Vol 78, No 10 (2007)

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Maternal serum concentration of angiogenic factors: PIGF, VEGF and VEGFR-1 and placental volume in pregnancies complicated by intrauterine growth restriction

Anna Semczuk-Sikora, Arkadiusz Krzyzanowski, Norbert Stachowicz, Jacek Robak, Janusz Kraczkowski, Maciej Kwiatek, Marian Semczuk
Ginekol Pol 2007;78(10).


INTRODUCTION: 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. AIM: 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. MATERIAL AND METHODS: 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). RESULTS: 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. CONCLUSIONS: 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.

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