Case Report
A woman in her 50s underwent a CT scan at a nearby hospital to investigate treatment-resistant hypertension and was found to have a left adrenal mass. Her blood test showed low ACTH and Cushing’s syndrome was suspected, so she was referred to the endocrinology department of our hospital. She was diagnosed with adrenal Cushing’s syndrome but was referred to our department because she was found to be HCV antibody positive. There is nothing special to note about her medical or family history. She had never smoked and drank very little. Her physical findings on admission were 164.5 cm tall, 92.6 kg in weight, and a BMI of 34.2 kg/m2. Her blood pressure was 179 / 73 mmHg, pulse 64 /min (rhythmic), body temperature 36.8°C, and respiratory rate 12 /min. She had findings of central obesity, moon face, buffalo hump, and red skin stretch marks. Her blood test findings (Table 1) showed an increase in ALT, HCV antibody positivity, and an HCV RNA concentration of 4.1 log IU/ml. The virus was genotype 2. Cortisol was within the reference range but ACTH was as low, less than 1.5 pg/ml. Her bedtime cortisol level was 7.07 μg/dl, which was above her reference of 5 μg/dl, suggesting the loss of diurnal variation in cortisol secretion. In an overnight low-dose dexamethasone suppression test, cortisol after loading was 6.61 μg/dl, which exceeded 5 μg/dl, suggesting that cortisol was autonomously secreted. Her contrast-enhanced CT scan (Fig. 1) revealed a tumor with a major axis of about 30 mm in her left adrenal gland. MRI scans showed mild hyperintensity in the “in phase” (Fig. 2a) and decreased signal in the “out of phase” (Fig. 2b), suggesting her adrenal mass was an adenoma. Based on the above test results, she was diagnosed with chronic hepatitis C and adrenal Cushing’s syndrome. She agreed to receive treatment with direct acting antiviral agents (DAAs) after resection of the left adrenal tumor. However, two months later, she had liver dysfunction with AST 116 U/L and ALT 213 U/L (Fig. 3). Because the HCV RNA concentration had increased to 6.4 logIU/mL, she was suspected to have an acute exacerbation of chronic hepatitis C and underwent percutaneous liver biopsy. The biopsy revealed an inflammatory cell infiltration, mostly composed of lymphocytes and plasma cells and mainly in the portal vein area (Fig. 4). Fibrosis and interface hepatitis also were observed and spotty necrosis was evident in the hepatic lobule. No clear fat deposits were found in the hepatocytes, ruling out NASH or NAFLD. According to the New Inuyama classification, hepatitis equivalent to A2-3 / F1-2 was considered. Because HBV DNA was not detected, no new drug was used and no cause of liver damage, such as biliary atresia, was found; the patient was diagnosed with liver damage due to reactivation of HCV, with acute exacerbation of chronic hepatitis C. The treatment policy was changed, in order to treat hepatitis C before the left adrenal resection, and administration of Glecaprevir / Pibrentasvir was started. A blood test two weeks after the start of treatment confirmed normalization of AST and ALT, and a rapid virological response was achieved (Fig. 3). Subsequently, HCV RNA remained negative, no liver damage was observed, and laparoscopic left adrenectomy was safely performed nine months after the initial diagnosis. The pathological findings were adrenal adenoma. After the operation, hypertension improved and weight loss was obtained (92.6 kg (BMI: 34.2 kg/m2) before the operation, but 77.0 kg (BMI: 28.5 kg/m2) one year after the operation). ACTH increased, and the adrenal Cushing’s syndrome was considered to have been cured. Regarding HCV infection, the sustained virological response has been maintained to date, more than two years after the completion of DAA therapy, and the follow-up continues.