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Summary: We sought to determine whether low-magnitude mechanical stimulation (LMMS) normalizes bone turnover among adolescents hospitalized for anorexia nervosa (AN). Brief, daily LMMS prevents the decline in bone turnover typically seen during bed rest in AN. LMMS may have application for patients with AN in the inpatient setting to protect bone health. Introduction: Malnourished adolescents with AN requiring medical hospitalization are at high risk for rapid reduction in skeletal quality. Even short-term bed rest can suppress normal patterns of bone turnover. We sought to determine whether LMMS normalizes bone turnover among adolescents hospitalized for complications of AN. Methods: In this randomized, double-blind trial, we prospectively enrolled adolescent females ( n = 41) with AN, age 16.3 ± 1.9 years (mean ± SD) and BMI 15.6 ± 1.7 kg/m. Participants were randomized to stand on a platform delivering LMMS (0.3 g at 32-37 Hz) or placebo platform for 10 min/day for 5 days. Serum markers of bone formation [bone-specific alkaline phosphatase (BSAP)], turnover [osteocalcin (OC)], and bone resorption [serum C-telopeptides (CTx)] were measured. From a random coefficients model, we constructed estimates and confidence intervals for all outcomes. Results: BSAP decreased by 2.8% per day in the placebo arm ( p = 0.03) but remained stable in the LMMS group ( p = 0.51, p = 0.04). CTx did not change with placebo ( p = 0.56) but increased in the LMMS arm (+6.2% per day, p = 0.04; p = 0.01). Serum OC did not change in either group ( p > 0.70). Conclusions: Bed rest during hospitalization for patients with AN is associated with a suppression of bone turnover, which may contribute to diminished bone quality. Brief, daily LMMS prevents a decline in bone turnover during bed rest in AN. Protocols prescribing strict bed rest may not be appropriate for protecting bone health for these patients. LMMS may have application for these patients in the inpatient setting. [ABSTRACT FROM AUTHOR]

Summary: This study evaluated bone health in adults with galactosemia. Associations between bone mineral density (BMD) and nutritional and biochemical variables were explored. Calcium level predicted hip and spine BMD, and gonadotropin levels were inversely associated with spinal BMD in women. These results afford insights into management strategies for these patients. Introduction: Bone loss is a complication of galactosemia. Dietary restriction, primary ovarian insufficiency in women, and disease-related alterations of bone metabolism may contribute. This study examined relationships between clinical factors and BMD in patients with galactosemia. Methods: This cross-sectional sample included 33 adults (16 women) with classic galactosemia, mean age 32.0 ± 11.8 years. BMD was measured by dual-energy X-ray absorptiometry, and was correlated with age, height, weight, fractures, nutritional factors, hormonal status, and bone biomarkers. Results: There was a significant difference in hip BMD between women and men (0.799 vs. 0.896 g/cm, p = 0.014). The percentage of subjects with BMD-Z <−2.0 was also greater for women than men [33 vs. 18 % (spine), 27 vs. 6 % (hip)], and more women reported sustaining fractures. Bivariate analyses yielded correlations between BMI and BMD-Z [at the hip in women ( r = 0.58, p < 0.05) and spine in men ( r = 0.53, p < 0.05)]. In women, weight was also correlated with BMD-Z ( r = 0.57, p < 0.05 at hip), and C-telopeptides ( r = −0.59 at spine and −0.63 hip, p < 0.05) and osteocalcin ( r = −0.71 at spine and −0.72 hip, p < 0.05) were inversely correlated with BMD-Z. In final regression models, higher gonadotropin levels were associated with lower spinal BMD in women ( p = 0.017); serum calcium was a significant predictor of hip ( p = 0.014) and spine ( p = 0.013) BMD in both sexes. Conclusions: Bone density in adults with galactosemia is low, indicating the potential for increased fracture risk, the etiology of which appears to be multifactorial. [ABSTRACT FROM AUTHOR]

A response from the authors of the article "Low prevalence of vitamin D deficiency among adolescents with anorexia nervosa" is presented.