Journal of endocrinological investigation · 2025
Association between vitamin D and central precocious puberty in children: Threshold effects and mediation mechanisms based on LC-MS/MS quantitation.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Le Juan, Dai Wen, Peng Rui, Wang Shaoting
Аннотация
PURPOSE: To investigate the association between serum 25-hydroxyvitamin D [25(OH)D] levels and central precocious puberty (CPP) in children, with emphasis on sex-specific threshold effects and mediation pathways.
METHODS: This cross-sectional study enrolled 494 CPP patients (female: 413; male: 81) and 2,259 age-matched healthy controls who underwent liquid chromatography-tandem mass spectrometry (LC-MS/MS) based 25(OH)D quantification, Tanner-Whitehouse 3 bone age assessment, and hormonal profiling. Dose-response relationships were analyzed via restricted cubic splines (RCS), and causal mediation analysis with 1,000 bootstrap resamples were quantified using structural equation models.
RESULTS: CPP patients exhibited significantly lower 25(OH)D levels than controls (median (IQR): females, 20.00 (14.00-24.20) vs. 23.40 (18.10-29.22) ng/mL, P < 0.001; males, 21.60 (16.00-27.10) vs. 23.30 (18.30-28.83) ng/mL, P = 0.033), with higher deficiency rates (females: 49.6% vs. 33.0%; males: 43.2% vs. 32.8%). RCS analysis revealed inverse 25(OH)D-CPP associations, with threshold concentrations at 35.4 ng/mL (females) and 19.5 ng/mL (males). Each 1 ng/mL increment in serum 25(OH)D was associated with 3.6% reduced risk of advanced pubic hair maturation (adjusted OR = 0.964, P = 0.009). Sex-stratified logistic regression showed elevated CPP risks in vitamin D-insufficient/deficient groups versus sufficient counterparts: females (OR = 2.13, P = 0.037; OR = 2.26, P = 0.030) and males (OR = 3.89, P = 0.059; OR = 4.71, P = 0.034). Mediation analysis identified bone age acceleration (64.6% mediation) and gonadotropin activation (14.6%) dominated pathways in females.
CONCLUSION: Vitamin D demonstrated sex-dimorphic associations with CPP risk, requiring higher protective thresholds in females. Bone age acceleration and gonadotropin activation emerged as primary mediators in females. These findings advocated sex-specific vitamin D supplementation strategies for CPP prevention.
METHODS: This cross-sectional study enrolled 494 CPP patients (female: 413; male: 81) and 2,259 age-matched healthy controls who underwent liquid chromatography-tandem mass spectrometry (LC-MS/MS) based 25(OH)D quantification, Tanner-Whitehouse 3 bone age assessment, and hormonal profiling. Dose-response relationships were analyzed via restricted cubic splines (RCS), and causal mediation analysis with 1,000 bootstrap resamples were quantified using structural equation models.
RESULTS: CPP patients exhibited significantly lower 25(OH)D levels than controls (median (IQR): females, 20.00 (14.00-24.20) vs. 23.40 (18.10-29.22) ng/mL, P < 0.001; males, 21.60 (16.00-27.10) vs. 23.30 (18.30-28.83) ng/mL, P = 0.033), with higher deficiency rates (females: 49.6% vs. 33.0%; males: 43.2% vs. 32.8%). RCS analysis revealed inverse 25(OH)D-CPP associations, with threshold concentrations at 35.4 ng/mL (females) and 19.5 ng/mL (males). Each 1 ng/mL increment in serum 25(OH)D was associated with 3.6% reduced risk of advanced pubic hair maturation (adjusted OR = 0.964, P = 0.009). Sex-stratified logistic regression showed elevated CPP risks in vitamin D-insufficient/deficient groups versus sufficient counterparts: females (OR = 2.13, P = 0.037; OR = 2.26, P = 0.030) and males (OR = 3.89, P = 0.059; OR = 4.71, P = 0.034). Mediation analysis identified bone age acceleration (64.6% mediation) and gonadotropin activation (14.6%) dominated pathways in females.
CONCLUSION: Vitamin D demonstrated sex-dimorphic associations with CPP risk, requiring higher protective thresholds in females. Bone age acceleration and gonadotropin activation emerged as primary mediators in females. These findings advocated sex-specific vitamin D supplementation strategies for CPP prevention.