Shaarawy Mohamed, Zaki Sameh, Ramzi Abdel-Megid, Salem Mahmoud E, El-Minawi Ahmed M
Department of Obstetrics and Gynecology, Kasr Al-Aini School of Medicine, Cairo University, Cairo, Egypt.
J Soc Gynecol Investig. 2005 Jul;12(5):343-8. doi: 10.1016/j.jsgi.2005.02.014.
To investigate feto-maternal bone turnover in normal pregnancy and preeclampsia and to test the hypothesis whether the reported low bone mass at birth in small-for-gestational age infants is associated with decreased bone formation or increased bone resorption.
Thirty-two patients with preeclampsia (17 mild and 15 severe) and 20 normotensive women (controls) with singleton gestations in the third trimester participated in this study. Furthermore, 25 nonpregnant healthy women were chosen as nonpregnant controls. Maternal 24-hour urine specimens and venous blood samples were collected. In addition, fetal cord blood and the first voided neonatal urine were also collected. The freshly separated sera were assayed for osteocalcin (OC) and carboxy-terminal propeptide of type 1 collagen (PICP) by radioimmunoassay. Urine samples were assayed for N-telopeptide of type 1 collagen (NTx) by enzyme-linked immunosorbent assay.
Maternal and cord serum OC and PICP levels were significantly decreased in severe preeclampsia, whereas maternal and first-voided neonatal urinary NTx level were significantly increased compared to the corresponding levels of controls. In both mother and fetus, the coupling index of markers of bone turnover in normal pregnancy or mild preeclampsia was in favor of bone formation, whereas in severe preeclampsia the markers suggested marked bone resorption.
Increased bone resorption and decreased bone formation occur in preeclampsia in both mother and fetus, being more pronounced in the latter. The increased osteoclastic activity in preeclampsia may be attributed to increased RANKL induced by increased interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor beta2 (TGF-beta2) production.
研究正常妊娠和子痫前期母胎骨转换情况，并验证以下假说：小于胎龄儿出生时低骨量是否与骨形成减少或骨吸收增加有关。
32例子痫前期患者（17例轻度，15例重度）和20例孕晚期单胎妊娠的血压正常女性（对照组）参与了本研究。此外，选取25名非妊娠健康女性作为非妊娠对照组。收集母体24小时尿液标本和静脉血样本。另外，还收集胎儿脐血和新生儿首次晨尿。采用放射免疫分析法检测新鲜分离血清中的骨钙素（OC）和1型胶原羧基端前肽（PICP）。采用酶联免疫吸附测定法检测尿液样本中的1型胶原N-端肽（NTx）。
与对照组相应水平相比，重度子痫前期患者母体和脐血血清OC和PICP水平显著降低，而母体和新生儿首次晨尿NTx水平显著升高。在母亲和胎儿中，正常妊娠或轻度子痫前期骨转换标志物的偶联指数有利于骨形成，而在重度子痫前期，标志物提示明显的骨吸收。
子痫前期母胎均出现骨吸收增加和骨形成减少，胎儿更为明显。子痫前期破骨细胞活性增加可能归因于白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）和转化生长因子β2（TGF-β2）产生增加导致的核因子κB受体活化因子配体（RANKL）增加。
