Use

This test, when used in conjunction with the measurement of 24‑hour urine cortisol, may help in the diagnosis of apparent mineralocorticoid excess (AME) syndrome. Cortisone is an inactive metabolite of cortisol converted by 11‑beta‑hydroxysteroid dehydrogenase type 2 (11‑beta‑HSD2) in the kidney. In patients with AME syndrome, deficiency of 11‑beta‑HSD2 impairs the deactivation of cortisol to cortisone. Consequently, accumulated cortisol activates mineralocorticoid receptors and leads to clinical manifestations resembling primary aldosteronism. Patients with AME typically present with low‑renin hypertension, hypokalemia, and metabolic alkalosis. Similarly, ingestion of certain compounds that inhibit 11‑beta‑HSD2 activity, such as glycyrrhetinic acid (in licorice), carbenoxolone, and phthalates, may also reduce the conversion of cortisol to cortisone. Therefore, a high cortisol‑to‑cortisone ratio measured in 24‑hour urine may help in identifying disorders caused by impaired activity of 11‑beta‑HSD2. This test should be used in conjunction with 24‑hour urine cortisol testing to evaluate the activity of 11‑beta‑HSD2. High serum cortisol‑to‑cortisone ratios in addition to low cortisone levels may also be helpful in the diagnosis of AME syndrome. The results of this test should be interpreted in the context of pertinent clinical and family history and physical examination findings.