Endocrine Abstracts

72 year old male has an incidental left adrenal lesion which was picked up by the ultrasound scan in 2014 for the flank pain. His medical background includes type2 Diabetes-Mellitus, hypertension, aortic stenosis, hypogonadotropic hypogonadism, well controlled asthma and sleep apnoea using CPAP. His Adrenal CT (late 2014) has shown pre-contrast of 4HU, portal-phase 20HU, and delayed-phase-18HU. His MRI adrenals showed fat rich left side 3 cm adrenal adenoma with stable appearances over a 13 month period. His biochemical profile is interesting as it showed probable hypercortisolism with the background of Type2 Diabetes-Mellitus. Clinically, he has central obesity, no striae in abdomen with BMI of 37. His serial 24 hour UFCs were showing variable results from 66 to 258nmol/24hour (Ref-0- 146nmol/24 hour). His ACTH levels were between 7-23 ng/l(Ref <50ng/l). His late night salivary cortisol levels were between 0.9-15nmol/l (Ref 20:00-22:00 <8nmol/l, 22:00-23:59 <4.3nmol/l. He failed OSDT with cortisol level of 126nmol/l and LDDST with cortisol level of 73, 105 and 113nmol/l respectively on three occasions. The cortisol day profile showed 9am-443, 11am-440, 1pm-366, 3pm-337, 5pm-276, 7pm-267, 9pm-261, midnight (awake)-204 and 224 (units–nmol/l). His recent tests showed testosterone level of 6.8nmol/l, LH-3.5mU/l, FSH-1.6mU/l, TSH-2.79mU/l, IGF-1 30.3mU/l, prolactin-96mU/l, DHEA 1.1umol/l, Hba1c 68mmol/mol and normal electrolytes. His HbA1c has deteriorated over the years. All his biochemical tests showed a like-hood of cortisol excess. As it is favouring to ACTH dependent, CT TAP was done but no show of ectopic tumours. Interestingly, the patient’s MRI pituitary showed a three millimetre left sided pituitary micro-adenoma. His blood pressure is controlled with Lisinopril and furosemide. He has a normal bone density scan result. This patient remains clinically well during the COVID period and he was followed up with a telephone appointment. His results continue to show a picture of mild hypercortisolism. The underlying cause for his Cushing Syndrome has not been identified. Adrenal autonomy was initially considered a possible aetiology after the identification of the left adrenal adenoma. However, the more recent ACTH levels would raise the possibility of a pituitary (or ectopic) origin. At this moment, we planned for him to optimise his diabetes control and repeat UFCs, late-night salivary cortisol and the day cortisol profile. This will be followed by CRH stimulation test if the above test results continue to show hypercortisolemia. The aetiology of cortisol excess remains unclear till the last clinic appointment.