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Anorexia nervosa, commonly occurring in peripubertal girls, is burdened by the highest mortality rate of any psychiatric disorder, due to the organic complications induced by the severe starvation and the high rate of suicide. Patients display dry, pale and yellowish skin, with lanugo hair growth. The clinical picture is characterized by muscle hypotrophy, dehydration, electrolyte disturbances, delayed gastric emptying, constipation, elevation of liver transaminases, leukopenia, bradycardia, hypotension, mitral valve prolapse, pericardial effusion, brain cortical atrophy. Endocrine complications, reversible with weight gain and recovery, can be interpreted as epiphenomena of the disease. Hypogonadotropic hypogonadism, of hypothalamic origin, is the cause of amenorrhea, which was considered in the past one of the diagnostic criteria of the disease. Gonadotropin secretion is characterized by a prepubertal pattern and serum sex steroid levels are low. The preferential conversion of T4 to reverse T3 rather than to T3 in peripheral tissues, common in all malnourishment states, leads to the so called low T3 syndrome. This mechanism, aimed at saving energy, although contributing to bradycardia in these patients, does not require replacement therapy. Like in other psychiatric disorders such as depression, the hypothalamic-pituitary-adrenal axis is activated: hypercortisolism might contribute to some clinical features of the disease such as osteopenia and brain cortical atrophy. The abnormalities of the somatotropin-somatomedin axis are substantially represented by a picture of acquired GH resistance: indeed, due to chronic malnutrition, circulating IGF-I is frankly low in spite of markedly enhanced GH release. Together with malnourishment and low body weight, hypogonadism, hypercortisolism and IGF-I deficiency contribute to bone demineralization, which in its turn leads to an increased fracture risk in the future of these patients.