Luiza Oliveira Perucci1, Kelerson Mauro de Castro Pinto2, Sirlaine Pio Gomes da Silva3, Eura Martins Lage4, Patrícia Gonçalves Teixeira5, Alexandre Simões Barbosa6, Patrícia Nessralla Alpoim7, Lirlândia Pires de Sousa8, André Talvani9, Luci Maria SantAna Dusse10. 1. Laboratory of Immunobiology of Inflammation, Department of Biological Sciences/ICEB, Federal University of Ouro Preto, Ouro Preto, Brazil; Nucleus of Research on Biological Sciences/NUPEB, Federal University of Ouro Preto, Ouro Preto, Brazil. Electronic address: luiza.perucci@ufop.edu.br. 2. Laboratory of Immunobiology of Inflammation, Department of Biological Sciences/ICEB, Federal University of Ouro Preto, Ouro Preto, Brazil; School of Physical Education, Federal University of Ouro Preto, Ouro Preto, Brazil. Electronic address: kelerson@ufop.edu.br. 3. Laboratory of Immunobiology of Inflammation, Department of Biological Sciences/ICEB, Federal University of Ouro Preto, Ouro Preto, Brazil. Electronic address: sirlainep10@gmail.com. 4. Department of Gynecology and Obstetrics, Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, Brazil. Electronic address: euramartinslage@gmail.com. 5. Department of Gynecology and Obstetrics, Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, Brazil. Electronic address: pgt2008@ufmg.br. 6. Department of Gynecology and Obstetrics, Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, Brazil. Electronic address: alexandre.oftalmo@gmail.com. 7. Department of Clinical and Toxicological Analysis, Faculty of Pharmacy, Federal University of Minas Gerais, Belo Horizonte, Brazil. Electronic address: patnessralla@yahoo.com.br. 8. Department of Clinical and Toxicological Analysis, Faculty of Pharmacy, Federal University of Minas Gerais, Belo Horizonte, Brazil. Electronic address: lipsousa72@gmail.com. 9. Laboratory of Immunobiology of Inflammation, Department of Biological Sciences/ICEB, Federal University of Ouro Preto, Ouro Preto, Brazil. Electronic address: talvani@ufop.edu.br. 10. Department of Clinical and Toxicological Analysis, Faculty of Pharmacy, Federal University of Minas Gerais, Belo Horizonte, Brazil. Electronic address: lucidusse@gmail.com.
Abstract
OBJECTIVES: We carried out a longitudinal study to compare leukotriene B4 (LTB4), lipoxin A4 (LXA4), and resolvin D1 (RvD1) levels in pregnant women with risk factors for PE - who did (N = 11) or did not develop (N = 17) this clinical condition. DESIGN & METHODS: For both groups, plasma levels of the lipid mediators were measured using immunoassays at 12-19, 20-29, and 30-34 weeks of gestation. RESULTS: LTB4 tended to be upregulated throughout gestation in women who developed PE. Moreover, this increase was significant at 30-34 weeks. Although LXA4 levels also tended to be higher in the PE group, this difference was not significant for the evaluated gestational periods. Pregnant women with PE had lower RvD1 levels and a low RvD1/LTB4 ratio at 30-34 weeks, compared to those in the normotensive pregnant women. Contrarily, RvD1 levels increased at weeks 12-19 in pregnant women who developed PE. Particularly, LXA4 and RvD1 levels were higher at 30-34 weeks than those at 20-29 weeks considering both groups of women. We observed an interaction between the gestational outcome and the gestational period in case of RvD1. CONCLUSIONS: The imbalance among LTB4, LXA4, and RvD1 levels in these preeclamptic women is consistent with the excessive inflammation that underlies the pathogenesis of PE. Although our data highlight the potential for the use of these lipid mediators as clinical markers for PE development, future longitudinal studies must be carried out to confirm these findings.
OBJECTIVES: We carried out a longitudinal study to compare leukotriene B4 (LTB4), lipoxin A4 (LXA4), and resolvin D1 (RvD1) levels in pregnant women with risk factors for PE - who did (N = 11) or did not develop (N = 17) this clinical condition. DESIGN & METHODS: For both groups, plasma levels of the lipid mediators were measured using immunoassays at 12-19, 20-29, and 30-34 weeks of gestation. RESULTS: LTB4 tended to be upregulated throughout gestation in women who developed PE. Moreover, this increase was significant at 30-34 weeks. Although LXA4 levels also tended to be higher in the PE group, this difference was not significant for the evaluated gestational periods. Pregnant women with PE had lower RvD1 levels and a low RvD1/LTB4 ratio at 30-34 weeks, compared to those in the normotensive pregnant women. Contrarily, RvD1 levels increased at weeks 12-19 in pregnant women who developed PE. Particularly, LXA4 and RvD1 levels were higher at 30-34 weeks than those at 20-29 weeks considering both groups of women. We observed an interaction between the gestational outcome and the gestational period in case of RvD1. CONCLUSIONS: The imbalance among LTB4, LXA4, and RvD1 levels in these preeclamptic women is consistent with the excessive inflammation that underlies the pathogenesis of PE. Although our data highlight the potential for the use of these lipid mediators as clinical markers for PE development, future longitudinal studies must be carried out to confirm these findings.