Endocrine Abstracts

Corticosteroids are major contributors to normal blood pressure control and to hypertension. The diagnosis of 'primary aldosteronism' based on raised aldosterone: renin ratios is now common although demonstration of an adrenocortical tumour remains rare. Moreover, the relationship between aldosterone and renin or angiotensin II in essential hypertension is often disturbed, suggestive of altered control of aldosterone biosynthesis. Aldosterone is synthesised from 11-deoxycortic...

Introduction. As for many minor metabolites of steroids, no authentic standard is commercially available for 18-OH-THA. This compound is the principal urinary metabolite of 18-hydroxycorticosterone, a putative intermediate in the synthesis of aldosterone and of diagnostic value in screening for hypermineralocorticoidism. Since de novo synthesis is time-consuming and expensive, we tested the possibility of using beta-cortol, which produces an ion at m/z 457 in common wit...

18-hydroxycortisol (18-OHF) and 18-oxocortisol (18oxo-F) are derivatives of cortisol whose origin and regulation are uncertain. 18-OHF is synthesised by zona fasciculata 11-beta hydroxylase; 18-oxoF can only be produced by zona glomerulosa aldosterone synthase. Levels of both steroids are increased in patients with Primary Aldosteronism. However, the origin of these steroids in normal subjects is not known.8 normal subjects and 6 subjects with primary adrenal failure performed...

Urine 18-hydroxy cortisol ('18OHF') measurements are claimed to have the potential to discriminate between primary hyperaldosteronism due to either Conn's syndrome/adrenal adenoma (increased values) or idiopathic adrenal hyperplasia (normal values), and also to identify cases of glucocorticoid-suppressible hyperaldosteronism ('GSH').We have evaluated three urine 18-OHF methods using a panel of samples from patients with primary hyperaldosteronism [due to either adenoma (N=...

INTRODUCTIONThe plasma concentrations and urinary excretion rates of 18-OH-F and 18-oxo-F are high in Conn's syndrome and glucocorticoid suppressible hyperaldosteronism, reputedly because aldosterone synthase (AS) has abnormal access to cortisol (F). However, both compounds are also excreted in normal subjects. Two enzymes, 11beta-hydroxylase (11OH) and AS, located in the zona fasiculata (ZF) and zona glomerulosa (ZG) respectively, are capable of 18-hydroxylation but only ...