Hepatocellular injuries observed in patients with an eating disorder prior to nutritional treatment.

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.

[1]  K. Tsuneyama,et al.  A case report of oxidative stress in a patient with anorexia nervosa. , 2006, The International journal of eating disorders.

[2]  A. Tanaka,et al.  Severe steatosis resulted from anorexia nervosa leading to fatal hepatic failure , 2006, Journal of Gastroenterology.

[3]  F. Contaldo,et al.  Severe acute liver damage in anorexia nervosa: two case reports. , 2006, Nutrition.

[4]  A. Klibanski,et al.  Medical findings in outpatients with anorexia nervosa. , 2005, Archives of internal medicine.

[5]  N. Paquot,et al.  Fatty liver in the intensive care unit , 2005, Current opinion in clinical nutrition and metabolic care.

[6]  L. Caregaro,et al.  Acute liver damage in anorexia nervosa. , 2004, The International journal of eating disorders.

[7]  J. Yaryura-Tobias,et al.  Anorexia nervosa, diabetes mellitus, brain atrophy, and fatty liver. , 2001, The International journal of eating disorders.

[8]  S. Furuta,et al.  Anorexia nervosa with severe liver dysfunction and subsequent critical complications. , 1999, Internal medicine.

[9]  Y. Shishiba,et al.  Elevation of serum aminotransferase as a sign of multiorgan-disorders in severely emaciated anorexia nervosa. , 1998, Internal medicine.

[10]  安二 中沼,et al.  神経因性食欲不振症の経過中, 著明な肝腫大を呈し, 肝不全にて死亡したnonalcoholic steatohepatitisの1例 , 1997 .

[11]  P. Holt,et al.  Hepatobiliary complications of total parenteral nutrition. , 1994, Journal of clinical gastroenterology.

[12]  J. Rabe-Jabłońska,et al.  [Affective disorders in the fourth edition of the classification of mental disorders prepared by the American Psychiatric Association -- diagnostic and statistical manual of mental disorders]. , 1993, Psychiatria polska.