Liver Damage Is Related to the Degree of Being Underweight in Anorexia Nervosa and Improves Rapidly with Weight Gain

Background: The present study investigates the relationship between hypertransaminasemia and malnutrition on the basis of a very large number of patients. We assume that the level of transaminases not only reflects the extent of underlying liver cell damage but also provides information about the metabolic situation under conditions of energy deficiency. Methods: We present an observational study in two different samples. The first sample consists of 3755 patients (mean age 22.7 years, Range 12–73 years; mean BMI 15.4 kg/m(2), range 8.1–25.7) out of a total of 4212 patients with anorexia nervosa treated in the Roseneck Clinic within five years for whom a complete admission laboratory was available. The second sample was obtained from a special ward for medically at-risk patients with eating disorders. During the period in question, four hundred and ten patients with anorexia nervosa were treated. One hundred and forty-two female patients (mean age 26.4 years, Range 18–63 years; mean BMI 11.5 kg/m(2), range 8.4–13) had a BMI of thirteen or less and a complete data set was obtained at admission and weekly in the following four weeks after admission. Results: The increase in liver transaminases shows a very high correlation with weight in sample one (N = 3755). The analysis of variance shows highly significant (<0.001) correlations with an F-value of 55 for GOT/AST and 63 for GPT/ALT. Nevertheless, the variance within the groups with the same BMI is quite high. With re-nutrition in sample two, GOT/AST decreased on average from 71 U/L to 26 U/L (MANOVA F 10.7, p < 0.001) and GPT/ALT from 88 to 41 U/L (F = 9.9, p < 0.001) within four weeks. Discussion: Below a BMI of about 13, the nutritional status of the patients becomes so critical that the energy supply of the patient is increasingly dependent on the autophagy of the liver, which can be seen in the very strong increase in transaminases here. Refeeding leads very quickly to the normalisation of the transaminases and, thus, a stabilisation of the metabolism leading also to a decrease in autophagy.