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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

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

.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

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

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

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

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

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

(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

-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