Abstract
IntroductionLiver injury is a frequent complication associated with anorexia nervosa, and steatosis of the liver is thought to be the major underlying pathology. However, acute hepatic failure with transaminase levels over 1000 IU/mL and deep coma are very rare complications and the mechanism of pathogenesis is largely unknown.Case presentationA 37-year-old Japanese woman showed features of acute liver failure and hepatic coma which were not associated with hypoglycemia or hyper-ammonemia. Our patient's consciousness was significantly improved with the recovery of liver function and normalization of transaminase levels after administration of nutritional support.ConclusionsOur case report demonstrates that transaminase levels had an inverse relationship with the consciousness of our patient, although the pathogenesis of coma remains largely unknown. This indicates that transaminase levels can be one of the key predictors of impending coma in patients with anorexia nervosa. Therefore, frequent monitoring of transaminase levels combined with rigorous treatment of the underlying nutritional deficiency and psychiatric disorder are necessary to prevent this severe complication.
Highlights
Liver injury is a frequent complication associated with anorexia nervosa, and steatosis of the liver is thought to be the major underlying pathology
Our case report demonstrates that transaminase levels had an inverse relationship with the consciousness of our patient, the pathogenesis of coma remains largely unknown
This indicates that transaminase levels can be one of the key predictors of impending coma in patients with anorexia nervosa
Summary
Our case report of a patient with AN and high transaminase levels in a deep coma indicates that severe starvationinduced hepatocyte autophagy and apoptosis may lead to a diagnosis of acute liver failure. We hypothesize that patients with AN and mild liver dysfunction may develop lower degrees of encephalopathy that may escape routine detection. It is important to note that the severe hepatitis and encephalopathy observed in our patient were completely reversed after institution of appropriate parenteral and enteral nutrition. Author details 1Department of Gastroenterology, Internal Medicine, TMG Asakadai Central General Hospital, Saitama 351-8551, Japan. Authors’ contributions SY and MS contributed to the management of the patient and the researching for and writing of this manuscript. All authors read and approved the final manuscript.
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