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Pediatric Neuroendocrinology

Editor(s): Loche S. (Cagliari) 
Cappa M. (Rome) 
Ghizzoni L. (Turin) 
Maghnie M. (Genova) 
Savage M.O. (London) 
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Neuroendocrine Consequences of Anorexia Nervosa in Adolescents

Misra M. · Klibanski A.
Neuroendocrine and Pediatric Endocrine Units, Massachusetts General Hospital and Harvard Medical School, Boston, Mass., USA Loche S, Cappa M, Ghizzoni L, Maghnie M, Savage MO (eds): Pediatric Neuroendocrinology. Endocr Dev. Basel, Karger, 2010, vol 17, pp 197–214 (DOI:10.1159/000262540)

Abstract

Anorexia nervosa (AN) is a condition of severe undernutrition characterized by alterations in multiple neuroendocrine axes and peptides that signal or regulate energy intake. These alterations include a state of hypogonadotropic hypogonadism, a nutritionally acquired resistance to growth hormone (GH) with low IGF-1 levels, relative hypercortisolemia, low total T3 despite normal TSH, low levels of leptin and insulin, and elevated levels of ghrelin, peptide YY (PYY) and possibly adiponectin. Although many of these changes are adaptive to low weight, they can impact bone metabolism, body composition, reproductive function and statural growth. Low bone mass is characteristic of AN in both adolescent boys and girls. In girls, sites of trabecular bone are more likely to be affected than sites of cortical bone, whereas in boys with AN, sites of cortical bone are more commonly affected. Bone microarchitecture is also affected in adolescent girls with AN, with a decrease in trabecular thickness and bone trabecular volume, and an increase in trabecular separation. Important predictors of low bone density include nutritional factors, body composition, hypogonadism, low IGF-1, elevated cortisol and PYY levels, with possible contributions of low insulin. Weight gain is associated with a stabilization of bone density, although residual deficits persist in the short term, and in some cases, long term.

 

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