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Interactions between growth and body composition in children treated with high-dose chronic glucocorticoids
Bethany J Foster1, Justine Shults, Babette S Zemel
1Department of Pediatrics, Division of Nephrology, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, USA. beth.foster@muhc.mcgill.ca
Insights
Children with steroid-sensitive nephrotic syndrome (SSNS) treated with glucocorticoids often become obese, impacting growth. Despite this, their final adult height remains normal due to a higher body mass index (BMI).
Area of Science:
- Pediatric Endocrinology
- Metabolic Disorders
- Growth and Development
Background:
- Glucocorticoid therapy is known to impede growth and cause Cushingoid body habitus in children.
- Children with steroid-sensitive nephrotic syndrome (SSNS) often achieve near-normal adult height despite prolonged glucocorticoid treatment.
- Limited data exists on the body composition of children undergoing long-term glucocorticoid therapy for SSNS.
Purpose of the Study:
- To evaluate the impact of chronic glucocorticoid therapy on height and body composition in children with SSNS.
- To compare body composition metrics in children with SSNS against healthy reference children.
- To test the hypothesis that glucocorticoids lead to obesity, reduced lean mass, and altered fat/lean distribution.
Main Methods:
- A cross-sectional study involving 52 children with SSNS (aged 4-21 years) and 259 healthy reference children.
- Assessment of height, weight, and pubertal status.
- Dual-energy X-ray absorptiometry (DXA) used to measure fat and lean mass in all participants.
- Recording of lifetime glucocorticoid exposure for SSNS patients; outcomes expressed as SD scores (SDS).
Main Results:
- 41% of SSNS patients were obese (BMI > 95th percentile), with normal regional fat distribution.
- SSNS patients exhibited higher mean total lean mass-for-height (0.43 SD) but lower mean appendicular lean mass-for-total-lean-mass (-0.39 SD) compared to controls.
- Mean height-SDS in SSNS was -0.08 SD, but significantly decreased with increasing obesity; height-SDS positively correlated with BMI-SDS.
Conclusions:
- Glucocorticoid therapy for SSNS is associated with obesity and reduced appendicular lean mass.
- Normal overall height-SDS in SSNS patients is attributed to a mitigating effect of elevated BMI on glucocorticoid-induced growth retardation.
Background:
Glucocorticoid therapy retards growth during childhood and is believed to lead to a Cushingoid body habitus. However, despite prolonged, repeated courses of glucocorticoid, children with steroid-sensitive nephrotic syndrome (SSNS) have almost normal adult height. Little information exists on body composition.
Objective:
We sought to assess the effect of glucocorticoids on height and body composition by comparing children with SSNS with concurrent healthy reference children. We hypothesized that chronic glucocorticoid therapy leads to obesity, decreased lean mass, and distorted distributions of fat and lean.
Design:
We performed a cross-sectional study of 52 subjects with SSNS (4-21 y) and 259 reference subjects. The evaluation included height, weight, and pubertal status. Fat and lean masses were assessed by dual-energy X-ray absorptiometry in all subjects. Lifetime glucocorticoid exposure was recorded for subjects with SSNS. Outcomes were expressed as SD scores (SDS).
Results:
Forty-one percent of subjects with SSNS were obese [body mass index (BMI) > 95th percentile], but regional fat distribution was normal. Mean total lean mass-for-height was 0.43 SD (95% CI: 0.15, 0.72) higher and mean appendicular lean mass-for-total-lean-mass was lower (-0.39 SD; 95% CI: -0.64, -0.14) in SSNS compared with reference children. The mean height-SDS in SSNS was -0.08 SD (95% CI: -0.37, 0.21) relative to national reference data, but height-SDS was significantly decreased given the degree of obesity. Height-SDS was positively associated with BMI-SDS among subjects with SSNS.
Conclusion:
Glucocorticoid therapy for SSNS is complicated by obesity and relatively low appendicular lean mass. Overall height-SDS is normal because of a mitigating effect of elevated BMI on glucocorticoid-induced growth retardation.
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