Abstract
Insulin resistance is central to the pathogenesis of NASH and is also frequently observed in patients with depression. A 32-year-old woman began treatment for a major depressive disorder when she was 27. She was mildly obese (BMI of 26.7 kg/m^2) and had hypertriglycemia (406 mg/dl) and normal fasting plasma glucose value. Mild elevation of serum levels of transaminases (AST, 32 IU/l; ALT, 32 IU/l) was detected. Both hepatitis B surface antigen and anti-hepatitis C virus antibody were seronegative. Abdominal ultrasonography showed typical fatty liver. She had not been drinking alcohol. Her depression was treated with tricyclic antidepressants, an anti-anxiety drug, levomepromazine and a hypnotic. Her depressive symptoms gradually improved and she was able to begin working after two years. Her serum levels of transaminases has been remained within normal limits. After 5 years, her depression was aggravated by life events (marital conflict and her sister's diagnosis of and surgery for a brain tumor). She also gained weight (BMI of 30.2 kg/m^2) because of stress-related overeating. Her serum levels of transaminases increased (AST, 174 IU/l; ALT, 183 IU/l). She was referred to the Department of Gastroenterology, and a liver biopsy was performed. Liver specimens showed macrovesicular steatosis (>30% hepatocytes), hepatocellular ballooning, pericellular and perivenular fibrosis, and Mallory bodies, and she was diagnosed as having NASH. She was negative for antinuclear antibody. Although a 75 g oral glucose tolerance test showed a normal glucose profile, hyperinsulinemia and insulin resistance (homeostasis model assessment index: 2.28) were found. Treatment with pioglitazone (30 mg daily) resulted in normalization of serum aminotransferase levels. Aggravation of depression, which was induced by stressful life events, might have been a factor in the development of steatohepatitis from fatty liver in this case.
