Endocrine Abstracts

Objective: Functional hypercortisolism associated with alcohol abuse is an infrequently diagnosed entity of unknown prevalence. Ethanol elicits hypothalamic oversecretion of CRH with subsequent increase in ACTH and cortisol. It may simulate Cushing’s disease both clinically and biochemically but there are no anatomic lesions and the diagnosis is confirmed by normalization of the biochemical pattern after at least 1 month of abstinence from alcohol. We hereby report a clinical case in order to increase the awareness of alcohol-induced functional hypercortisolism.

Methods: Review of the patient’s record and of the relevant literature

Clinical Case: A male, 43-year-old patient was referred to our Endocrinology Clinic with suspected Cushing’s syndrome, because of the typical phenotype, with central obesity and proximal muscle atrophy, round face, interscapular fat pad, violaceous striae and ecchymosis. These signs had appeared gradually during the last 5-8 years but in the last few months he complained of progressive incapacitating asthenia. The patient showed borderline central obesity (BMI 29.4 kg/m²), with enlarged liver without palpable lumps, high blood pressure (154/92 mmHg) and inability to stand up from the sitting position without arm support Lab tests; Routine normal except fasting glucose 112 mg/dl, HbA1c 6.2%, triglycerides 368 mg/dl, AST 124 U/l, ALT 98 U/l, GGT 169 U/l, cyanocobalamin <137 pg/ml, folate 2.1 ng/ml, MCV 102 fL, platelets 127000/mm³, FIB-4 index 4.73. Hormones: Normal except ACTH 57.2 pg/ml, fasting cortisol after 1 mg dexamethasone suppression 18.1 µg/dl; 24-hour cortisol excretion 211 µg. After 14 days the results were similar (61.4 pg/ml, 21.8 µg/dl, 198 µg respectively). Abdominal ultrasonography: hepatomegaly and intense steatosis without nodules: both adrenals were normal. Pituitary MRI was normal. Thoracic/abdominal CT showed no additional findings Petrosal sinus sampling was scheduled but then the patient revealed alcohol abuse for the last 10 years, with usual daily intake of half a liter of rum plus variable amounts of beer, wine and other spirits. The patient was encouraged to abstain from alcohol and treated with vitamin B complex supplements. After 3 months, the Cushing phenotype was largely reversed, the patient could stand up easily, and the biochemical profile was normal (cortisol 1.4 µg/dl after dexamethasone, excretion 32 µg, fasting ACTH 26 pg/ml).

Conclusions: This case illustrates a probably underdiagnosed entity. Alcohol abuse may go unreported and patients may remain in a diagnostic quagmire. When hypercortisolism is unexplained, functional causes such as alcohol abuse, major depression, chronic emotional stress, etc. must be ruled out.