The patient is instructed to take a 1-mg oral dose of dexamethasone between 11 PM and midnight and fast overnight.1
Initial Screening
THE 1-MG DEXAMETHASONE SUPPRESSION TEST (DST)
According to guidelines, the 1-mg DST is recognized as being sensitive for the detection of all etiologies of hypercortisolism.1,2 The 1-mg DST is also considered a reliable test for screening patients with adrenal autonomous cortisol secretion, which is common in patients who present with difficult-to-control T2D and hypertension.3,4 It is inexpensive, accessible, and relatively easy to manage.5
A sample of blood is drawn the next morning between 8 AM and 9 AM to measure plasma cortisol.1
An AM dexamethasone level ≥140 ng/dL confirms adequate HPA axis suppression occurred and verifies the DST cortisol result.6
A post-DST cortisol >1.8 μg/dL with AM dexamethasone ≥140 ng/dL is indicative of a hypercortisolism diagnosis.6
A POST 1-MG DST CORTISOL >1.8 μg/dL IS RECOMMENDED FOR SCREENING2,4
1-MG DST
Measures suppression of adrenocorticotropic hormone and autonomous cortisol secretion
post 1-mg-DST cortisol level of>1.8 μg/dL
Indicates evidence of possible hypercortisolism. Subsequent testing is needed to support a diagnosis and identify the source of hypercortisolism.
After an initial post 1-mg-DST cortisol level of >1.8 μg/dL, subsequent tests and further evaluation may be needed to confirm hypercortisolism and will be needed to identify the source of hypercortisolism.
How reliable is the 1-mg DST?
Other screening tests, such as the late-night salivary cortisol (LNSC) test and urinary-free cortisol (UFC) test, may have a low sensitivity and may be less reliable.2,7,8
The LNSC test often has discordant results in patients with an adrenal source of hypercortisolism8
Patients with confirmed hypercortisolism often have UFC levels in the normal range3,7
Nearly 1 in 4 patients with difficult-to-control T2D had endogenous hypercortisolism6
Do you have patients who may need a hypercortisolism specialist?
Discuss the recent prevalence data with a Corcept representative
References
1. DeFronzo RA, Auchus RJ, Bancos I, et al. BMJ Open. 2024;14(7):e081121. doi:10.1136/bmjopen-2023-081121 2. Nieman LK, Biller BM, Findling JW, et al. J Clin Endocrinol Metab. 2008;93(5):1526-1540. doi:10.1210/jc.2008-0125 3. Chiodini I, Ramos-Rivera A, Marcus AO, Yau H. J Endocr Soc. 2019;3(5):1097-1109. doi:10.1210/js.2018-00382 4. Fassnacht M, Tsagarakis S, Terzolo M, et al. Eur J Endocrinol. 2023;189(1):G1-G42. doi:10.1093/ejendo/lvad066 5. Ciftel S, Mercantepe F. Cureus. 2023;15(11):e48383. doi:10.7759/cureus.48383 6. Buse JB, Kahn SE, Aroda VR, et al. Diabetes Care. 2025;48(00):1-9. doi:10.2337/dc24-2841 7. Giovanelli L, Aresta C, Favero V, et al. J Endocrinol Invest. 2021;44(8):1581-1596. doi:10.1007/s40618-020-01484-2 8. Kuzu I, Zuhur SS, Demir N, Aktas G, Yener Ozturk F, Altuntas Y. Endokrynol Pol. 2016;67(5):487-492. doi:10.5603/EP.a2016.0028