Severe acute liver damage in anorexia nervosa: two case reports.

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.

[Clinical nutritional outcome in patients recovering in a psychiatric setting from severe protein-energy malnutrition of anorexia nervosa]. / Aspetti clinico-nutrizionali di pazienti ricoverati in ambiente psichiatrico per grave malnutrizione proteico-energetica da anoressia nervosa.

Protein energy malnutrition due to anorexia nervosa, either restrictive or bulimic, requires an integrated medical psychiatric intervention to be treated. The aim of this study was to evaluate the effectiveness of this integrated treatment in severely malnourished anorectic patients requiring to be hospitalized in Psychiatry Unit. Fifteen patients (14 females, 1 male, mean age 19.6 +/- 4.7 years, body mass index 14.0 +/- 1.9 kg/m2) 13 of whom affected by restrictive anorexia nervosa and 2 by bulimic anorexia nervosa, have been hospitalized in the Psychiatry Unit of the Federico II University Hospital, Naples from September 2000 to July 2003, always without requiring compulsory sanitary treatment. Hospitalization was due to failure of the outpatient treatment in all of them, complicated by uncontrolled weight loss in 7, hydroelectrolytic unbalance in 2, edema in 1 patient. All were hypotensive and 4 had marked bradycardia. Forced nutrition was never necessary. Enteral nutrition by nasogastric tube was prescribed in 4 patients, oral nutrition supplements with diet in 4 and only diet in the remaining 7. All patients received vitamin and mineral supplements, if necessary parenterally. A mild body weight increase and satisfactory normalization of biochemical parameters was obtained in all patients during hospitalization. Thereafter they were enrolled in an outpatient integrated medical/psychiatric protocol, including group therapy. Only in 1 case, a few months later, a second hospitalization was necessary. In conclusion, integrated medical psychiatric treatment represents an effective intervention also in severely malnourished anorectic patient requiring hospitalization.