PDF(Pubmed)
Abstract：
Prenatal exposure to maternal metabolic conditions associated with inflammation and steroid dysregulation has previously been linked to increased autism risk. Steroid-related maternal serum biomarkers have also provided insight into the in utero steroid environment for offspring who develop autism.
This study examines the link between autism among offspring and early second trimester maternal steroid-related serum biomarkers from pregnancies enriched for prenatal metabolic syndrome (PNMS) exposure.
Early second trimester maternal steroid-related serum biomarkers (i.e., estradiol, free testosterone, total testosterone, and sex hormone binding globulin) were compared between pregnancies corresponding to offspring with (N = 68) and without (N = 68) autism. Multiple logistic regression analyses were stratified by sex and gestational duration. One-way ANCOVA with post hoc tests was performed for groups defined by autism status and PNMS exposure.
Increased estradiol was significantly associated with autism only in males (AOR = 1.13 per 100 pg/ml, 95% CI 1.01-1.27, p = 0.036) and only term pregnancies (AOR = 1.17 per 100 pg/ml, 95% CI 1.04-1.32, p = 0.010). Autism status was significantly associated with decreased sex hormone binding globulin (AOR = 0.65 per 50 nmol/L, 95% CI 0.55-0.78, p < 0.001) overall and when stratified by sex and term pregnancy status. The inverse association between sex hormone binding globulin and autism was independent of PNMS exposure.
The relative racial and ethnic homogeneity of Utah\'s population limits the generalizability of study results. Although significant differences by autism status were identified in concentrations of sex hormone binding globulin overall and of estradiol in participant subgroups, differences by PNMS exposure failed to reach statistical significance, which may reflect insufficient statistical power.
Both elevated maternal serum estradiol in males only and low maternal serum sex hormone binding globulin in both sexes are associated with increased autism risk. Further investigation is merited to identify how steroid, metabolic, and inflammatory processes can interact to influence neurodevelopment in early second trimester.
This study examines the link between autism among offspring and early second trimester maternal steroid-related serum biomarkers from pregnancies enriched for prenatal metabolic syndrome (PNMS) exposure.
Early second trimester maternal steroid-related serum biomarkers (i.e., estradiol, free testosterone, total testosterone, and sex hormone binding globulin) were compared between pregnancies corresponding to offspring with (N = 68) and without (N = 68) autism. Multiple logistic regression analyses were stratified by sex and gestational duration. One-way ANCOVA with post hoc tests was performed for groups defined by autism status and PNMS exposure.
Increased estradiol was significantly associated with autism only in males (AOR = 1.13 per 100 pg/ml, 95% CI 1.01-1.27, p = 0.036) and only term pregnancies (AOR = 1.17 per 100 pg/ml, 95% CI 1.04-1.32, p = 0.010). Autism status was significantly associated with decreased sex hormone binding globulin (AOR = 0.65 per 50 nmol/L, 95% CI 0.55-0.78, p < 0.001) overall and when stratified by sex and term pregnancy status. The inverse association between sex hormone binding globulin and autism was independent of PNMS exposure.
The relative racial and ethnic homogeneity of Utah\'s population limits the generalizability of study results. Although significant differences by autism status were identified in concentrations of sex hormone binding globulin overall and of estradiol in participant subgroups, differences by PNMS exposure failed to reach statistical significance, which may reflect insufficient statistical power.
Both elevated maternal serum estradiol in males only and low maternal serum sex hormone binding globulin in both sexes are associated with increased autism risk. Further investigation is merited to identify how steroid, metabolic, and inflammatory processes can interact to influence neurodevelopment in early second trimester.
摘要：
背景：以前，与炎症和类固醇失调相关的母体代谢疾病的产前暴露与自闭症风险增加有关。类固醇相关的母体血清生物标志物也为患有自闭症的后代提供了子宫内类固醇环境的见解。
目的：本研究探讨了后代孤独症与孕中期母体类固醇相关血清生物标志物之间的联系，这些标志物来自富含产前代谢综合征（PNMS）暴露的妊娠。
方法：妊娠中期早期母体类固醇相关血清生物标志物（即，雌二醇,游离的睾酮,总睾酮,和性激素结合球蛋白）在对应于患有（N=68）和没有（N=68）自闭症的后代的怀孕之间进行了比较。多因素logistic回归分析按性别和妊娠时间分层。对由自闭症状态和PNMS暴露定义的组进行单向ANCOVA和事后测试。
结果：雌二醇增加仅在男性中与自闭症显着相关（AOR=1.13/100pg/ml，95％CI1.01-1.27，p=0.036）和仅足月妊娠（AOR=每100pg/ml1.17，95%CI1.04-1.32，p=0.010）。自闭症状态与性激素结合球蛋白降低显着相关（AOR=0.65每50nmol/L，95％CI0.55-0.78，p<0.001）总体上以及按性别和足月妊娠状态分层时。性激素结合球蛋白与自闭症之间的负相关与PNMS暴露无关。
结论：犹他州人口的相对种族和民族同质性限制了研究结果的普遍性。尽管在参与者亚组中，性激素结合球蛋白和雌二醇的浓度在自闭症状态方面存在显着差异，PNMS暴露的差异没有达到统计学意义，这可能反映出统计能力不足。
结论：仅男性的母体血清雌二醇升高和两种性别的母体血清性激素结合球蛋白降低均与自闭症风险增加相关。值得进一步调查以确定类固醇，新陈代谢，和炎症过程可以相互作用，影响早孕中期的神经发育。
目的：本研究探讨了后代孤独症与孕中期母体类固醇相关血清生物标志物之间的联系，这些标志物来自富含产前代谢综合征（PNMS）暴露的妊娠。
方法：妊娠中期早期母体类固醇相关血清生物标志物（即，雌二醇,游离的睾酮,总睾酮,和性激素结合球蛋白）在对应于患有（N=68）和没有（N=68）自闭症的后代的怀孕之间进行了比较。多因素logistic回归分析按性别和妊娠时间分层。对由自闭症状态和PNMS暴露定义的组进行单向ANCOVA和事后测试。
结果：雌二醇增加仅在男性中与自闭症显着相关（AOR=1.13/100pg/ml，95％CI1.01-1.27，p=0.036）和仅足月妊娠（AOR=每100pg/ml1.17，95%CI1.04-1.32，p=0.010）。自闭症状态与性激素结合球蛋白降低显着相关（AOR=0.65每50nmol/L，95％CI0.55-0.78，p<0.001）总体上以及按性别和足月妊娠状态分层时。性激素结合球蛋白与自闭症之间的负相关与PNMS暴露无关。
结论：犹他州人口的相对种族和民族同质性限制了研究结果的普遍性。尽管在参与者亚组中，性激素结合球蛋白和雌二醇的浓度在自闭症状态方面存在显着差异，PNMS暴露的差异没有达到统计学意义，这可能反映出统计能力不足。
结论：仅男性的母体血清雌二醇升高和两种性别的母体血清性激素结合球蛋白降低均与自闭症风险增加相关。值得进一步调查以确定类固醇，新陈代谢，和炎症过程可以相互作用，影响早孕中期的神经发育。
