Table 2.
Summary of studies developed in Latin America evaluating the role of genetic variation in vascular- and angiogenesis-related genes in PE.
| Factors | Sample size† | Key findings | Country | References |
|---|---|---|---|---|
| eNOS (−786T>C, intron-4 b/a, Glu298Asp) | 322/522 | Association with PE risk: 298Asp/Asp genotype and eNOS C-b-Asp haplotype. | Colombia | Serrano et al., 2004 |
| eNOS (−786T>C, intron-4 b/a, Glu298Asp) | 216/110a | Association with PE and GH risk: eNOS C-a-Glu haplotype. Association with protection for PE and GH: eNOS T-a-Glu haplotype |
Brazil | Sandrim et al., 2008 |
| eNOS (−786T>C, intron-4 b/a, Glu298Asp) | 127/263 | Association with PE risk: 298Asp/Asp genotype and eNOS C-b-Asp. | Mexico | Díaz-Olguín et al., 2011 |
|
eNOS (−786T>C, intron-4 b/a, Glu298Asp) MMP2 (C-1306T) MMP9 (C-1562T) |
77/266 | Association with PE risk and severity: −786CC genotype and −786C allele, respectively. | Brazil | Leonardo et al., 2015 |
| eNOS (−786T>C, intron-4 b/a, Glu298Asp) | 98/103b | Association with late-onset PE risk: 298Asp/Asp genotype and 298Asp allele; intron-4 aa genotype and a allele; eNOS C-b-Asp. | Brazil | Alpoim et al., 2014 |
| eNOS (−786T>C), intron-4 b/a, Glu298Asp | 152/152c | Association with anti-hypertensive therapy in PE, eNOS haplotypes: C-a-Glu responsive and T-a-Asp non-responsive. | Brazil | Sandrim et al., 2010a |
| eNOS (−786T>C, intron-4 b/a, Glu298Asp, rs743506, rs7830) | 295/122d | Association with protection for PE and GH: eNOS C-b-Glu-G-C haplotype. | Brazil | Muniz et al., 2012 |
| eNOS (C-1026A, G2087A) | 353/212e | Association with PE risk: 2087GA genotype and the 2087A allele. | Brazil | Amaral et al., 2012 |
| HP (Hp1-1, Hp2-1, Hp2-2) | 92/105 | No association with PE risk. Nitric Oxide byproducts in PE associated with Hp2-1 and Hp2-2 genotypes. | Brazil | Sertório et al., 2013 |
| TAFI (G505A, C1040T, G-438A) | 87/87 | No association with PE. | Mexico | Acosta-Tejeda et al., 2011 |
|
MTHFR (C677T) FV LEIDEN (G1691A) PROTHROMBIN (G20210A) |
28/41 | No association with PE. | Mexico | Rojas et al., 2010 |
| MTHFR (C677T) | 148/490f | No association with PE | Mexico | Pérez-Mutul et al., 2004 |
| MTHFR (C677T, A1298C) | 150/150 | Association with PE risk: 1298CC genotype. | Ecuador | Chedraui et al., 2014 |
| MTHFR (C677T) | 125/274 | Association with protection for PE: 677TT genotype and 677T allele. | Mexico | Canto et al., 2008 |
| VEGF (C-2578A, G-1154A, G-634C) | 195/108g | Association with protection for PE: VEGF−2578C/-1154G/-634C haplotype. Low proportion of-2578AA and−634GG genotypes in white PE women. | Brazil | Sandrim et al., 2009 |
| VEGF (C936T, C-2578A) | 52/28 | Association with protection for PE: VEGF−2578A allele. | Brazil | Cunha et al., 2011 |
| VEGF (C2578A, G634C) | 113h | No association with PE. | Brazil | Sandrim et al., 2015 |
|
VEGF (G634C) IL1A (rs3783550) |
79/210 | Association with PE risk: IL1A rs3783550 “A” allele. | Brazil | Silva et al., 2015 |
| VEGF (A2578C, C1498T, A1154G, C634G,C936T) | 31/31i | No association with PE. | Ecuador | Chedraui et al., 2013 |
|
eNOS (T786C, VNTR, G894T) MTHFR (C677T) AGT (C704T) |
230/350 | No association with PE. | Mexico | Coral-Vázquez et al., 2013 |
| MMP9 (C1562T, (CA)n repeats) | 300/176j | Association with risk for GH: MMP9 C1562 T allele. No association with PE. | Brazil | Palei et al., 2010 |
|
eNOS (T786C, VNTR, G894T) MMP9 (C1562T, (CA)n repeats) VEGF (C2578A, G634C) |
