Wolfrum R, Bordasch C, Holweg J
J Perinat Med. 1975;3(4):248-59. doi: 10.1515/jpme.1975.3.4.248.
A reliable method for surveillance of chronic impairment of nutritive placental function is described. The techniques are simple, tested for their reliability, without need for isotopes or special apparatus and hence inexpensive. Using 222 pregnancies at risk it is shown that the simultaneous determination of a fetal (estrogen) and a placental (pregnandiol) parameter makes the early diagnosis of intrauterine growth retardation possible. Estrogen diagnosis alone has a reliability of 90.1% with 1.8% falsely pathological and 8.1% falsely normal findings (Tab. I). Simultaneous pregnandiol determinations increase the number of falsely pathological findings to 8.1% but reduce that of falsely normal ones to 2.7%. No small for date (SGA) infants are found here. It consists of 5 cases of imminent (3 times actual) premature delivery and one postmature one. Hence our technique indicates the risk of intrauterine growth retardation in all cases but not the risk of premature or postmature delivery. Early diagnosis (from week 20) indicates that impairment of placental function as indicated by decreased pregnandiol excretion, occurs weeks or months earlier than decreased estrogen excretion (Fig. 1). This can be explained only by assuming that the rate of estrogen excretion is usually not dependent on the placenta but on the capacity of the fetal adrenals and liver. Thus our results indirectly confirm those of others who claim that the fetus can synthetize estrogen precursors without the need for placental pregnenolon by using acetate. Thus it appears that the synthetic pathway is independent of the placenta at the beginning plays a quantitative role also. Since the placenta can form aromatic compounds even when its nutritive function is severely impaired, our finding is further proof that estrogen excretion reflects fetal and not fetoplacental well-being. It follows that pathological estrogen excretion indicates fetal injury that has already occurred. The requirement that a sensitive parameter of placental function be hence determined in time is met by pregnandiol assays. Low pregnandiol excretion often precedes low estrogen excretion which leads to a SGA infant, indicating that pregnandiol excretion is closely correlated to placental nutritive function. Synthetic reactions in the fetus require energy and hence depend on the placenta. Normal estrogen excretion frequently observed in the presence of prolonged decreased pregnandiol excretion must hence indicate that the fetus can compensate for placental insufficiency. In the placenta this can be demonstrated by hyperplasia of the capillaries. This is reflected in the undulating excretion of pregnandiol (Fig. 1), where compensation (new vessel formation) and depression (lesion of vessels) make these contradictory placental processes "visible". The functional unity of the fetus and the placenta is finally also demonstrated by the fact that each prolonged compensatory phase of the placenta is reponded to by the fetus with a clearly compensatory excretion of estrogen (Fig. 1)...
本文描述了一种用于监测胎盘营养功能慢性损害的可靠方法。该技术简单，经过可靠性测试，无需同位素或特殊设备，因此成本低廉。通过对222例高危妊娠的研究表明，同时测定胎儿（雌激素）和胎盘（孕二醇）参数可实现宫内生长迟缓的早期诊断。仅雌激素诊断的可靠性为90.1%，假阳性病理结果为1.8%，假阴性正常结果为8.1%（表I）。同时测定孕二醇会使假阳性病理结果增加到8.1%，但假阴性正常结果减少到2.7%。这里未发现小于孕周（SGA）的婴儿。其中包括5例即将发生（3例实际发生）的早产和1例过期产。因此，我们的技术在所有情况下都能表明宫内生长迟缓的风险，但不能表明早产或过期产的风险。早期诊断（从第20周开始）表明，孕二醇排泄减少所提示的胎盘功能损害比雌激素排泄减少早数周或数月出现（图1）。这只能通过假设雌激素排泄率通常不依赖于胎盘，而是依赖于胎儿肾上腺和肝脏的能力来解释。因此，我们的结果间接证实了其他人的观点，即胎儿可以通过利用醋酸盐合成雌激素前体而无需胎盘孕烯醇酮。因此，似乎合成途径一开始就独立于胎盘，并且也起到了定量作用。由于即使胎盘的营养功能严重受损，它仍能形成芳香族化合物，我们的发现进一步证明雌激素排泄反映的是胎儿的健康状况，而不是胎儿 - 胎盘的健康状况。由此可见，病理性雌激素排泄表明已经发生了胎儿损伤。孕二醇测定满足了及时确定胎盘功能敏感参数的要求。低孕二醇排泄通常先于低雌激素排泄出现，而低雌激素排泄会导致SGA婴儿，这表明孕二醇排泄与胎盘营养功能密切相关。胎儿体内的合成反应需要能量，因此依赖于胎盘。在孕二醇排泄长期减少的情况下经常观察到正常的雌激素排泄，这必然表明胎儿可以补偿胎盘功能不全。在胎盘中，这可以通过毛细血管增生来证明。这反映在孕二醇的波动排泄上（图1），其中补偿（新血管形成）和抑制（血管损伤）使这些相互矛盾的胎盘过程“可见”。胎儿和胎盘的功能统一性最终也通过以下事实得到证明：胎盘的每个延长的补偿阶段都会引起胎儿明显的雌激素补偿性排泄（图1）……
