Angiogenesis is one of the most important steps during pregnancy for placental and fetal development. Based on the hypothesis that vascular insufficiency and altered angiogenesis may lead to early pregnancy loss, the present study was aimed to understand the role of Vascular endothelial growth factor (VEGFA) and Placental growth factor (PLGF) gene expression in placental angiogenesis in the pathogenesis of Recurrent pregnancy loss (RPL). Gene expression analysis of VEGFA and PLGF was carried out in the placental tissue collected from 30 women with recurrent pregnancy loss and compared with the placenta obtained from 16 women with medically terminated pregnancy. The mRNA expression of both VEGFA and PLGF genes were significantly downregulated in the placenta of recurrent pregnancy loss in comparison to the placenta of medically terminated pregnancies. In conclusion the results of the present study suggest that altered expression of VEGFA and PLGF genes in placenta disturb the angiogenesis and contribute to the pathogenesis of recurrent pregnancy loss.
Background: Lupus nephritis (LN) is one of the most severe manifestations of systemic lupus erythematosus (SLE). There are increased studies examining the role of different markers that would facilitate diagnosis, LN activity monitoring, relapse occurrence, and the right time to introduce maintenance therapy. We aimed to examine the importance of determining the neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), systemic immuneinflammatory index (SII) and systemic inflammatory response index (SIRI) in LN, comparing their significance with other standard parameters of active disease.
Methods: The clinical examination included 66 patients (34 with active and 32 with LN in remission) and 23 healthy controls. The investigated parameters were CRP, CBC, creatinine, albumin, GFR, C3, C4, ANA, anti-ds DNA Ab, in urine: sediment analysis, SLEDAI/r, proteinuria 24h and Up/cre. We determined the derived markers: NLR, PLR, SIRI, and SII and their correlation with other parameters of active disease.