The Adrenal Corticoids profile is a consideration for baseline or follow up testing for patients with concerns that are particular to HPA axis and corticoid health. This non-invasive test requires only 4 or 5 separate urine collections. Patient FAQs and Best Practices for HuMap [ LEARN MORE]
5 to 7 days
Note: Turnaround times on results are an estimate and are not guaranteed. The lab may need additional time due to holidays, confirmation/repeat testing, etc. You can contact us to discuss when your results should be ready.
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The major site of cortisol metabolism is the liver. There it is reduced, oxidized or hydroxylated. The enzymes that directly metabolize cortisol are 11 beta hydroxysteroid dehydrogenase 1 and 2 (11-B HSD1 and 11B HSD2), the A-ring reductases (5 alpha and 5 beta reductases), 3 alpha hydroxysteroid dehydrogenase and 20 alpha and 20 beta hydroxysteroid dehydrogenases.
Cortisone protects the tissues from effects of cortisol, therefore if 11 B HSD activity is functioning properly, there should be twice as much cortisone as cortisol, measured in the cortisone (E)/cortisol (F) ratio. This ratio indicates 11B HSD 2 activity and infers tissue-specific concentrations of cortisol (which normally cannot be measured without a biopsy). A lower ratio suggests decreased cortisol clearance which may be associated with hypothyroidism (but isn’t associated with elevated free cortisol).
HSD 11B (1 and 2):
The primary function of 11B-HSD2 is to limit the cortisol effects upon cells with mineralocorticoid receptors (MR). Since cortisol has the same affinity for MR as aldosterone and is present in much higher concentrations, the conversion of cortisol to cortisone through the liver via 11B-HSD2 protects these cells from glucocorticoid intrusion on the mineralocorticoid system. It has been shown that the effects of excessive glucocorticoid activation in many of these tissues result from the actions of 11B-HSD1 due to the re-conversion of cortisone back to cortisol, rather than merely the excessive production of cortisol through classic HPA axis processes. In fact, the human liver/ splanchnic bed is responsible for 20-40% of the daily cortisol production making the inactive cortisone pool a major reservoir for systemic cortisol availability.
Thyroid hormone plays a role in this conversion process. Increased cortisol metabolism is associated with hyperthyroidism while hypothyroidism has been shown to slow cortisol metabolism, resulting in lower levels of metabolized cortisol.