Purpose of review
Following the introduction of an increasing number of investigational procedures, the use of dexamethasone suppression testing as a main mean in the assessment of endogenous hypercortisolism has been questioned. We will discuss the indications for dexamethasone suppression testing, the variations currently used, and address areas of debate in an attempt to suggest the most appropriate diagnostic approaches.
The biochemical confirmation of endogenous hypercortisolism (Cushing syndrome) has relied on the low-dose dexamethasone suppression testing, whereas the high-dose dexamethasone suppression testing has been used to define the cause. Cushing syndrome is currently considered earlier, when the clinical and biochemical evidence of hypercortisolism is mild; in addition, a number of other common conditions can exhibit a similar phenotype. Following changes in the methodology of cortisol measurement, the ability to measure salivary cortisol and the improvement in other investigational procedures, the use of the low-dose dexamethasone suppression testing as a mean to facilitate the diagnosis of Cushing syndrome has been questioned. However, a number of recent studies have provided evidence that the low-dose dexamethasone suppression testing, measuring serum instead of urinary cortisol and using lower cut-off limits to define adequate suppression, remains a highly sensitive and specific test. In addition, the combination of the low-dose dexamethasone suppression testing with other tests can be of high diagnostic accuracy and obviate the need for other diagnostic procedures.
The low-dose dexamethasone suppression testing is a simple test that can identify patients with mild Cushing syndrome and differentiate between the different subtypes of ACTH-dependent Cushing syndrome.