dr ruman
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hayee i em quite confused about interpretation of metyrapone test,well it inhibits 11 hydroxylase preventing cortisol formation and buildup of deoxycortisone,fine! but how do we interpret in hypocotisolism and cushing ,by both pituitary and adrenal
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| shivaniab
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Metyrapone blocks the conversion of 11-deoxycortisol to cortisol by CYP11B1 (11-beta-hydroxylase, P-450c11), the last step in the synthesis of cortisol, and induces a rapid fall of cortisol and an increase of 11-deoxycortisol in serum.
Because it is essentially devoid of glucocorticoid activity, 11-deoxycortisol does not inhibit ACTH secretion. Thus, in healthy individuals, the fall in serum cortisol concentrations leads sequentially to increases in ACTH secretion, adrenal steroidogenesis, and the secretion of cortisol precursors, in particular, 11-deoxycortisol, the substrate of CYP11B1, which can be measured by radioimmunoassay, HPLC, or in urine as a 17-hydroxycorticosteroid (17-OHCS) [3].
The increase in serum 11-deoxycortisol concentrations or in urinary 17-OHCS excretion provides an index of the increase in ACTH release; a failure of these values to rise can indicate either ACTH deficiency or primary adrenal disease. Thus, if the metyrapone test is abnormal, the ability of the adrenal gland to respond to exogenous ACTH must be assessed to distinguish between these disorders.
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| SmokyWaters
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| dr ruman
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thx 
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Living each day as a preparation for the next is an exciting way to live. Looking forward to something is much more fun than looking back at something—so lets do it together
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| imnalini
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Increased 11 deoxycortisol (weak mineralocoticoid) leads to HYPERTENSION in 11 hydroxylase deficiency----------------imp clue in clinical vignettes.
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