Endocrine Abstracts

A 44 years old lady was reviewed by endocrinology team in January 2020 for weight gain, increased fat deposition around the neck, constant fatigue and decreased libido. She denied usage of exogenous steroids. She was normal BMI, normotensive and did not display signs of Cushing’s syndrome in first visit. Although overnight dexamethasone suppression was failed to suppress: cortisol of 141 nmol/l and ACTH 78 ng/l, Low dose dexamethasone suppression test (LDSST) was adequately suppressed with cortisol was 38nmol/l. The diagnosis of mild autonomous cortisol secretion (MACS) was made and regularly following up for cardiovascular risks. Unfortunately, she defaulted follow-up. She presented with worsening of fatigue, 15 kg weight gain and easy bruising skin one year later. She had purple striae in abdomen, increase dorso-cervical fat pad and proximal myopathy on examination. Her BMI was 36.8 kg/m2. She was diabetic with Hb A1c of 70 mmol/mol, hypertensive and sustained osteoporotic rib fracture. BMD reported osteopenia Potassium was normal with random cortisol 971 nmol/l. 24 h Urinary cortisol was > 1396. LDDST showed cortisol of 607 nmol/l with ACTH 290 ng/l. Pituitary profile showed secondary hypogonadism with low FSH, LH and oestradiol. Formal visual field reported as normal. MRI pituitary demonstrated 20x15mm adenoma with no chiasmatic compression. Metyropone was initiated and it was discussed in pituitary MDT. Transphenoidal hypophysectomy was performed. Histology confirmed corticotroph adenoma positive for ACTH and TPIT with Ki67 1-2%. Subsequently she developed panhypopituitism which requiring full pituitary hormone replacement. However, glycaemic control and quality of life have improved dramatically post operation. In conclusion, diagnosis of Cushing syndrome is always challenging as there is no single test or scan is absolutely sensitive and specific. Management of MACS should be individualised with close monitoring of cardiovascular risks and progression of Cushing syndrome