229/102k | Association with protection for PE: combination of MMP9-1562CC with VEGF-634GG genotypes. Association with PE risk: combination of MMP9-1562CC with VEGF-634CC or MMP9-1562CT with VEGF-634CC or-634GG genotypes. |
Brazil | Luizon et al., 2012 |
| MMP2 (C1306T, C735T) | 263/130l | No association with PE. | Brazil | Palei et al., 2012a |
| MMP9 (C1562T, (CA)n repeats) | 399/214m | Association with GH: combination of the “T” allele for the C1562T and “H” allele of 90(CA)13–25. | Brazil | Palei et al., 2012b |
|
MTHFR (C677T) Factor II (G20210A) FV LEIDEN (G1691A) PAI1 (4G/5G I/D) |
75/145 | No association with PE. | Brazil | Dalmáz et al., 2006 |
|
MTHFR (C677T) FV LEIDEN (G1691A) |
33/62 | No association with PE. | Mexico | Dávalos et al., 2005 |
| ACVR2A (rs1424954, rs1014064, rs1424941, rs2161983, rs3768687) | 613/693n | Association with severe early-onset PE risk: SNPs rs1014064 “G,” rs1424954 “A,” and rs2161983 “A.” | Brazil | Ferreira et al., 2015 |
| ACE (287 bp I/D in intron 16) | 51/71 | No association with PE. | Brazil | Galão et al., 2004 |
|
FV LEIDEN (G1691A) Factor II (G20210A) MTHFR (C677T) |
30/83 | No association with PE. | Brazil | Dusse et al., 2007 |
| ACE (287 bp I/D in intron 16) | 66/37 | Association with risk for PE: ACE “DD” genotype. | Mexico | González-Garrido et al., 2017 |
| EDN1 (G5665T) | 61/49o | Association with protection for PE: paternal EDN1 “GG” and “GT” genotypes. | Mexico | Galaviz-Hernandez et al., 2016 |
| MTHFR (C677T, A1298C) | 50/50p | Association with risk for PE: MTHFR 677TT genotype. | Ecuador | Chedraui et al, 2015 |
| ACE (287 bp I/D in intron 16) | 665/1,046 | No association with PE. | Colombia | Serrano et al., 2006 |
| HIF1A (C1772T, G1790A) | 150/105 | No association with PE. | Mexico | Nava-Salazar et al., 2011 |
| VDR (FokI, ApaI, BsmI) | 316/213q | No association with PE. | Brazil | Rezende et al., 2012 |
| COMT (rs6269, rs4633, rs4680, and rs4818), MTHFR (C677T) | 528/575r | Association with PE risk: “ATCA” haplotype of COMT (SNPs rs6269, rs4633, rs4818, rs4680, and MTHFR 677T) | Chile | Hill et al., 2011a |
Pooled cases/controls.
Cases were stratified in PE (n = 113) and gestational hypertension (GH, n = 103).
Cases were stratified in early severe PE (n = 53) and late severe PE (n = 45).
Cases were stratified in PE (n = 152) and GH (n = 152).
Cases were stratified in PE (n = 157) and GH (n = 138).
Cases were stratified in PE (n = 187) and GH (n = 166).
Sample size composed by PE cases (n = 148), health pregnant woman (N = 177), and health non-pregnant volunteers (313).
Cases were stratified in PE (n = 94) and GH (n = 101).
Sample size was composed by 113 PE white women who were responsive (n = 46) and non-responsive (n = 67) to anti-hypertensive treatment.
Sample size was composed by 62 cord vessels of singleton gestations with severe PE (n = 31) and controls (n = 31).
Cases were stratified in PE (n = 154) and GH (n = 146).
Cases were stratified in PE (n = 122) and GH (n = 107).
Cases were stratified in PE (n = 133) and GH (n = 130).
Cases were stratified in PE (n = 214) and GH (n = 185).
Cases were stratified in PE (n = 443), eclampsia (n = 138), and HELLP syndrome (n = 693).
°Sample size composed by PE cases (n = 61) and their partners (n = 61), and the control group was health pregnant woman (N = 49) and their partners (n = 49).
Sample size composed by 100 placental tissues of PE cases (n = 50) and controls (n = 50).
Cases were stratified in PE (n = 162) and GH (n = 154).
Sample size was composed by maternal-fetus dyads from PE cases (n = 528) and controls (n = 575).