Endocrine Abstracts

Exposure to supraphysiologic doses of exogenous glucocorticoids is associated with gastrointestinal (GI) complications such as peptic ulcer disease, gastrointestinal hemorrhage, duodenal ulcer, and colonic diverticular perforation (DP). Patients receiving high dose glucocorticoids, for rheumatological or autoimmune disease are at increased risk for lower gastrointestinal tract abscesses and perforation. However, little is known about GI complications in endogenous hypercortisolism caused by Cushing syndrome (CS). Here we present a case with Cushing Disease (CD) who developed sudden diverticular perforation (DP) that necessitated surgical intervention. 29 years old female patient was first admitted to outpatient clinic with symptoms of weight gain, edema, weakness, easy bruising, wide purplish stria, hirsutism and skin atrophy. There was history of refractory hypertension, diabetes mellitus,heart failure, asthma bronchiale and menstrual irregularity. She was married and had two children. On presentation the patient had a blood pressure of 190/95 mmHg and a potassium level of 2.6 meq/L. Her physical exam was significant for a moon and plethoric face, dorsocervical fat pad, abdominal obesity and skin thinning with several large areas of ecchymosis. Biochemical evaluation confirmed severe hypercortisolism: Cortisole: 25.13 μg/dl, 1 mg dexamethason suppression test (DST): 24.9 μg/dl, 2 day 2 mg DST: 19 μg/dl, ACTH- 210 pg/ml, 24-hour urinary free cortisol (UFC) 690 mg, diurnal rhythm was disturbed midnight 0300 h cortisole: 20 μg/dl. MRI of the pituitary showed an area of 5 mm in the left lobe of the pituitary that had decreased uptake of contrast on early dynamic screening. Transphenoidal hypophysectomy was performed and ACTH secreting adenoma (Kİ67: <%1) was found on pathological examination. While she was being followed with symptoms due to diabetes insipidus and hypokalemia, 15 days following surgery, the patient also developed symptoms of abdominal pain and vomiting. Laparotomy revealed an intra-abdominal abscess and extensive colonic diverticulitis with evidence of perforation at the ascending colon. Right hemicolectomy with colostomy was performed and pathological specimen revealed diverticular disease complicated with supurative inflammation, diverticulitis, multiple intraabdominal abscesses. This case illustrates the potential for fulminant diverticular disease complications in patients with Cushing’s disease. Multiple elements contribute to the increased risk of diverticular perforation in association with hypercortisolism. Surgeons and endocrinologists should be aware of this potentially fatal complication when caring for patients with Cushing’s disease. When treating such patients, this risk should be eliminated through management of malnutrition, uremia, hypokalemia, constipation, early detection and aggressive management of diverticulitis and DP.