Article and Find Full Text PDFEndocr Connect
November 2017
Department of Endocrinology and MetabolismAcademic Medical Center, Amsterdam, The Netherlands
Innate immune cells have recently been identified as novel thyroid hormone (TH) target cells in which intracellular TH levels appear to play an important functional role. The possible involvement of TH receptor alpha (TRα), which is the predominant TR in these cells, has not been studied to date. Studies in TRα mice suggest a role for this receptor in innate immune function.
View Article and Find Full Text PDFJ Endocrinol
February 2017
Department of Endocrinology and MetabolismAcademic Medical Center, Amsterdam, The Netherlands
Thyroid hormone (TH) metabolism and thyroid status have been linked to various aspects of the immune response. There is extensive literature available on the effects of thyroid hormone on innate immune cells. However, only recently have authors begun to study the mechanisms behind these effects and the role of intracellular TH metabolism in innate immune cell function during inflammation.
View Article and Find Full Text PDFJ Endocrinol
January 2017
Department of Endocrinology and MetabolismAcademic Medical Center, University of Amsterdam, the Netherlands
We showed previously that rats on a free-choice high-fat, high-sugar (fcHFHS) diet become rapidly obese and develop glucose intolerance within a week. Interestingly, neither rats on a free-choice high-fat diet (fcHF), although equally obese and hyperphagic, nor rats on a free-choice high-sugar (fcHS) diet consuming more sugar water, develop glucose intolerance. Here, we investigate whether changes in insulin sensitivity contribute to the observed glucose intolerance and whether this is related to consumption of saturated fat and/or sugar water.
View Article and Find Full Text PDFJ Endocrinol
April 2016
Department of Endocrinology and MetabolismAcademic Medical Center (AMC), University of Amsterdam, Amsterdam, the Netherlands.
In addition to the direct effects of thyroid hormone (TH) on peripheral organs, recent work showed metabolic effects of TH on the liver and brown adipose tissue via neural pathways originating in the hypothalamic paraventricular and ventromedial nucleus (PVN and VMH). So far, these experiments focused on short-term administration of TH. The aim of this study is to develop a technique for chronic and nucleus-specific intrahypothalamic administration of the biologically active TH tri-iodothyronine (T3).
View Article and Find Full Text PDFEur J Endocrinol
November 2014
Department of Endocrinology and MetabolismAcademic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The NetherlandsHypothalamic Integration MechanismsNetherlands Institute for Neuroscience, Amsterdam, The Netherlands.
The hypothalamus-pituitary-thyroid (HPT) axis represents a classical example of an endocrine feedback loop. This review discusses dynamic changes in HPT axis setpoint regulation, identifying their molecular and cellular determinants, and speculates about their functional role. Hypothalamic thyrotropin-releasing hormone neurons were identified as key components of thyroid hormone (TH) setpoint regulation already in the 1980s, and this was followed by the demonstration of a pivotal role for the thyroid hormone receptor beta in negative feedback of TH on the hypothalamic and pituitary level.
View Article and Find Full Text PDFEur J Endocrinol
June 2014
Department of Endocrinology and MetabolismAcademic Medical Center, Room F5-169, University of Amsterdam, Meibergdreef 9, Amsterdam 1105AZ, The Netherlands
The last 10 years have seen some progress in understanding the etiology of autoimmune thyroid disease (AITD). The female preponderance can now be explained - at least in part - by fetal microchimerism and X-chromosome inactivation. The number of identified susceptibility genes for AITD is increasing (among others now including TSHR, TG, HLA, CTLA4, PTPN22, CD40, FCRL3, IL2RA, and FOXP3), but these genes together probably do not explain more than about 10% of the heritability of AITD.
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