50 The Korean Journal of Internal Medicine : Vol. 23, No. 1, March 2008 Figure 1. There is no obvious Cushingoid features such as hirsuitism, acne or a moon face. CASE REPORT A 39-year-old woman had been previously diagnosed with endometrial hyperplasia and hypertension, and she was referred to our department for further evaluation and management of persistent menometrorrhagia despite being treated with progestin and ten dilatation and curettage procedures in 2 years. Her past medical history was negative for diabetes mellitus, but positive for hypertension. She had been treated with antihypertensive medication for 2 years, but her blood pressure control was not satisfactory. The patient had gained 7 kg in body weight over the past 4 years. The patient had delivered two children vaginally without complication, at the ages of 25 and 28, respectively, and she had a negative history of spontaneous or elective abortion. She was a former nurse and denied using alcohol. At the time of her referral, her blood pressure was 155/92 mmHg. She presented with mild central obesity (waist to hip ratio, 0.90); her weight was 60 kg, and her BMI was 22.9 kg/m2. No violet striae, proximal myopathy, hirsutism or acne were observed, but minor bruising was present on her forearm (Figure 1). Her hormone levels during the early follicular phase, which had been determined 2 years earlier upon a previous visit to a local clinic for abnormal uterine bleeding prior to her referral, were LH: 3.2 mIU/mL (normal range: 2.0-15.0 mIU/mL), FSH: 6.6 mIU/mL (3.0-20.0 mIU/mL), estrone (E1): 15.0 pg/mL (1.5-15.0 pg/mL) and estradiol (E2): 6.3 pg/mL (20.0-145.0 pg/mL). However, her progesterone level was very low at 0.2 Figure 2. An adrenal CT scan of patient shows a 3.1-cm sized well-marginated mass in the left adrenal gland (arrows). ng/mL (3.0-20.0 ng/mL), suggesting chronic anovulation and dysfunctional uterine bleeding. At that time, the results of a thyroid function test, a prolactin level test, a liver function test and the platelet count were all within normal ranges. Other biochemical laboratory tests gave the following results: protein, 7.1 g/dL (6.0-8.1 g/dL), albumin: 4.2 g/dL (3.2-5.3 g/dL), cholesterol: 149 mg/dL (120-220 mg/dL), LDL-cholesterol: 100 mg/dL (0-130 mg/dL), HDL-cholesterol: 45mg/dL (35-80 mg/dL), triglyceride: 79 mg/dL (35-200 mg/dL), alkaline phosphatase: 66 IU/L (39-120 IU/L) and creatinine: 0.9 mg/dL (0.5-1.1 mg/dL). An oral glucose tolerance test indicated impaired glucose tolerance (fasting glucose: 74 mg/dL, 2-h: 187 mg/dL). Ultrasonography showed a 15.6 mm thickness of the endometrium. Endometrial biopsy revealed simple endometrial hyperplasia without atypia. Ultrasonography revealed a 2.5 cm size simple cyst on the left ovary; otherwise, the architecture of both ovaries was normal. Although she did not present with the typical features of Cushing's syndrome, we ordered laboratory tests for cortisol and ACTH as well as the sex hormone, gonadotropin and prolactin levels to investigate the cause of her chronic anovulation and the persistent menstrual irregularity. The results were 24-h urine free cortisol: 454.5 μg/24h (20.0-70.0 μg/24h), serum ACTH: 2.0 pg/dL (6.0-76.0 pg/dL) and midnight serum cortisol: 15.3 g/dL (0-10.0 μg/dL); this all suggested hypercortisolemia and loss of the circadian rhythm. The 24-h urine free estrone and free estradiol levels were 3.3 g/24h (2.0-39.0 μg/24h) and 1.9 μ g/24h (1.0-23.0 μg/24h), respectively. The E1/E2 ratio was elevated in the serum and urine (2.4 and 1.7, respectively). The serum testosterone was below the detectable range of 0.10 ng/mL. A CT scan revealed a 3.1-cm, hyperechoic, well-