Longitudinal assessment of maternal-fetal Doppler parameters and maternal plasma level of matrix metalloproteinases 2 and 9.

OBJECTIVE: To assess the behavior as well as the comparison between maternal circulating level of biochemical markers (matrix metalloproteinases - MMP-9 and MMP-2) and maternal-fetal Doppler parameters in all three trimesters of pregnancy. METHODS: We performed a prospective longitudinal study with 33 healthy pregnant women in three periods of pregnancy: A1 (12w0-14w6d), A2 (22w0d-24w6d) and A3 (34w0d and 36w6d). The following maternal Doppler parameters were assessed: mean pulsatility index (PI) uterine artery, resistance index (RI) umbilical artery and RI middle cerebral artery. The maternal plasma concentrations of MMP-2 and MMP-9 were determined by enzyme immunoassay (ELISA). To compare two (A2 and A3) and three assessments (A1, A2 and A3), we used the paired Student t test and linear regression, respectively. To compare the biomechanical markers and maternal-fetal Doppler parameter, we used the Spearman correlation coefficient (ρ). RESULTS: We observed a significant decrease of PI uterine artery Doppler over the three trimesters of pregnancy (p < 0.01) and RI umbilical artery Doppler overt second to three trimester of pregnancy (p < 0.05). We did not observe significant difference in the maternal plasma level of MMP-2 and MMP-9 between the three trimesters. We did not also observe significant correlation between biochemical markers and maternal-fetal Doppler parameters. CONCLUSION: Maternal circulating level of MMPs did not modify throughout pregnancy and it did not show correlation with maternal-fetal Doppler parameters.

Polymorphisms and haplotypes in candidate genes related to angiogenesis and endothelial dysfunction in preeclampsia.

Valenzuela and colleagues have recently reviewed some polymorphisms in important candidate genes involved in different pathogenic mechanisms related to preeclampsia (PE) and concluded that various studies in different populations have identified maternal polymorphisms associated with PE. However, we would like to contribute to some studies regarding candidate genes related to angiogenesis and endothelial dysfunction in PE performed in the Brazilian population. Specifically, genotypes and haplotypes formed by polymorphisms of VEGF, eNOS and MMP-9, along with an example of the interaction among these genes in the prediction of PE. Our suggestions may provide additional information with clinical relevance to PE susceptibility.