IBMS BoneKEy | Perspective

Skeletal abnormalities in anorexia nervosa

Elka Jacobson-Dickman
Madhusmita Misra



Anorexia nervosa (AN) is a condition of self-imposed starvation associated with multiple endocrine abnormalities that contribute to low bone density in both males and females. Hormonal alterations in AN include a state of acquired growth hormone (GH) resistance with low IGF-1 levels, hypogonadism, relative hypercortisolemia, elevations in levels of ghrelin, peptide YY and adiponectin, and reductions in leptin. Weight gain associated with menstrual recovery leads to stabilization of bone density, whereas persistence of low weight and amenorrhea causes further decreases in bone density. Low bone density in AN is refractory to oral estrogen replacement, although a combination of oral estrogen with rhIGF-1 causes an increase in bone density in adult women with AN. In addition to low bone density, alterations in bone microarchitecture have been reported in AN, with reductions in apparent bone trabecular volume, trabecular thickness and number, and an increase in trabecular separation. AN may also impact stature adversely, particularly when it begins before epiphyseal fusion and is long-standing.

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