adrenal-corticoids-profile-urine adrenal-corticoids-profile-urine
Adrenal Corticoids Profile; urine Adrenal Corticoids Profile; urine

Adrenal Corticoids Profile; urine

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]

Useful for:

  • Fatigue
  • Insomnia
  • Mood or cognitive concerns
  • Thyroid pathologies
  • Inflammation
  • Libido
  • Weight gain

Turnaround Time

5 to 7 days

Analytes Tested

Click any analyte name for additional clinical information, including reference ranges, specimen collection, stability and rejection criteria.


List price applies when filing with insurance or Medicare, or when billing a patient directly. Prompt payment pricing applies when billing to a physician account or prepayment is received with the test.

Doctor's Data offers profiles containing multiple analytes. *Multiple analytes may be billed under a single CPT code. Many analytes can be ordered individually. Pricing may vary. Click on a specific analyte for more information or read our detailed billing and payment policies.

The CPT codes listed on our website are for informational purposes only. This information is our interpretation of CPT coding requirements and may not necessarily be correct. You are advised to consult the CPT Coding Manual published by the American Medical Association. Doctor's Data, Inc. takes no responsibility for billing errors due to your use of any CPT information from our website.

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Detailed Information

Corticoids:

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.