Marozio Luca, Garofalo Anna, Berchialla Paola, Tavella Anna Maria, Salton Loredana, Cavallo Franco, Benedetto Chiara
Department of Surgical Sciences, Obstetrics and Gynecology, University of Turin, Sant'Anna University Hospital, Turin, Italy.
Department of Clinical and Biological Sciences, University of Turin, Turin, Italy.
J Obstet Gynaecol Res. 2017 Sep;43(9):1391-1396. doi: 10.1111/jog.13377. Epub 2017 Jul 10.
Abnormal placentation is a common pathogenic mechanism of many placenta-mediated complications of late pregnancy, including pre-eclampsia, fetal growth restriction, stillbirth, and placental abruption. During successful placentation, the trophoblast (which is a semi-allograft) is not rejected by decidual immune cells because of maternal immune tolerance, mainly induced by human leukocyte antigen G (HLA-G). Deficient HLA-G expression seems to be associated with the development of complications of pregnancy. The aim of this study was to determine whether low soluble HLA-G (sHLA-G) levels in maternal blood at the beginning of pregnancy may be associated with subsequent placenta-mediated complications.
For this retrospective case-control study, 117 cases of placenta-mediated complications of pregnancy and 234 controls with uneventful pregnancy were selected. Plasma sHLA-G levels were measured at 11-13 weeks' gestation by the enzyme-linked immunosorbent assay method in blood samples previously obtained at first-trimester prenatal screening for chromosomal fetal abnormalities.
Women who subsequently developed placenta-mediated complications had significantly lower sHLA-G levels at the beginning of pregnancy (median, 43.08 IU/mL) than controls (median, 49.10 IU/mL; P = 0.008). An sHLA-G level lower than 43.50 IU/mL at the end of the first trimester was associated with a twofold increased risk of developing a pregnancy complication (odds ratio, 1.82; 95% confidence interval, 1.22-2.73). The strongest association, although only moderately strong, was observed with severe pre-eclampsia (odds ratio, 2.66; 95% confidence interval, 1.08-6.56).
Placenta-mediated complications of pregnancy may be associated with low sHLA-G levels in the first trimester, suggesting a potential role of sHLA-G in the early stages of placentation.
胎盘形成异常是许多晚期妊娠胎盘介导并发症的常见致病机制，包括子痫前期、胎儿生长受限、死产和胎盘早剥。在成功的胎盘形成过程中，滋养层细胞（一种半同种异体移植物）由于主要由人类白细胞抗原G（HLA-G）诱导的母体免疫耐受而不被蜕膜免疫细胞排斥。HLA-G表达不足似乎与妊娠并发症的发生有关。本研究的目的是确定妊娠初期母体血液中低可溶性HLA-G（sHLA-G）水平是否与随后的胎盘介导并发症有关。
在这项回顾性病例对照研究中，选择了117例妊娠胎盘介导并发症患者和234例妊娠结局正常的对照者。在妊娠11-13周时，采用酶联免疫吸附测定法，对孕早期产前筛查染色体胎儿异常时采集的血样中的血浆sHLA-G水平进行测定。
随后发生胎盘介导并发症的女性在妊娠初期的sHLA-G水平（中位数为43.08 IU/mL）显著低于对照组（中位数为49.10 IU/mL；P = 0.008）。孕早期末sHLA-G水平低于43.50 IU/mL与发生妊娠并发症的风险增加两倍相关（比值比为1.82；95%置信区间为1.22-2.73）。观察到与重度子痫前期的关联最强，尽管强度仅为中等（比值比为2.66；95%置信区间为1.08-6.56）。
妊娠胎盘介导并发症可能与孕早期低sHLA-G水平有关，提示sHLA-G在胎盘形成早期可能发挥潜在作用。
