Format

Send to

Choose Destination
J Endocrinol Invest. 2011 Apr;34(4):324-32. doi: 10.3275/7505. Epub 2011 Feb 7.

Bone metabolism in adolescents with anorexia nervosa.

Author information

1
Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. mmisra@partners.org

Abstract

Adolescents with anorexia nervosa (AN) are at risk for low bone mass at multiple sites, associated with decreased bone turnover. Bone microarchitecture is also affected, with a decrease in bone trabecular volume and trabecular thickness, and an increase in trabecular separation. The adolescent years are typically the time when marked increases occur in bone mass accrual towards the attainment of peak bone mass, an important determinant of bone health and fracture risk in later life. AN often begins in the adolescent years, and decreased rates of bone mass accrual at this critical time are therefore also concerning for deficits in peak bone mass. Factors contributing to low bone density and decreased rates of bone accrual include alterations in body composition such as low body mass index and lean body mass, and hormonal alterations such as hypogonadism, a nutritionally acquired resistance to GH and low levels of IGF-I, relative hypercortisolemia, low levels of leptin, and increased adiponectin (for fat mass) and peptide YY. Therapeutic strategies include optimizing weight and menstrual recovery, and adequate calcium and vitamin D replacement. Oral estrogen-progesterone combination pills are not effective in increasing bone density in adolescents with AN. Recombinant human IGF-I increases levels of bone formation markers in the short term, while long-term effects remain to be determined. Bisphosphonates act by decreasing bone resorption, and are not optimal for use in adolescents with AN, in whom the primary defect is low bone formation.

PMID:
21301203
PMCID:
PMC3671890
DOI:
10.1007/BF03347094
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Springer Icon for PubMed Central
Loading ...
Support Center