Frequently Asked Questions

The definition of difficult-to-control T2D varies by patient, clinical practice, and experience. Consider the following characteristics to determine if a treatment-adherent patient may have difficult-to-control T2D:

  • Persistently elevated glucose levels despite standard diabetes management including lifestyle changes
  • Treated with multiple diabetes medications or higher doses than frequently observed in clinical practice

While clinical studies have not universally defined difficult-to-control T2D patients, identifying these patients is a critical step to improving health outcomes and minimizing the risk of complications. Some clinical studies recommend screening for hypercortisolism in patients with certain clinical characteristics of T2D.1,2 A 2021 meta-analysis by Aresta et al recommends screening for hypercortisolism in patients with T2D treated with at least 3 drugs and presenting with associated comorbidities.3 The Endocrine Society Guidelines recommend screening for hypercortisolism in patients with T2D who have overlapping conditions and features.4

Moon face, dorsocervical fat pad/buffalo hump, and striae are considered highly specific Cushingoid features. However, there are many patients with hypercortisolism who do not present with these phenotypic features.

These patients may have multiple progressive metabolic derangements and feature comorbidities commonly seen in the general population (eg, obesity, diabetes, hypertension, and depression). The absence of Cushingoid physical features does not exclude patients from having hypercortisolism. Patients with an adrenal source of hypercortisolism do not typically display Cushingoid phenotypic features. In a meta-analysis published in 2019, patients with adrenal incidentalomas, only 0.2% (n=6/2745) of patients with adrenal incidentalomas developed overt Cushingoid features, and these patients had an increased risk for developing cardiometabolic conditions.5

Many patients who do not present with Cushingoid features are at risk for delayed or even missed hypercortisolism diagnosis. A retrospective study of 198 patients with adrenal adenomas from DiDalmazi et al revealed that patients with post-DST cortisol levels >1.8 μg/dL who did not have overt Cushingoid features had a greater risk for morbidity and mortality.6

Multiple publications support the use of DST to screen for ACS.1-3 The Endocrine Society Guidelines recommend a 1-mg DST cutoff of >1.8 µg/dL to screen patients who do not exhibit the clinical features or signs and symptoms but are suspected of having ACS. A 1-mg DST cutoff of >1.8 µg/dL achieves sensitivity rates greater than 95%.4

The following factors may interfere with the reliability and accuracy of the results from a 1-mg DST4:

  • Drugs that may alter dexamethasone metabolism (eg, anticonvulsants, or other drugs that may induce CYP450 or CYP3A4 metabolism)
  • Alcoholism
  • Psychiatric illness
  • Women on estrogen therapy
  • Non-compliance with testing instructions

To help ensure accurate test results in your patients, use this 1-mg DST Patient Tool that provides directions and guidance on what to expect with screening.

No, a patient with elevated post-DST cortisol levels and normal UFC results may still have an adrenal source of excess cortisol secretion. In patients suspected of having an adrenal adenoma, UFC results are often normal and cannot be used to confirm a diagnosis.1

The Endocrine Society Guidelines recommend the use of a 1-mg DST or LNSC over a UFC test.4 Diagnostic tests should be used in combination with a high degree of clinical suspicion to reduce the likelihood of false positive results.


1. Giovanelli L, Aresta C, Favero V, et al. J Endocrinol Invest. 2021;44(8):1581-1596. doi:10.1007/s40618-020-01484-2 2. Chiodini I, Albani A, Ambrogio AG, et al. Endocrine. 2017;56(2):262-266. doi:10.1007/s12020-016-1017-3 3. Aresta C, Soranna D, Giovanelli L, et al. Endocr Pract. 2021;27(12):1216-1224. doi:10.1016/j.eprac.2021.07.014 4. Nieman LK, Biller BM, Findling JW, et al. J Clin Endocrinol Metab. 2008;93(5):1526-1540. doi:10.1210/jc.2008-01 5. Elhassan YS, Alahdab F, Prete A, et al. Ann Intern Med. 2019;171(2):107-116. doi:10.7326/M18-3630 6. Di Dalmazi G, Vivennati V, Garelli S, et al. Lancet Diabetes Endocrinol. 2014;2(5):396-405. doi:10.1016/S2213-8587(13)70211-0.