A polygenic score for height identifies an unmeasured genetic predisposition among pediatric patients with idiopathic short stature

身高多基因评分可以识别特发性矮小症患儿中未被测量的遗传易感性。

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Abstract

BACKGROUND: A subset of children with short stature do not have an identified clinical explanation after extensive diagnostic evaluation. We hypothesized that a polygenic score for height (PGS(height)) could identify children with non-familial idiopathic short stature (ISS-NF) who carry a polygenic predisposition to shorter height that is not accounted for by existing measures. METHODS: We studied 534 pediatric participants in an electronic health record (EHR)-linked DNA biobank (BioVU) who had been evaluated for short stature by an endocrinologist. Participants were classified as having one of five short stature subtypes: primary growth disorders, secondary growth disorders, idiopathic short stature (ISS), which was sub-classified into familial (ISS-F) and non-familial (ISS-NF), and constitutional delay of puberty (ISS-DP). Differences in polygenic predisposition between subtypes were analyzed using a validated PGS(height) which was standardized to a standard deviation score (SDS). Adult height predictions were generated using the PGS(height) and mid-parental height (MPH). Within-child differences in height predictions were compared across subtypes. Logistic regression models and AUC analyses were used to test the ability of the PGS(height) to differentiate ISS-NF from growth disorders. The incremental improvement (ΔAUC) of adding the PGS(height) to prediction models with MPH was also estimated. RESULTS: Among the 534 participants, 29.0% had secondary growth disorders, 24.9% had ISS-F, 20.2% had ISS-NF, 17.2% had ISS-DP, and 8.6% had primary growth disorders. Participants with ISS-NF had similar PGS(height) values to those with ISS-F (difference [Δ] in PGS(height) SDS [95% CI] = 0.19 [- 0.31 to 0.70], p = 0.75). Predicted heights generated by the PGS(height) were lower than the MPH estimate for children with ISS-NF (Δ[PGS(height) - MPH] =  - 0.37 SDS; p = 3.2 × 10(-9)) but not for children with ISS-F (Δ =  - 0.07; p = 0.56). Children with ISS-NF also had lower PGS(height) than children with primary growth disorders (ΔPGS(height) =  - 0.53 [- 1.03 to - 0.04], p = 0.03) and secondary growth disorders (Δ =  - 0.45 [- 0.80 to - 0.10], p = 0.005). The PGS(height) improved model discrimination between ISS-NF and children with primary (ΔAUC, + 0.07 [95% CI, 0.02 to 0.17]) and secondary growth disorders (ΔAUC, + 0.03 [95% CI, 0.01 to 0.10]). CONCLUSIONS: Some children with ISS-NF have an unrecognized polygenic predisposition to shorter height, similar to children with ISS-F and greater than those with growth disorders. A PGS(height) could aid clinicians in identifying children with a benign, polygenic predisposition to shorter height.

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