PDF(Pubmed)
Abstract：
UNASSIGNED: Pantothenate (vitamin B5) is a precursor for coenzyme A (CoA) synthesis, which serves as a cofactor for hundreds of metabolic reactions. Cysteine is an amino acid in the CoA synthesis pathway. To date, research on the combined role of early life pantothenate and cysteine levels in childhood neurodevelopmental disabilities is scarce.
UNASSIGNED: To study the association between cord pantothenate and cysteine levels and risk of autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD) and other developmental disabilities (DD) in children born term and preterm.
UNASSIGNED: The study sample (n = 996, 177 born preterm) derived from the Boston Birth Cohort included 416 neurotypical children, 87 ASD, 269 ADHD, and 224 other DD children, who were mutually exclusive. Participants were enrolled at birth and were followed up prospectively (from October 1, 1998, to June 30, 2018) at the Boston Medical Center. Cord blood sample was collected at birth. Plasma pantothenate and cysteine levels were measured using liquid chromatography-tandem mass spectrometry.
UNASSIGNED: Higher cord pantothenate (≥50th percentile vs. <50th percentile) was associated with a greater risk of ASD (adjusted odds ratio [aOR]: 1.94, 95% confidence interval [CI]: 1.06, 3.55) and ADHD (aOR: 1.66, 95% CI: 1.14, 2.40), after adjusting for potential confounders. However, cord cysteine alone was not associated with risk of ASD, ADHD, or other DD. When considering the joint association, greater ASD risk was noted when both cord pantothenate and cysteine levels were elevated (≥50th percentile) (aOR: 3.11, 95% CI: 1.24, 7.79), when compared to children with low cord pantothenate (<50th percentile) and high cysteine. Even though preterm and higher pantothenate independently increased the ASD risk, the greatest risk was found in preterm children who also had elevated pantothenate (≥50th percentile), which was true for all three outcomes: ASD (aOR: 5.36, 95% CI: 2.09, 13.75), ADHD (aOR: 3.31, 95% CI: 1.78, 6.16), and other DD (aOR: 3.39, 95% CI: 1.85, 6.24).
UNASSIGNED: In this prospective birth cohort, we showed that higher cord pantothenate individually and in combination with higher cysteine or preterm birth were associated with increased risk of ASD and ADHD. More study is needed to explore this biologically plausible pathway.
UNASSIGNED: To study the association between cord pantothenate and cysteine levels and risk of autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD) and other developmental disabilities (DD) in children born term and preterm.
UNASSIGNED: The study sample (n = 996, 177 born preterm) derived from the Boston Birth Cohort included 416 neurotypical children, 87 ASD, 269 ADHD, and 224 other DD children, who were mutually exclusive. Participants were enrolled at birth and were followed up prospectively (from October 1, 1998, to June 30, 2018) at the Boston Medical Center. Cord blood sample was collected at birth. Plasma pantothenate and cysteine levels were measured using liquid chromatography-tandem mass spectrometry.
UNASSIGNED: Higher cord pantothenate (≥50th percentile vs. <50th percentile) was associated with a greater risk of ASD (adjusted odds ratio [aOR]: 1.94, 95% confidence interval [CI]: 1.06, 3.55) and ADHD (aOR: 1.66, 95% CI: 1.14, 2.40), after adjusting for potential confounders. However, cord cysteine alone was not associated with risk of ASD, ADHD, or other DD. When considering the joint association, greater ASD risk was noted when both cord pantothenate and cysteine levels were elevated (≥50th percentile) (aOR: 3.11, 95% CI: 1.24, 7.79), when compared to children with low cord pantothenate (<50th percentile) and high cysteine. Even though preterm and higher pantothenate independently increased the ASD risk, the greatest risk was found in preterm children who also had elevated pantothenate (≥50th percentile), which was true for all three outcomes: ASD (aOR: 5.36, 95% CI: 2.09, 13.75), ADHD (aOR: 3.31, 95% CI: 1.78, 6.16), and other DD (aOR: 3.39, 95% CI: 1.85, 6.24).
UNASSIGNED: In this prospective birth cohort, we showed that higher cord pantothenate individually and in combination with higher cysteine or preterm birth were associated with increased risk of ASD and ADHD. More study is needed to explore this biologically plausible pathway.
