Cushing syndrome in patient with thyroid orbitopathy (case report)
Peter Vanuga, Michal Kulich & Dusan Pavai
Authors present a 35-year-old female with thyroid orbitopathy (EO) associated with Graves disease. After initial antithyroid therapy, thyroidectomy was indicated and performed uneventenfully. Due to persisting severe clinically active EO, thyroablative therapy with 131I was performed three years later, intravenous pulse of methylprednisolone was given and consecutive oral therapy with prednisone initiated. This caused weight gain (from 63 to 80 kg) and iatrogenic Cushing syndrome. Afterwards, prednisone was changed to cyclophosphamide. After initial decrease of body weight, we noticed repeated weight gain (from 76 to 91 kg). Patient underwent an laparoscopic cholecystectomy for biliary colic. This was complicated by haemorrhage and computer tomography (CT) was performed postoperatively. CT study showed a hypodense expansion originating from the medial limb of left adrenal gland (30 mm in diameter), indicating investigations of the adrenal hormonal status. Renin and aldosterone in saline infusion test (6.40…3.40 IU/l, and 0.28…0.14 nmol/l, respectively) and metanephrine and normetanephrine in clonidine test (0.156…0.241…0.145 nmol/l, respectively 0.332…0.738…0.224 nmol/l) were normal. Surprisingly, elevated levels of urinary free cortisol (UFC) (653…833 nmol/day, normal values 20-220 nmol/day) were found. These findings were confirmed by loss of diurnal variation of serum cortisol (FP at 8 AM 559 nmol/l, FP at 12 PM 578 nmol/l), supressed ACTH values (4.8…2.3 pg/ml) and lack of supression of FP and UFC in 2 mg and 8 mg dexamethasone tests (FP 650 nmol/l, and 621 nmol/l, UFC 888 nmol/day, and 1018 nmol/day). Macroscopically, an ochre tumor was found at laparoscopic adrenalectomy, confirmed by histological finding of a cortical adenoma.