Endocrine Abstracts

A 29yrs lady presented to endocrinology clinic with 2-3 stone weight gain over a 3 year period which was central in nature, associated with rounding of her face, muscle weakness, fatigue and ease of bruising. She was plethoric and had a number of violaceous striae since age 22yrs suggesting her Cushing’s syndrome was long-standing. Her past history included renal calculi, liver focal nodular hyperplasia and hidradenitis suppurativa. Initial investigations showed LH 5.5iu/l, FSH 6.9iu/l, testosterone 1.9nmol/l, HbA1c 43mmol/mol; ODST on two occasions showed 9am cortisol 491nmol/land 530nmol/L; Urinary free cortisol 339 (>147) nmol/d. ACTH was raised on two occasions. A diagnosis of ACTH-dependent Cushing’s syndrome was made. MRI pituitary showed minor asymmetry with no discreet nodule but suggestion the left aspect of the gland was larger. High-resolution MRI suggested a focal area of hypoenhancement within the midline anterior superior aspect of the adenohypophysis. IPSS confirmed a pituitary source with lateralised to the left. She was commenced on metyrapone whilst awaiting surgery. During pre-assessment she was diagnosed with severe OSA and was commenced on CPAP. Metyrapone was discontinued on the day endonasal transphenoidal resection. Histology confirmed an ACTH-secreting adenoma. Ki67: 14% with scattered p53 positivity in <5% of cells. The surgery was undertaken in the morning and by the evening she complained of dysuria. Bladder scan showed 500ml of urine. She was catheterised and her urine output in the following hour was >1500ml. Paired blood and urine samples showed serum sodium 142mmol/l, creatinine 60umol/l, serum osmolality 294mOsmol/kg and urine osmolality 168mOsmol/kg. Input-output monitoring was undertaken. She was reviewed by the endocrine team when she complained of thirst and passing clear urine. Serum sodium was 154mmol/l and I/O in 12 hours was 6550/4040. Repeated urine osmolality was 42mOsmol/kg and serum osmolality 314mOsmol/kg. A diagnosis of likely AVP-deficiency was made. Her sodium improved to 147mmol/lon IV fluids to compensate for the urinary loss. She received 50 mg desmopressin orally. Six hours after desmopressin her sodium level improved to 144mmol/laccompanied by reduction in thirst, urine output and sodium levels stabilised without further desmopressin. She was commenced on parenteral then converted to oral hydrocortisone post-operatively, as per protocol. Day 2 post-op 9am cortisol was 53nmol/l indicating surgical success. She was discharged on maintenance hydrocortisone and enoxaparin prophylaxis for a period of 6 weeks. Her hydrocortisone dose was doubled at her day 7 follow up as she had adrenal insufficiency symptoms.