Semczuk-Sikora Anna, Krzyzanowski Arkadiusz, Stachowicz Norbert, Robak Jacek, Kraczkowski Janusz, Kwiatek Maciej, Semczuk Marian
Klinika Połoznictwa i Patologii Ciazy AM im F. Skubiszewskiego w Lublinie.
Ginekol Pol. 2007 Oct;78(10):783-6.
Pathomechanism of intrauterine growth restriction is a complex issue, involving many different factors, and is still undergoing an investigation. Improper placental angiogenesis, resulting in placental pathology, is considered to be one of the most important causes of IUGR. Placental vascular growth factors--placental growth factor (PIGF), vascular endothelial growth factor (VEGF) and its receptor (VEGFR-1), are involved in the mechanism of placental vascular development and maternal endothelial function during the pregnancy.
The aim of our study was to evaluate the maternal serum concentration of vascular growth factors (PIGF, VEGF) and their receptor (VEGFR-1), as well as the placental volume in pregnancies complicated by IUGR, and to compare the results with healthy control groups.
20 patients with intrauterine growth restriction and 18 healthy pregnant women were recruited. Their blood serum samples were assayed for the placental growth factor (PIGF), vascular endothelial growth factor (VEGF) and their receptor (VEGFR-1). These placental factors were measured with the ELISA- method (R@D Systems Kits. In all cases the placental volume was assessed with an ultrasound (Voluson V730 GE) with VOCAL (Virtual Organ Komputer-aided AnaLysis).
Our investigation revealed significantly lower maternal serum concentrations of PIGF in pregnancies with IUGR, comparing to the controls in the third trimester. In most cases, VEGF concentrations were undetectable in the maternal serum both, in the second as well as in the third trimester. In the 2nd trimester VEGFR-1 concentrations were statistically higher in the investigated group. In the 3rd trimester the concentrations of VEGFR-1 were higher in the investigated group, but the difference has not achieved the level of statistical importance. The mean placental volume was lower in the investigated group but with not statistical gnificance.
Presented and documented dependencies may indicate the involvement of angiogenic factors in a pathomechanism of intrauterine growth restriction process. It seems that the measurement of placental volume may be useful in IUGR diagnosis. However, it should be a complementary examination only, due to technical limitations.
胎儿宫内生长受限的发病机制是一个复杂的问题,涉及许多不同因素,仍在研究中。胎盘血管生成不当导致胎盘病变,被认为是胎儿宫内生长受限最重要的原因之一。胎盘血管生长因子——胎盘生长因子(PIGF)、血管内皮生长因子(VEGF)及其受体(VEGFR-1),参与孕期胎盘血管发育和母体血管内皮功能机制。
我们研究的目的是评估合并胎儿宫内生长受限的孕妇血清中血管生长因子(PIGF、VEGF)及其受体(VEGFR-1)的浓度,以及胎盘体积,并将结果与健康对照组进行比较。
招募20例胎儿宫内生长受限患者和18例健康孕妇。检测她们血清中的胎盘生长因子(PIGF)、血管内皮生长因子(VEGF)及其受体(VEGFR-1)。这些胎盘因子采用ELISA法(R@D Systems试剂盒)进行检测。所有病例均使用配备VOCAL(虚拟器官计算机辅助分析)的超声(Voluson V730 GE)评估胎盘体积。
我们的研究显示,与孕晚期对照组相比,胎儿宫内生长受限孕妇血清中PIGF浓度显著降低。在大多数情况下,孕中期和孕晚期母体血清中均未检测到VEGF浓度。孕中期,研究组VEGFR-1浓度在统计学上较高。孕晚期,研究组VEGFR-1浓度较高,但差异未达到统计学意义水平。研究组平均胎盘体积较低,但无统计学意义。
所呈现和记录的相关性可能表明血管生成因子参与了胎儿宫内生长受限过程的发病机制。胎盘体积测量似乎对胎儿宫内生长受限的诊断有用。然而,由于技术限制,它仅应作为一项补充检查。