Facultad de Medicina, Universidad Complutense de Madrid, Madrid, España
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Servicio de Endocrinología y Nutrición. Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Hospital Clínico San Carlos, Madrid, España
Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Madrid, España
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Servicio de Endocrinología y Nutrición. Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Hospital Clínico San Carlos, Madrid, España
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Servicio de Endocrinología y Nutrición. Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Hospital Clínico San Carlos, Madrid, España
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Servicio de Endocrinología y Nutrición. Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Hospital Clínico San Carlos, Madrid, España
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Introduction Aldosterone and cortisol are the two main mineralocorticoids in humans. Under physiological conditions, aldosterone is the chief stimulatory ligand of the mineralocorticoid receptor (MR) in the principal cells of the distal
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) or cortisone acetate, requires two-three daily doses to maintain adequate plasma cortisol levels, with the highest dose administered in the morning and a lower dose in the afternoon or, if required, in the evening ( 1 ), exposing patients to
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Department of Endocrine and Metabolic Diseases, Istituto Auxologico Italiano IRCCS, Milan, Italy
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, which is required for the conversion of cholesterol to cortisol and aldosterone, rendering it either partly or completely ineffective ( 2 , 3 ). Patients with classic CAH, therefore, experience glucocorticoid (GC) and mineralocorticoid deficiency
Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
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Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
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Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Krakow, Poland
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the number of thrombotic episodes or with the level of cortisol was observed ( 3 ). The role of hypercortisolemia in triggering thrombotic episodes is still being studied, with a possible inverse correlation between aPTT and urine free cortisol (UFC
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AmCare Genomics Lab, Guangzhou, People’s Republic of China
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Introduction Congenital adrenal hyperplasia (CAH) is one of the most severe disorders of metabolism with an overall incidence of approximately 1:15,000 worldwide ( 1 ). CAH encompasses a group of enzymatic deficiencies of cortisol synthesis
Tulane University School of Medicine, Department of Psychiatry, Division of Child and Adolescent Psychiatry, Tulane University, New Orleans, Louisiana, USA
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Tulane University School of Medicine, Department of Psychiatry, Division of Child and Adolescent Psychiatry, Tulane University, New Orleans, Louisiana, USA
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stress on TL, and other subsequent biological systems known to deteriorate with aging. Pathway 2: the antiglucocorticoid hypothesis In vitro cortisol exposure is associated with decreased telomerase ( 23 ), the enzyme responsible for repairing
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cannulation was considered successful if the adrenal vein/inferior vena cava cortisol gradient (selectivity index) was >3.0. Lateralization was considered when the aldosterone:cortisol ratio (A/C) from one adrenal gland was at least three times greater than
Harvard Medical School, Boston, Massachusetts, USA
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hypocortisolism with low serum cortisol (<5 μg/dL) and/or low urinary free cortisol (<20 mg per 24 h), and/or low cortisol (<1.8 mg/dL) level after 1 mg dexamethasone. Most of the studies also defined eucortisolism as remission ( 15 , 17 , 18 , 25 , 28 , 29
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previously described ( 11 ). Morning fasting venous blood samples were collected to measure lipids, glucose (GLU), insulin (INS), TSH, fT4, cortisol and aminotransferases. Plasma total cholesterol (T Chol), high-density lipoprotein cholesterol (HDL-Chol) and
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and hypokalemia include 11-beta hydroxylase and 17-alpha hydroxylase deficiency, which are characterized by increased production of cortisol and aldosterone precursors due to chronic stimulation of the adrenal cortex by ACTH ( 42 ). In 11-beta