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M S Elston, V B Crawford, M Swarbrick, M S Dray, M Head, and J V Conaglen

showed a hypokalaemic metabolic alkalosis ( Table 1 ). Hypercortisolaemia was confirmed with morning cortisol >1655 nmol/L, absence of diurnal cortisol rhythm and markedly increased 24-h urinary free cortisol excretion (24-h UFC). Table 1 Pertinent

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Jülide Durmuşoğlu, Henri J L M Timmers, Pepijn van Houten, Johan F Langenhuijsen, Ad R M M Hermus, and Annenienke C van de Ven

rates of ACC after resection are high ( 6 , 8 ). ACC may be classified as functional (hormone-secreting) or nonfunctional. Functional adrenal tumors of the cortex can produce cortisol, androgens, estrogens and aldosterone. A functional ACC can cause

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Amit Kumar, Maria Ghosh, and Jubbin Jagan Jacob

.2%, respectively. For precision testing, the CV% for low to normal and high sodium levels was 1.1 and 0.4 mmol/L, respectively. Quantitative determination of serum cortisol was performed using Elecsys Cortisol II kit on Cobas e411/601 fully automated analyzer

Open access

Masafumi Tetsuka and Misato Tanakadate

2) ( 13 ). The former is a reductase that predominantly catalyzes inactive cortisone to active cortisol, while the latter is an oxidase that catalyzes the opposite reaction ( 14 ). The expression of these HSD11Bs appeared to be differentially

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T P Parikh, B Stolze, Y Ozarda, J Jonklaas, K Welsh, L Masika, M Hill, A DeCherney, and S J Soldin

Introduction Diurnal variations in the serum concentration of steroid hormones and their metabolism, as assessed by urinary excretion, have long been known for cortisol and testosterone ( 1 , 2 , 3 ). Less information exists for the other up

Open access

Jana Ernst, Katharina Gert, Frank Bernhard Kraus, Ulrike Elisabeth Rolle-Kampczyk, Martin Wabitsch, Faramarz Dehghani, and Kristina Schaedlich

concentration of cortisone. Cholesterol and steroid hormones (cortisol, DHEAS, estradiol, progesterone, testosterone) were analyzed in the Central Laboratory of the University Hospital Halle. Cholesterol was measured using a colorimetric assay (CHOL2

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Peter Wolf, Yvonne Winhofer, Martin Krššák, and Michael Krebs

morphology of the heart in patients suffering from T2DM and hypothyroidism. Cortisol Death from cardiovascular disease, including heart failure, coronary artery disease and cardiac thromboembolism, is the leading cause of increased mortality observed

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Sandra R Dahl, Ingrid Nermoen, Ingeborg Brønstad, Eystein S Husebye, Kristian Løvås, and Per M Thorsby

Introduction Congenital adrenal hyperplasia (CAH) is a group of autosomal recessive disorders with impaired biosynthesis of adrenal glucocorticosteroids and defects in cortisol biosynthesis. More than 95% of cases are caused by mutations in

Open access

Ali Abbara, Sophie Clarke, Pei Chia Eng, James Milburn, Devavrata Joshi, Alexander N Comninos, Rozana Ramli, Amrish Mehta, Brynmor Jones, Florian Wernig, Ramesh Nair, Nigel Mendoza, Amir H Sam, Emma Hatfield, Karim Meeran, Waljit S Dhillo, and Niamh M Martin

(persistent hiccup). One patient was hypotensive (systolic BP <90 mmHg; serum cortisol of 118 nmol/L and serum sodium of 115 nmol/L on admission). However, 11/30 were hypertensive at presentation (systolic BP >140 mmHg) ( Table 2 ). Symptoms consistent with

Open access

Peter Ergang, Anna Mikulecká, Martin Vodicˇka, Karla Vagnerová, Ivan Mikšík, and Jirˇí Pácha

-hydroxysteroid dehydrogenase type 1 (11HSD1) and type 2 (11HSD2). 11HSD2 is an enzyme that catalyzes the oxidations of cortisol and corticosterone to the inactive cortisone and 11-dehydrocorticosterone, reducing the local glucocorticoid signals. In contrast, 11HSD1 converts