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Endocrine Abstracts (2026) 117 P7 | DOI: 10.1530/endoabs.117.P7

SFEBES2026 Poster Presentations Adrenal and Cardiovascular (54 abstracts)

Adrenal adenomata displaying mild autonomous cortisol secretion:a service evaluation of cardiometabolic profile routinely screened patients

Adrian Heald 1,2 , Callum Stables 1,2 , Sarah Jamil 2 , Waseem Majeed 1,2 , Sangeeth Veluchamy 2 , Rupinder Kochchar 2 , Akheel Syed 1,2 , Rajshekhar Mudaliar 2 , Fahmy Hannah 3 , David Marshall 4 , Ian Laing 5 , Anthony Fryer 6 , Yasitha Illangasekera 7,8 , Adhithya Sankar 1,2 & Brian Keevil 4


1University of Manchester, Manchester, United Kingdom; 2Salford Royal Hospital, Salford, United Kingdom; 3University Hospital North Midland, Stoke on-Trent, United Kingdom; 4Wythenshaw Hospital, Manchester, United Kingdom; 5Royal Preston Hospitak, Preston, United Kingdom; 6Keele University, Keele, United Kingdom; 7Sheffield Hallam University, Sheffield, United Kingdom; 8University of Peradeniya, Peradeniya, Sri Lanka


Introduction: The increasing use of high-resolution imaging has led to rising detection of adrenal incidentalomas (AIs), with a proportion of these exhibiting autonomous cortisol secretion, now termed Mild Autonomous Cortisol Secretion (MACS), is defined biochemically by a post-1 mg overnight dexamethasone suppression test(ONDST) cortisol between 51 and 137nmol/l with some variation in relation to assay platforms. Our primary objective was to identify the group of individuals with adrenal adenomata and associated MACS, and comprehensively to characterize their cardiometabolic profile

Methods: We undertook service evaluation of the cardiometabolic profile of adrenal adenomata presenting over a period of 3-years at a single centre. All subsequently evaluated had a 0900 post-midnight dexamethasone of >50 nmol/l which was deemed a ‘fail’ on basis of ONDST serum cortisol level on our assay. A subcategorization into MACS1 (ONDST cortisol of 50-137nmol/l) and MACS2 (ONDST cortisol of >1387nmol/l was created to take account of those individuals with ONDST cortisol of >137nmol/l and no diagnosis of Cushing’s syndrome. on subsequent evaluation.

Results: The diagnosis of MACS1 was associated with a higher diagnosis rate of cardiovascular disease (CVD) (17.7% in MACS 1) vs non-MACS = non-functioning adenoma (NFA) (3.7%)(P = 0.009) and higher rates of prescription of lipid lowering agents (51.6%) vs (29.6%) (P = 0.01). ONDST cortisol levels in MACS1 patients correlated with a more adverse lipid profile (for higher LDL-cholesterol r2=0.404, P = 0.007; HDL-cholesterol r2 =-0.346, P = 0.023 for; for higher serum triglycerides r2=0.282, P = 0.02) in spite of higher rates of statin prescribing. Dunn’s post hoc analysis indicated an overall more adverse lipid profile in MACS1.

Conclusion: The positive direction of association observed between serum cortisol and lipid measures, highlights that MACS carries a metabolically adverse lipid profile. The question remains as to whether a specific directed treatment of MACS should be offered over and above risk factor mitigating management.

Volume 117

Society for Endocrinology BES 2026

Harrogate, United Kingdom
02 Mar 2026 - 04 Mar 2026

Society for Endocrinology 

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