Article

Sclerostin levels and bone turnover markers in adolescents with anorexia nervosa and healthy adolescent girls.

Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Bone (impact factor: 4.02). 06/2012; 51(3):474-9. DOI:10.1016/j.bone.2012.06.006 pp.474-9
Source: PubMed

ABSTRACT Sclerostin, product of the SOST gene, is an important determinant of bone formation and resorption. Adolescents with anorexia nervosa (AN) have low bone density and decreased levels of bone turnover markers. However, sclerostin has not been examined in AN as a potential mediator of impaired bone metabolism. Our study objectives were to (i) assess associations of sclerostin with surrogate bone turnover markers in girls with AN and controls and (ii) examine effects of transdermal estradiol on sclerostin in AN. 69 girls (44 with AN and 25 normal-weight controls) 13-18 years old were studied at baseline. 22 AN girls were randomized to transdermal estradiol (plus cyclic medroxyprogesterone) or placebo in a double-blind study for 12 months. Sclerostin correlated positively with P1NP and CTX in controls (r=0.67 and 0.53, p=0.0002 and 0.005, respectively) but not in AN despite comparable levels at baseline. Changes in sclerostin over twelve months did not differ in girls randomized to estradiol or placebo. The relationship between sclerostin and bone turnover markers is disrupted in adolescent girls with AN. Despite an increase in BMD with estradiol administration in AN, estrogen does not impact sclerostin levels in this group.

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Keywords

12 months
 
25 normal-weight controls
 
adolescent girls
 
anorexia nervosa
 
bone formation
 
bone metabolism
 
bone turnover markers
 
comparable levels
 
cyclic medroxyprogesterone
 
double-blind study
 
estradiol administration
 
estrogen
 
girls
 
girls randomized
 
potential mediator
 
Sclerostin correlated
 
SOST gene
 
study objectives
 
surrogate bone turnover markers
 
transdermal estradiol