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Hormonal Regulation and Hypertension / Pituitary Gland Disorders and Treatments / Adrenal Hormones and Disorders · Journal article
Diabetes Obesity and Metabolism · August 13, 2026
A consensus or society position rather than new primary data.
This is a clinical guidance document reviewing the epidemiology, diagnosis, and screening of hypercortisolism (including mild autonomous cortisol secretion) in Type 2 diabetes patients. The authors recommend targeted case-finding using a 1-mg overnight dexamethasone suppression test in high-risk phenotypes (resistant diabetes, resistant hypertension, adrenal incidentalomas) rather than universal screening, with confirmatory dexamethasone level ≥140 ng/dL.
Journal article. Patients with Type 2 diabetes, particularly those with resistant hyperglycaemia, severe insulin resistance, resistant hypertension, adrenal incidentalomas, or physical findings suggestive of cortisol excess..
Abnormal cortisol suppression following 1-mg overnight DST occurs more frequently in patients with difficult-to-control T2D and resistant hypertension than previously appreciated Overnight 1-mg DST is recommended as the preferred initial screening test because it is practical, inexpensive and widely available Interpretation supported by confirmatory dexamethasone level ≥140 ng/dL
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
Clinicians should adopt targeted screening for hypercortisolism in high-risk T2D phenotypes using the 1-mg overnight DST rather than screening all diabetic patients. Recognition of resistant cardiometabolic disease patterns may identify treatable cortisol excess and improve outcomes.
A narrative review synthesizing current evidence on hypercortisolism in Type 2 diabetes, recommending targeted case-finding strategy and DST screening approach rather than universal screening.
Quoted from the source exactly as published.
Clinicians should adopt targeted screening for hypercortisolism in high-risk T2D phenotypes using the 1-mg overnight DST rather than screening all diabetic patients. Recognition of resistant cardiometabolic disease patterns may identify treatable cortisol excess and improve outcomes.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
ABSTRACT Importance Hypercortisolism is an underdiagnosed contributor to metabolic dysfunction in people with Type 2 diabetes (T2D). Although overt Cushing syndrome is rare, milder forms of cortisol excess, commonly termed mild autonomous cortisol secretion (MACS), appear substantially more common in selected high‐risk populations. Observations Chronic cortisol excess contributes directly to insulin resistance, hepatic gluconeogenesis, visceral adiposity, hypertension, dyslipidaemia and cardiovascular disease. Many patients with hypercortisolism lack classic cushingoid features and instead present with resistant diabetes, resistant hypertension, obesity or progressive cardiometabolic disease. Emerging evidence suggests that abnormal cortisol suppression following a 1‐mg overnight dexamethasone suppression test (DST) occurs more frequently in patients with difficult‐to‐control T2D and resistant hypertension than previously appreciated. Current evidence supports a targeted case‐finding approach rather than universal screening. Patients most likely to benefit from evaluation include those with persistent hyperglycaemia despite intensive therapy, severe insulin resistance, resistant hypertension, adrenal incidentalomas or physical findings suggestive of cortisol excess. The overnight 1‐mg DST remains the preferred initial screening test because it is practical, inexpensive and widely available. Interpretation is supported by a confirmatory dexamethasone level ≥ 140 ng/dL and requires careful consideration of medication interactions, obesity, psychiatric disease, alcohol use, sleep disorders and assay variability. Conclusions and Relevance Hypercortisolism likely contributes to metabolic dysfunction in a subset of patients with T2D, particularly those with resistant cardiometabolic disease. Recognition of high‐risk phenotypes and appropriate use of the DST may improve identification of patients with potentially treatable cortisol excess. Additional prospective studies are needed to clarify optimal screening strategies and determine whether earlier diagnosis and treatment improve long‐term cardiometabolic outcomes.
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