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Expected Turnaround Time
6 - 10 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Specimen Requirements
Specimen
Serum (preferred) or plasma
Volume
1 mL
Minimum Volume
0.3 mL (Note: This volume does not allow for repeat testing.)
Container
Gel-barrier tube, red-top tube, lavender-top (EDTA) tube or green-top (heparin) tube
Collection
Serum/plasma must be separated from cells within 45 minutes of venipuncture. Send serum/plasma in a plastic transport tube
Storage Instructions
Freeze (preferred) or refrigerate.
Stability Requirements
Temperature | Period |
|---|---|
Room temperature | 2 days |
Refrigerated | 2 days |
Frozen | 7 days |
Test Details
Use
The mineralocorticoid receptor binds cortisol as an active ligand, yet in normal people cortisol levels are not related to sodium retention. While in vitro the mineralocorticoid receptor has a similar affinity as aldosterone and cortisol, and in vivo cortisol is found in concentrations 100 to 1000 times higher than those of aldosterone, 11β-hydroxysteroid dehydrogenase 2 protects the mineralocorticoid receptor by reducing cortisol to cortisone, which is not an active ligand. This enzyme occurs in cells that contain the receptor. A similar enzyme is present in other tissues but works more slowly and backwards, converting cortisone to cortisol. Defects in this system can cause hypertension and can be diagnosed from the cortisol to cortisone ratio.1-6
Apparent mineralocorticoid excess (AME) is a rare recessive genetic disease that is characterized by childhood onset of hypertension, hypokalemic alkalosis, and low plasma renin and aldosterone levels.7-8 Hypertension is due to impaired conversion of cortisol to cortisone due to an inactive 11β-hydroxysteroid dehydrogenase (11βHSD). This condition may be diagnosed with elevated cortisol metabolite to cortisone metabolite ratios in urine or more recently with an elevated cortisol to cortisone ratio in serum.1 It is recommended that cortisol:cortisone ratios (F/E) be tested in hypokalemic hypertension cases in which aldosterone, deoxycorticosterone, and renin are all low.
Elevated cortisol:cortisone ratios may be found in chronic renal failure, excessive ingestion of glycyrrhetinic acid or derivatives, or in liver or bile-acid abnormalities.7 Even in these circumstances, however, determination of the cortisol:cortisone ratio is recommended to help shed light on the source of hypertension.
Limitations
Results of this test are for investigational purposes only. The performance characteristics of this assay have been determined by LabCorp. The result should not be used as a diagnostic procedure without confirmation of the diagnosis by another medically established diagnostic product or procedure.
Methodology
High-pressure liquid chromatography (HPLC)/tandem mass spectrometry
Footnotes
1. Inada M, Iwasaki KC, Imai C, et al. Spironolactone effective hypertension in the elderly due to 11-β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) impairment: Contributory role of determining serum cortisol/cortisone ratio as a marker of 11β-HSD2 activity. Intern Med. 2008; 47(24):2157-2164.19075542
2. Carvajal CA, González AA, Romero DG, et al. Two homozygous mutations in the 11β-hydroxsteroid dehydrogenase type 2 gene in a case of apparent mineralocorticoid excess.J Clin Endocrinol Metab. 2003; 88(6):2501-2507.12788846
3. Morineau G, Sulmont V, Salomon R, et al. Apparent mineralocorticoid excess: Report of six new cases and extensive personal experience.J Am Soc Nephrol. 2006; 17(11):3176-3184.17035606
4. Palermo M, Quinkler M, Stewart PM. Apparent mineralocorticoid excess syndrome: An overview. Arq Bras Endocrinol Metabol. 2004; 48(5):687-696.15761540
5. Schroth M, Plank C, Rauh M, et al. Pediatric renal allograft transplantation does not normalize the increased cortisol/cortisone ratios of chronic renal failure. Eur J Endocrinol. 2006; 154(4):555-561.16556718
6. Lawson AJ, Walker EA, Lavery GG, et al. Cortisone reductase deficiency associated with heterozygous mutations in 11β-hydrozysteroid dehydrogenase type 1. Proc Natl Acad Sci USA. 2011; 108(10):4111-4116. Available at www.pnas.org/cgi/doi/10.1073/pnas.101493410821325058
7. Quinkler M, Stewart PM. Hypertension and the cortisol-cortisone shuttle. J Clin Endocrinol Metab. 2003; 88(6):2384-2392.12788832
8. Draper N, Stewart PM. 11β-hydroxysteroid dehydrogenase and the pre-receptor regulation of corticosteroid hormone action. J Endocrinol. 2005; 186(2):251-271.16079253
LOINC® Map
| Order Code | Order Code Name | Order Loinc | Result Code | Result Code Name | UofM | Result LOINC |
|---|---|---|---|---|---|---|
| 503715 | Cortisol-Cortisone Ratio Prof. | 500155 | Cortisol, Serum LCMS | ug/dL | 2143-6 | |
| 503715 | Cortisol-Cortisone Ratio Prof. | 503716 | Cortisone, Serum, LCMS | ug/dL | 14159-8 | |
| 503715 | Cortisol-Cortisone Ratio Prof. | 503717 | Cortisol/Cortisone Ratio | 72392-4 |
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