Endocrine Abstracts

Introduction

The most common causes of pseudo Cushing syndrome are alcoholism, chronic kidney disease, neuropsychiatric diseases, pregnancy, uncontrolled diabetes, and drugs. We present a patient who was operated on suspected Cushing syndrome based on abnormal results in overnight dexamethasone suppression tests.

Case presentation

A 49-year-old female patient was referred to our clinic for reoperation due to persistant cushing syndrome after first pituitary surgery in another center. Cortisol had been found to be 10.2 µg/dl after overnight 1 mg dexamethasone suppression test (DST) performed in aforementioned center with suspicion of cushing syndrome in the patient with type 2 diabetes mellitus and obesity. Basal morning ACTH and cortisol had been found 44 pg/ml and 12.7 µg/dl respectively. The cortisol response to 48-h, 2 mg/day low-dose DST was 6.24 µg/dl. 24-h urinary free cortisol (UFC) had beenfound to be normal. Heterogeneous contrast enhancement was observed in the right half of the pituitary gland, and no mass lesion had been detected in pituitary magnetic resonance imaging, . She was diagnosed with bilateral cushing disease in inferior petrosal sinus sampling and operated. On the first postoperative day morning cortisol was 14 µg/dl. At the 3rd month control, the cortisol levels after 1 mg DST was 4.4 µg/dl. The patient was referred to our clinic with the diagnosis of persistant cushing disease. Beside facial plethorea and abdominal obesity (body mass index 41.2 kg/m²) her physical examination was unremarkable. Past medical history revealed carbamazepine use for 10 years due to epilepsy. Recurrent tests performed in our clinic showed that, midnight serum cortisol was 1.79 µg/dl, and 24-hour UFC was 150 µg/day (43-403). No pathological signal change was observed in the control pituitary MRI. When the pathological specimens were re-evaluated in the pathology department no adenoma was identified, it was observed that the normal reticulin structure was preserved, Ki67 proliferation index was < 1%, and diffuse strong cytoplasmic staining was observed with GH, ACTH and PRL. Telangiectasias of the face were evaluated in favor of rosacea disease by the dermatology clinic. We concluded that there was no clinical evidence of Cushing’s syndrome and that failed dexamethasone suppression tests were due to the effect of carbamazepine.

Conclusion

Some drugs such as carbamazepine induce CYP3A4 activity and may lead to false positive dexamethasone suppression test results. The results must be properly evaluated to avoid misdiagnosis.