Developmental medicine and child neurology · 2026
Vitamin D deficiency in early pregnancy and the risk of developing cerebral palsy: A case-control study.
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.
Bergman Ebba, Rylander Lars, Lindh Christian, Thacher Jesse D
Аннотация
AIM: To investigate whether maternal deficiency of vitamin D in early pregnancy increases the risk of cerebral palsy (CP) in offspring.
METHOD: This registry and biobank-based case-control study consisted of mother-child pairs from Scania, Sweden. Cases (n = 322) were identified from a nationwide CP-register born between 1995 and 2014. Random population controls (n = 343) and preterm controls (n = 258) were identified from a birth registry. Serum samples taken during pregnancy were obtained from a biobank and 25(OH)D3 concentrations were categorized into three groups: sufficient (≥ 75 nmol/L), insufficient (50-74.9 nmol/L), and deficient (< 50 nmol/L). Logistic regression was used to investigate associations between 25(OH)D3 concentrations and CP. Separate analyses were completed among children born preterm and at term, as well as for subtypes of CP.
RESULTS: Deficiency of 25(OH)D3 was not associated with a significantly higher risk of CP compared with sufficient values in the studied groups of all children (odds ratio [OR]: 1.34; 95% confidence interval [CI]: 0.86-2.10), children born at term (OR: 1.48; 95% CI: 0.89-2.44), and children born preterm (OR: 0.74; 95% CI: 0.37-1.46).
INTERPRETATION: No apparent association between 25(OH)D3 and CP was observed; however, the relatively small sample size and reliance on a single vitamin D measurement may have limited the detection of modest effects.
METHOD: This registry and biobank-based case-control study consisted of mother-child pairs from Scania, Sweden. Cases (n = 322) were identified from a nationwide CP-register born between 1995 and 2014. Random population controls (n = 343) and preterm controls (n = 258) were identified from a birth registry. Serum samples taken during pregnancy were obtained from a biobank and 25(OH)D3 concentrations were categorized into three groups: sufficient (≥ 75 nmol/L), insufficient (50-74.9 nmol/L), and deficient (< 50 nmol/L). Logistic regression was used to investigate associations between 25(OH)D3 concentrations and CP. Separate analyses were completed among children born preterm and at term, as well as for subtypes of CP.
RESULTS: Deficiency of 25(OH)D3 was not associated with a significantly higher risk of CP compared with sufficient values in the studied groups of all children (odds ratio [OR]: 1.34; 95% confidence interval [CI]: 0.86-2.10), children born at term (OR: 1.48; 95% CI: 0.89-2.44), and children born preterm (OR: 0.74; 95% CI: 0.37-1.46).
INTERPRETATION: No apparent association between 25(OH)D3 and CP was observed; however, the relatively small sample size and reliance on a single vitamin D measurement may have limited the detection of modest effects.