摘要：
■泛酸（维生素B5）是辅酶A（CoA）合成的前体，作为数百种代谢反应的辅因子。半胱氨酸是CoA合成途径中的氨基酸。迄今为止,关于生命早期泛酸和半胱氨酸水平在儿童神经发育障碍中的联合作用的研究很少。
■为了研究脐带泛酸和半胱氨酸水平与自闭症谱系障碍（ASD）风险之间的关系，足月和早产儿的注意缺陷多动障碍（ADHD）和其他发育障碍（DD）。
■来自波士顿出生队列的研究样本（n=996，177名早产）包括416名神经典型儿童，87ASD，269多动症,和其他224名DD儿童，他们是相互排斥的。参与者在出生时登记，并在波士顿医学中心进行前瞻性随访（从1998年10月1日至2018年6月30日）。在出生时收集脐带血样本。使用液相色谱-串联质谱法测量血浆泛酸和半胱氨酸水平。
■高索泛酸（≥50百分位数vs.<50百分位数）与更大的ASD风险相关（调整后的优势比[aOR]：1.94，95％置信区间[CI]：1.06，3.55）和ADHD（aOR：1.66，95％CI：1.14，2.40），在调整了潜在的混杂因素后。然而,单独的脐带半胱氨酸与ASD的风险无关，多动症,或其他DD。在考虑联合协会时，当脐带泛酸和半胱氨酸水平均升高（≥50百分位数）时，发现ASD风险更大（aOR：3.11，95％CI：1.24，7.79），与低脐带泛酸（<50百分位数）和高半胱氨酸的儿童相比。尽管早产和较高的泛酸独立地增加了ASD风险，在泛酸升高的早产儿中发现最大的风险（≥50百分位数），这对所有三个结果都是正确的：ASD(OR：5.36，95%CI：2.09，13.75)，多动症（AOR：3.31，95%CI：1.78，6.16），和其他DD（aOR：3.39，95%CI：1.85，6.24）。
■在这个前瞻性出生队列中，我们发现,单独使用较高的脐带神经泛酸盐,以及与较高的半胱氨酸或早产联合使用,与ASD和ADHD的风险增加相关.需要更多的研究来探索这种生物学上合理的途径。
■为了研究脐带泛酸和半胱氨酸水平与自闭症谱系障碍（ASD）风险之间的关系，足月和早产儿的注意缺陷多动障碍（ADHD）和其他发育障碍（DD）。
■来自波士顿出生队列的研究样本（n=996，177名早产）包括416名神经典型儿童，87ASD，269多动症,和其他224名DD儿童，他们是相互排斥的。参与者在出生时登记，并在波士顿医学中心进行前瞻性随访（从1998年10月1日至2018年6月30日）。在出生时收集脐带血样本。使用液相色谱-串联质谱法测量血浆泛酸和半胱氨酸水平。
■高索泛酸（≥50百分位数vs.<50百分位数）与更大的ASD风险相关（调整后的优势比[aOR]：1.94，95％置信区间[CI]：1.06，3.55）和ADHD（aOR：1.66，95％CI：1.14，2.40），在调整了潜在的混杂因素后。然而,单独的脐带半胱氨酸与ASD的风险无关，多动症,或其他DD。在考虑联合协会时，当脐带泛酸和半胱氨酸水平均升高（≥50百分位数）时，发现ASD风险更大（aOR：3.11，95％CI：1.24，7.79），与低脐带泛酸（<50百分位数）和高半胱氨酸的儿童相比。尽管早产和较高的泛酸独立地增加了ASD风险，在泛酸升高的早产儿中发现最大的风险（≥50百分位数），这对所有三个结果都是正确的：ASD(OR：5.36，95%CI：2.09，13.75)，多动症（AOR：3.31，95%CI：1.78，6.16），和其他DD（aOR：3.39，95%CI：1.85，6.24）。
■在这个前瞻性出生队列中，我们发现,单独使用较高的脐带神经泛酸盐,以及与较高的半胱氨酸或早产联合使用,与ASD和ADHD的风险增加相关.需要更多的研究来探索这种生物学上合理的途径。
