INITIAL SCREENING

CONSIDER THE SUSPECTED SOURCE OF EXCESS CORTISOL

A significant proportion of patients with hypercortisolism presenting initially with type 2 diabetes (T2D) will have an adrenal source1-4—it is important to select an initial screening test with sensitivity to detect all etiologies of hypercortisolism.

A majority of patients with T2D have an adrenal source of hypercortisolism1-4

Adrenal source of hypercortisolism

Studies depicting percentages of patients with type 2 diabetes who have an adrenal source of hypercortisolism.

THE 1-MG DEXAMETHASONE SUPPRESSION TEST (DST) IS RECOMMENDED FOR A SUSPECTED ADRENAL SOURCE OF HYPERCORTISOLISM5,6

The Endocrine Society Guidelines recommend a more sensitive 1-mg DST cutoff of >1.8 μg/dL to screen for a suspected adrenal source of hypercortisolism.5

1-MG DST

Measures suppression of adrenocorticotropic hormone and autonomous cortisol secretion

≤1.8 μg/dL

May exclude autonomous cortisol secretion

>1.8 μg/dL

Evidence of possible hypercortisolism.
Additional tests are needed to support a diagnosis

View further evaluation
  • The urinary-free cortisol (UFC) test may be less reliable in patients suspected of having an adrenal source of hypercortisolism, since these patients will often have normal UFC results4,7

    • The Endocrine Society Guidelines recommend a 1-mg DST rather than the UFC test for patients suspected of having an adrenal source of hypercortisolism5

  • The late-night salivary cortisol test may have a low sensitivity for predicting the presence of adrenal autonomous cortisol secretion8

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Additional tests may be needed to identify hypercortisolism

HOW TO EVALUATE
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How to confirm a hypercortisolism diagnosis

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References

1. Catargi B, Rigalleau V, Poussin A, et al. J Clin Endocrinol Metab. 2003;88(12):5808-5813. doi:10.1210/jc.2003-030254 2. Chiodini I, Torlontano M, Scillitani A, et al. Eur J Endocrinol. 2005;153(6):837-844. doi:10.1530/eje.1.02045 3. Steffensen C, Pereira AM, Dekkers OM, Jørgensen JO. Eur J Endocrinol. 2016;175(6):R247-R253. doi:10.1530/EJE-16-0434 4. Giovanelli L, Aresta C, Favero V, et al. J Endocrinol Invest. 2021;44(8):1581-1596. doi:10.1007/s40618-020-01484-2 5. Nieman LK, Biller BM, Findling JW, et al. J Clin Endocrinol Metab. 2008;93(5):1526-1540. doi:10.1210/jc.2008-0125 6. Fassnacht M, Tsagarakis S, Terzolo M, et al. Eur J Endocrinol. 2023;189(1):G1-G42. doi:10.1093/ejendo/lvad066 7. Chiodini I, Ramos-Rivera A, Marcus AO, Yau H. J Endocr Soc. 2019;3(5):1097-1109. doi:10.1210/js.2018-00382 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