Aldosterone, the major mineralocorticoid hormone and cortisol, the major glucocorticoid hormone are produced in the adrenal gland. Aldosterone binds intracellular mineralocorticoid receptors (MR) in the kidney promoting urinary reabsorption of sodium and water and excretion of potassium and hydrogen ions. Unregulated mineralocorticoid excess may, therefore, lead to high blood pressure due to sodium and water retention and hypokalaemic alkalosis.Blood concentrations of cortisol which has equal affinity for MR are 1000 fold greater than those of aldosterone. Therefore in order not to overwhelm MR, cortisol needs to be deactivated before it binds MR. This is achieved by the enzyme 11-beta hydroxysteroid dehydrogenase type 2 (11ßHSD-2) in the kidney which rapidly inactivates cortisol to cortisone(this process allows only aldosterone to bind MR). Reduced activity of 11ßHSD-2 leads to an accumulation of cortisol which binds MR and hence has the effect of aldosterone. Reduced Activity of 11ßHSD-2 may be seen in the inherited condition of ‘Apparent mineralocorticoid excess (AME)’ or in excessive liquorice ingestion. The diagnosis of AME and liquorice toxicity is difficult due to unavailability of diagnostic urine analysis in most general laboratories. Cortisol in the salivary glands, similarly to that in kidneys, is metabolised by 11β-HSD2 to cortisone. It is proposed that increased salivary cortisol/cortisone ratio could offer a simple and convenient diagnostic test for AME and liquorice toxicity and can be used as a surrogate marker of urinary cortisol/cortisone ratio. The advantages of salivary cortisol/cortisone include non-invasiveness making it stress free for the patient, no risk of needlestick injury and ease of collection allowing potential home testing and posting of samples.
