Severe acute liver damage in anorexia nervosa: two case reports

Abstract

Objective

Two female patients (18 and 30 y old, body mass indexes 14.1 and 13.2 kg/m²) with severe, restrictive anorexia nervosa developed sudden severe liver damage. In addition to overt protein-energy malnutrition, they showed marked hypotension, bradycardia, dry skin, acrocyanosis, and hypothermia. Most common causes of liver failure, such as hepatotropic viruses, hepatotoxic drugs, alcohol, cannabis, and cocaine abuse, were excluded.

Methods

Therapeutic intervention consisted of immediate plasma volume support, progressive parenteral or oral nutritional rehabilitation, and parenteral potassium and phosphorus supplements to avoid the refeeding syndrome.

Results and conclusion

Improvement of initial clinical symptoms and rapid recovery of liver enzymes after this type of treatment suggest that severe liver damage in anorexia nervosa may be secondary to acute hypoperfusion.

Introduction

Several studies have described an increase in serum liver enzymes in severely malnourished patients who are affected by anorexia nervosa (AN) [1], [2], [3], [4] and in the refeeding phase of therapeutic intervention [5]. In the case of anorectic patients, the slight to moderate increase in liver enzymes is expected to reflect a fatty liver that is typical of several protein-energy malnutrition states [6], [7], [8]. In these clinical circumstances, hepatic steatosis may well be a consequence of an unbalance between hepatic triacylglycerol synthesis and secretion, with decreased lipoprotein synthesis, due to decreased amino acid availability [9]. The few liver biopsies available from patients with AN, who generally present with a marked increase in liver enzymes, show moderate periportal inflammatory infiltrates, hepatocyte ballooning, (massive) fatty liver, and increased glycogen deposits [10], [11], [12], [13], [14], [15].

Nevertheless, very few cases of acute liver failure in AN have been described [10], [12], [16], [17]. Aside from malnutrition, several pathogenetic factors have been considered to justify the shift from normal or slightly increased serum liver enzymes to acute complications such as hepatotropic viruses (hepatitis A, B, and C; cytomegalovirus; Epstein-Barr virus), acute liver hypoperfusion, hypothermia, alcohol, cannabis, cocaine abuse, and hepatotoxic drugs (paroxetine, amphetamines, benzodiazepines, methadone, opiates, etc.) [16]. Therapeutic intervention should be based on careful consideration of these pathogenetic mechanisms.

We describe two patients who were affected by AN and presented with increased serum liver enzymes and discuss the possible etiopathogenic determinants and our medical intervention.