BACKGROUND/AIMS: Although hepatocellular injuries are occasionally observed in patients with an eating disorder, such as anorexia nervosa (AN), it remains unclear how malnutrition in patients with AN causes hepatocellular damage. In this retrospective study, we aimed to reveal the characteristics of hepatocellular injuries in patients with an eating disorder without any nutritional treatment, to eliminate the possible hepatotoxic effects of nutritional support. SUBJECTS AND METHODS: Twenty-five patients with an eating disorder who visited St. Luke's International Hospital were enrolled. No nutritional treatment had been performed for these patients. The diagnosis of eating disorder as well as typing (anorexia nervosa or bulimia nervosa) was made according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-4). We reviewed the charts of these patients and examined the clinical parameters. RESULTS: Elevation of serum alanine aminotransferase (ALT) was found in 13 out of 25 (52%), all of whom were categorized as AN. In 13 AN patients with elevated ALT, the median of serum ALT values was 92 [39-438] IU/L. The body mass index (BMI) was significantly lower (13.5 vs. 17.3, p=0.011), and the duration since the onset of AN was shorter (4.2 years vs. 8.9 years, p=0.037) in patients with elevated ALT. The age was younger in patients with elevated ALT, even though not significant (24.5 vs. 29.8, p=0.139). Logistic regression analysis revealed that only BMI was a significant determinant for the development of hepatocellular injuries (OR=3.46; 95% CI 1.06-11.34, p=0.041). Imaging studies failed to demonstrate any abnormalities, including fatty liver. CONCLUSION: The current study indicated that lower BMI might significantly contribute to the development of hepatocellular injuries in AN patients prior to any nutritional treatments.
BACKGROUND/AIMS: Although hepatocellular injuries are occasionally observed in patients with an eating disorder, such as anorexia nervosa (AN), it remains unclear how malnutrition in patients with AN causes hepatocellular damage. In this retrospective study, we aimed to reveal the characteristics of hepatocellular injuries in patients with an eating disorder without any nutritional treatment, to eliminate the possible hepatotoxic effects of nutritional support. SUBJECTS AND METHODS: Twenty-five patients with an eating disorder who visited St. Luke's International Hospital were enrolled. No nutritional treatment had been performed for these patients. The diagnosis of eating disorder as well as typing (anorexia nervosa or bulimia nervosa) was made according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-4). We reviewed the charts of these patients and examined the clinical parameters. RESULTS: Elevation of serum alanine aminotransferase (ALT) was found in 13 out of 25 (52%), all of whom were categorized as AN. In 13 AN patients with elevated ALT, the median of serum ALT values was 92 [39-438] IU/L. The body mass index (BMI) was significantly lower (13.5 vs. 17.3, p=0.011), and the duration since the onset of AN was shorter (4.2 years vs. 8.9 years, p=0.037) in patients with elevated ALT. The age was younger in patients with elevated ALT, even though not significant (24.5 vs. 29.8, p=0.139). Logistic regression analysis revealed that only BMI was a significant determinant for the development of hepatocellular injuries (OR=3.46; 95% CI 1.06-11.34, p=0.041). Imaging studies failed to demonstrate any abnormalities, including fatty liver. CONCLUSION: The current study indicated that lower BMI might significantly contribute to the development of hepatocellular injuries in AN patients prior to any nutritional treatments.