Abstract

Eating disorders (TCA per its abbreviation in Spanish) are common in young women, with an estimated prevalence of 4-5%. One of the physical complications of eating disorders, especially anorexia nervosa (AN) and eating disorder not otherwise specified (TANE) is bone mass loss, which affects both cortical and trabecular bone. The synergistic effect of malnutrition and estrogen deficiency produces significant bone mass loss, resulting from the uncoupling of bone turnover characterized by a decrease in osteoblastic bone formation and an increase in osteclastic bone resorption. The mechanisms implied in the pathogenesis of bone loss are the hypoestrogenism, hypercortisolism, serum leptin levels and insulin-like growth factor decrease. Severity of bone loss in anorexia nervosa varies depending on duration of illness, the minimal weight ever and sedentarism or strenuous exercise. Long term consequences occur, such as a fracture risk increase in patients who have suffered anorexia nervosa, compared with the general population. The first treatment line to recover bone mass is nutritional rehabilitation together with weight gain. Hormonal replacement therapy may be effective if combined with an anabolic method. Osteopenia and osteoporosis are terms adopted to define the deficiency of bone mass in adults. Authors have used these terms to define densitometric data in young subjects who have not reached their peak bone mass. We suggest the term "hypo-osteogenesia" to define the deficiency in the development of bone mass in adolescents or children.

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