Abstract

To evaluate the amino acid profile in a group of adolescents with anorexia nervosa, and to apply alternative ways of presenting and assessing results, so as to increase the information available for understanding the metabolic abnormalities developed in these patients. Plasma amino acid concentrations of a random group of patients with anorexia nervosa compared with values obtained from a 'healthy' adolescent population. The study was performed at the tertiary children's Hospital Sant Joan de Deu. Female adolescents (n = 92, age: 15+/-1.8 y) at diagnosis of anorexia nervosa. Reference values for amino acids were obtained from apparently healthy adolescents (by history and analytical data) who underwent presurgical analysis for minor operations. Plasma amino acid concentrations were measured by ion exchange chromatography. Basic laboratory analysis, carnitine and IGF-I were also determined. In anorexic patients plasma concentrations of taurine, asparagine, glutamine, glycine, methionine, phenylalanine, ornithine, and histidine were significantly higher than reference values (Mann-Whitney, P < 0.01-0.0001), whereas arginine and cystine were lower than our reference values (P < 0.0001). Relative amino acid values (the molar fraction of the patient medians relative to control medians) were plotted. The ratios of some amino acids were significantly greater than those obtained from the reference population: Phe/Tyr (P < 0.001), Met/Cys (P < 0.0001), and Gly/Val (P < 0.01). A trend to hyperaminoacidemia is a common feature in anorexia nervosa. Although absolute amino acid values cannot play a significant role in the assessment of nutritional status in this condition, the calculation of some ratios (Phe/Tyr, Met/Cys and Gly/Val) and the graphical representation of relative values may be useful. The plasma amino acid profile in anorexia nervosa is different from those of other severe malnutrition states, showing a marasmic pattern of balanced protein-energy undernutrition. Cystine and arginine may be considered limiting amino acids in this disease, and the consequences of their deficient concentrations for oxidative damage should be further evaluated.

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