Endocrine Abstracts

Diagnostic work-up for Cushing Syndrome (CS) can be challenging and is based on clinical and biochemical assessment. Biochemical evidence of endogenous steroid excess is demonstrated through overnight dexamethasone suppression test (ODST), low dose dexamethasone suppression test and/or 24-hour urinary free cortisol estimation (UFC). Once endogenous steroid excess is confirmed, random serum ACTH measurement is key in determining the suspected source of steroid excess: ACTH-independent (adrenal cause) or ACTH-dependent Cushing (pituitary or ectopic ACTH secretion). We report a case of CS where the serum ACTH caused diagnostic confusion during work-up for adrenal incidentalomas. 55-year-old female with history of Type II diabetes mellitus, Hypertension, psychosis and Ischaemic heart disease was seen for an incidental finding of Left adrenal mass. She was on medication for ischemic heart disease, diabetes, arthritis and centrally acting drugs in the form of Quetiapine, gabapentin, Duloxetine. She was seen 5 years back at another hospital for same and discharged labelled as normal hormonal work up. She reported Ongoing weight gain, Excessive hair growth and she had Cushingoid features Flushed face, thinning of skin, abdominal striae, Central adiposity, Proximal myopathy and diabetes was poorly controlled despite been on insulin. Her Random ACTH were 13 and 17. Her cortisol didn’t suppress on Low dose and high dose dexamethasone suppression test. Her urinary steroid profile was supportive of Cushing’s. The reason for ACTH not being fully suppressed was unclear. We reviewed imaging in MDT and it was found that there was Left adrenal adenoma which was static in size but there was hyperplasia of right adrenal on retrospective review. DDAVP was positive with Increase in ACTH and cortisol. MRI pituitary was discussed in MDT and there was debate whether it is normal or there is small adenoma. IPSS was positive with lateralization to one side confirming pituitary Cushing. ACTH was low despite being pituitary Cushing likely due to centrally acting drugs. This leads to discussion around the Cushing’s work-up in patients presenting through the adrenal incidentaloma pathway:

• Clinical assessment of pretest probability is very important

• ACTH levels and Dex suppression testing should be interpreted carefully

• We should take into consideration centrally-acting drugs

• Review CT adrenals in MDT – is the ‘normal’ adrenal normal looking?