Anogenital distance in newborn daughters of women with polycystic ovary syndrome indicates fetal testosterone exposure.
Anogenital distance in newborn daughters of women with polycystic ovary syndrome indicates fetal testosterone exposure.
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DOI：
10.1017/s2040174417001118
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发表时间：
2018-06
影响因子：
1.7
通讯作者：
Swan SH
中科院分区：
文献类型：
--
作者：
Barrett ES;Hoeger KM;Sathyanarayana S;Abbott DH;Redmon JB;Nguyen RHN;Swan SH
多囊卵巢综合症 (PCOS) 影响大约 7% 的育龄妇女。尽管其病因尚不清楚，但在动物中，过量的产前睾酮 (T) 暴露会诱发 PCOS 样表型。虽然在人类中测量胎儿 T 是不可行的，但使用可靠的新生儿生物标志物肛门生殖器距离 (AGD) 证明子宫内雄激素暴露将为 PCOS 的胎儿起源提供证据，并可能识别处于危险中的女孩。利用妊娠队列（婴儿发育与环境研究）的数据，我们测试了一个新假设，即患有 PCOS 的女性所生的女婴比无 PCOS 的女性所生的女婴具有更长的 AGD，这表明胎儿 T 暴露更高。在怀孕期间，女性报告她们是否曾经被诊断出患有多囊卵巢综合症。出生后，女婴接受了两次 AGD 测量：肛门距离 [AGD-AF] 和肛门阴蒂距离 [AGD-AC]。我们拟合调整后的线性回归模型来检查母亲 PCOS 和女孩 AGD 之间的关联。总共有 300 名母女拥有完整的数据，其中 23 名母亲报告患有 PCOS。与未诊断出 PCOS 的女性的女儿相比，诊断出 PCOS 的女性的 AGD 更长（AGD-AF：β=1.21，p=0.05；AGD-AC：β=1.05，p=0.18）。仅限于足月出生的分析结果更强（AGD-AF：β=1.65，p=0.02；AGD-AC：β=1.43，p=0.09）。我们的研究是第一个检查多囊卵巢综合症女性后代 AGD 的研究。我们的结果与 PCOS 女性 AGD 较长的发现一致，并表明在 PCOS 怀孕期间，女儿可能会经历较高的 T 暴露。确定多囊卵巢综合症的根本原因可能有助于对高危人群进行早期识别和干预。
Polycystic ovary syndrome (PCOS) affects approximately 7% of reproductive age women. Although its etiology is unknown, in animals, excess prenatal testosterone (T) exposure induces PCOS-like phenotypes. While measuring fetal T in humans is infeasible, demonstrating in utero androgen exposure using a reliable newborn biomarker, anogenital distance (AGD), would provide evidence for a fetal origin of PCOS and potentially identify girls at risk. Using data from a pregnancy cohort (The Infant Development and the Environment Study), we tested the novel hypothesis that infant girls born to women with PCOS have longer AGD, suggesting higher fetal T exposure, than girls born to women without PCOS. During pregnancy, women reported whether they ever had a PCOS diagnosis. After birth, infant girls underwent two AGD measurements: anofourchette distance [AGD-AF] and anoclitoral distance [AGD-AC]. We fit adjusted linear regression models to examine the association between maternal PCOS and girls’ AGD. In total, 300 mother-daughter dyads had complete data and 23 mothers reported PCOS. AGD was longer in the daughters of women with a PCOS diagnosis compared to daughters of women with no diagnosis (AGD-AF:β=1.21, p=0.05; AGD-AC:β=1.05, p=0.18). Results were stronger in analyses limited to term births (AGD-AF:β=1.65, p=0.02; AGD-AC:β=1.43, p=0.09). Our study is the first to examine AGD in offspring of women with PCOS. Our results are consistent with findings that women with PCOS have longer AGD and suggest that during PCOS pregnancies, daughters may experience elevated T exposure. Identifying the underlying causes of PCOS may facilitate early identification and intervention for those at risk.