Table 3.
Summary of studies in Latin America evaluating the role of genetic variants in histocompatibility-related genes in PE.
| Factors | Sample size† | Key findings | Country | References |
|---|---|---|---|---|
| HLA-A, -G, -DRB1, -DQA1, -DQB1 alleles | 27/29a | Association with PE risk: HLA-G*0104 allele, DRB1*07 DQA1*0201 DQB1*0201 haplotype and DRB1*07 and/or DRB1*06 alleles in presence of HCMV detection. | Venezuela | Carreiras et al., 2002 |
| HLA-G (14 bp ins/del) | 157/162 | No association with PE. | Brazil | Vianna et al., 2007 |
| KIR inhibitory(2DL1, 2DL2, 2DL3, 2DL4, 2DL5, 3DL1, 3DL2, 3DL3); activating (2DS1, 2DS2, 2DS3, 2DS4, 2DS5, 3DS1); pseudogenes (2PQ1, 3DP1) | 90/86 | No association with PE. | Mexico | Sánchez-Rodríguez et al., 2011 |
| HLA-G (14 bp ins/del, +3142C>G). | 26/32b | No association with PE. | Brazil | Vianna et al., 2016 |
| HLA-G (14 bp ins/del) | 409/332c | No association with PE. | Brazil | Ferreira et al., 2017 |
| ERAP2 (rs2549782, rs17408150) | 528/575d | No association with PE. | Chile | Hill et al., 2011b |
†
Pooled cases/controls.
a
Samples were mother-neonate dyads.
b
Controls were grouped in non-PE (n = 25) and healthy group (n = 7).
c
Cases were grouped in PE (n = 246), eclampsia (n = 57), and HELLP (n = 106). PE, preeclampsia; HLA, human leukocyte antigen; HCMV, human cytomegalovirus; ins, insertion; del, deletion; KIR, killer cell immunoglobulin-like receptor; ERAP2, endoplasmic reticulum aminopeptidase-2
d
Only Chilean mother-neonate dyads.