Parker C R, Hauth J C, Goldenberg R L, Cooper R L, Dubard M B
Department of Obstetrics and Gynecology and the Center for Obstetrics Research, The University of Alabama at Birmingham, 35233-7333, USA.
J Matern Fetal Med. 2000 Jul-Aug;9(4):209-15. doi: 10.1002/1520-6661(200007/08)9:4<209::AID-MFM4>3.0.CO;2-S.
Our aim was to quantify thromboxane B2 (TXB2) in umbilical cord serum of term infants of nulliparous, low-risk women who were randomly assigned to either placebo or low-dose (60 mg) aspirin (ASA) on a daily basis from 24 weeks' gestation through delivery as part of a randomized clinical trial for prevention of preeclampsia.
Umbilical cord sera from 230 singleton, term infants whose mothers were involved in our low-dose ASA trial were assayed for TXB2, the stable metabolite of thromboxane A2, without knowledge of treatment or outcome data. The data were related to assigned treatment group, longitudinal pattern of maternal serum TXB2 levels, and other maternal and newborn characteristics. The data also were analyzed according to whether or not maternal serum levels of TXB2 at 29-31, 34-36, and delivery were reduced > or =50% compared to values prior to initiation of the trial.
Umbilical cord TXB2 levels (ng/ml, mean +/- SE) were significantly lower at term in the ASA group (36.1 +/- 3.3, n = 111) than in the placebo group (56.6 +/- 5.7, n = 119; P = 0.002). Umbilical cord TXB2 levels were correlated to those in maternal serum at delivery in the ASA group (r = 0.3441; P = 0.0005) but not in the placebo group (r = 0.0626; P = 0.53). Regardless of assigned treatment group, infants whose mothers had a > or =50% longitudinal reduction in serum TXB2 had lower umbilical cord TXB2 levels (39.2 +/- 3.6, n = 114) than infants whose mothers had <50% reductions in TXB2 (54.6 +/- 5.9, n = 116; P = 0.027). Birthweights of these infants correlated inversely (r = 0.1678, P = 0.017) with maternal serum TXB2 at delivery but not to umbilical cord TXB2 levels; the best correlation between birthweight and maternal serum TXB2 was noted in pregnancies assigned to receive placebo (r = -0.2558, P = 0.009).
Umbilical cord serum levels of TXB2 1) are reduced in instances of long-term maternal ingestion of ASA, 2) correlate well with maternal serum levels of TXB2 at delivery when there is evidence for consistent maternal use of ASA, but 3) do not correlate with maternal serum TXB2 levels when there is no evidence for frequent maternal ingestion of cyclooxygenase inhibitors. These data suggest that the capacity for platelet production of TXA2 in fetal and maternal compartments are regulated independently. Finally, there is an inverse relationship between maternal serum TXB2 levels at delivery and birthweight of newborn infants that is most evident among the pregnancies assigned to placebo and also among pregnancies in which there was little evidence to suggest a pattern of cyclooxygenase inhibitor use during pregnancy.
作为预防子痫前期的一项随机临床试验的一部分，我们的目的是对未生育、低风险孕妇足月婴儿脐带血清中的血栓素B2（TXB2）进行定量分析。这些孕妇从妊娠24周起至分娩期间被随机分配至安慰剂组或每日服用低剂量（60毫克）阿司匹林（ASA）组。
对230名单胎足月婴儿的脐带血清进行TXB2检测，这些婴儿的母亲参与了我们的低剂量ASA试验。检测时不知道治疗情况或结局数据。数据与指定的治疗组、母亲血清TXB2水平的纵向模式以及其他母亲和新生儿特征相关。还根据母亲在妊娠29 - 31周、34 - 36周和分娩时血清TXB2水平与试验开始前相比是否降低≥50%对数据进行分析。
ASA组足月时脐带TXB2水平（纳克/毫升，均值±标准误）显著低于安慰剂组（36.1±3.3，n = 111）（56.6±5.7，n = 119；P = 0.002）。ASA组分娩时脐带TXB2水平与母亲血清中的水平相关（r = 0.3441；P = 0.0005），而安慰剂组则无相关性（r = 0.0626；P = 0.53）。无论指定的治疗组如何，母亲血清TXB2水平纵向降低≥50%的婴儿，其脐带TXB2水平（39.2±3.6，n = 114）低于母亲TXB2水平降低<50%的婴儿（54.6±5.9，n = 116；P = 0.027）。这些婴儿的出生体重与母亲分娩时血清TXB2呈负相关（r = 0.1678，P = 0.017），但与脐带TXB2水平无关；在分配接受安慰剂的妊娠中，出生体重与母亲血清TXB2之间的相关性最佳（r = -0.2558，P = 0.009）。
脐带血清TXB2水平1）在母亲长期摄入ASA的情况下会降低，2）当有证据表明母亲持续使用ASA时，与母亲分娩时血清TXB2水平密切相关，但3）当没有证据表明母亲频繁摄入环氧化酶抑制剂时，与母亲血清TXB2水平无关。这些数据表明，胎儿和母体血小板产生TXA2的能力是独立调节的。最后，母亲分娩时血清TXB2水平与新生儿出生体重之间存在负相关关系，这在分配接受安慰剂的妊娠中最为明显，在几乎没有证据表明孕期使用环氧化酶抑制剂模式的妊娠中也是如此。
