Journal of pediatric orthopedics · 2025
Effect of Vitamin D Deficiency on Development of Slipped Capital Femoral Epiphysis.
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Torres-Izquierdo Beltran, Galan-Olleros Maria, Momtaz David, Mittal Mehul M, Gonuguntla Rishi, Tippabhatla Abhishek, Hosseinzadeh Pooya
Аннотация
OBJECTIVE: Slipped capital femoral epiphysis (SCFE) is one of the most common hip disorders in adolescents, often linked to obesity. However, other factors, such as vitamin D deficiency, may also contribute to SCFE development. This study investigates the impact of vitamin D deficiency on SCFE development in a large cohort.
METHODS: We utilized the TriNetX national database to query pediatric patients with documented calcidiol levels. Patients with a recorded visit below the age of 9 and subsequent documented calcidiol levels were followed until SCFE occurrence or age 18. Patients were categorized into vitamin D adequate (≥ 30 ng/mL) and deficient (< 30 ng/mL) groups. Propensity score matching was performed using a multivariable logistic regression model to adjust for baseline characteristics, including age, sex, race, and body mass index percentile. Significance testing was conducted using the Fisher exact test and χ 2 tests to compare SCFE risk between the cohorts, with a significance level set at P <0.05.
RESULTS: On preliminary analysis, 98,045 patients met the inclusion criteria. After matching, 34,552 individuals in both vitamin D deficient and adequate groups were included, with an average age of 8.4 years at the time of their first visit and 50% females. SCFE occurred in 136 (0.39%) and 48 (0.14%) patients in the vitamin D deficient and adequate groups, respectively ( P < 0.0001). Vitamin D deficiency significantly increased SCFE risk, with a relative risk of 2.8 (95% CI: 2-3.9; P < 0.0001) and a hazard ratio of 1.6 (95% CI: 1.1-2.2; P < 0.0001).
CONCLUSION: This study, one of the largest to date, establishes a significant association between vitamin D deficiency and SCFE development. After controlling for potential confounding variables, including body mass index, individuals with vitamin D deficiency were ∼2.83 times more likely to develop SCFE. The study findings highlight the need for further research to evaluate whether supplementation could mitigate this risk of developing SCFE.
LEVEL OF EVIDENCE: Level III.
METHODS: We utilized the TriNetX national database to query pediatric patients with documented calcidiol levels. Patients with a recorded visit below the age of 9 and subsequent documented calcidiol levels were followed until SCFE occurrence or age 18. Patients were categorized into vitamin D adequate (≥ 30 ng/mL) and deficient (< 30 ng/mL) groups. Propensity score matching was performed using a multivariable logistic regression model to adjust for baseline characteristics, including age, sex, race, and body mass index percentile. Significance testing was conducted using the Fisher exact test and χ 2 tests to compare SCFE risk between the cohorts, with a significance level set at P <0.05.
RESULTS: On preliminary analysis, 98,045 patients met the inclusion criteria. After matching, 34,552 individuals in both vitamin D deficient and adequate groups were included, with an average age of 8.4 years at the time of their first visit and 50% females. SCFE occurred in 136 (0.39%) and 48 (0.14%) patients in the vitamin D deficient and adequate groups, respectively ( P < 0.0001). Vitamin D deficiency significantly increased SCFE risk, with a relative risk of 2.8 (95% CI: 2-3.9; P < 0.0001) and a hazard ratio of 1.6 (95% CI: 1.1-2.2; P < 0.0001).
CONCLUSION: This study, one of the largest to date, establishes a significant association between vitamin D deficiency and SCFE development. After controlling for potential confounding variables, including body mass index, individuals with vitamin D deficiency were ∼2.83 times more likely to develop SCFE. The study findings highlight the need for further research to evaluate whether supplementation could mitigate this risk of developing SCFE.
LEVEL OF EVIDENCE: Level III.