PubMed · 14758334
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Judith Korby. 2004. Abruptio placentae.. https://doi.org/10.1097/00152193-200402000-00059
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OBJECTIVE: Several variables related to increased risk of placental abruption are also risk factors for venous thromboembolism. Prior second trimester-, third trimester, and repeated fetal loss are reported to be associated to thrombophilias. However, it is yet not known if they are also related to placental abruption. STUDY DESIGN: A retrospective case-control study of 161 women with placental abruption and 2371 unselected gravidae without placental abruption. The medical files were scrutinized and the selected variables were investigated in relation to the development of placental abruption. RESULTS: As compared to controls, previous second trimester-, third trimester-, repeated fetal loss, and prior placental abruption were related to a 3-, 13-, 3-, and a 25-fold increased risk of placental abruption, respectively. Several other factors were associated with a roughly three-fold increased risk such as: preeclampsia, IUGR, high maternal age (>35), family history of venous thromboembolism, smoking, and multiple birth. A risk score was created and as compared with those with no risk factors present, the risk of placental abruption was increasing from 2.5-fold for those with risk score=1, to almost 100-fold for risk score 4 or above. CONCLUSION: Easily obtainable information might be used to classify the risk of placental abruption.
OBJECTIVES: RCAS1 is a membrane protein that plays a role in the maintenance of maternal immune tolerance during pregnancy. The work presented here demonstrates the results of RCAS1 expression in placenta in cases of placental abruption and patients with retained placental tissue during the third stage of labor. STUDY DESIGN: The placenta tissue samples were obtained during vaginal and cesarean delivery (derived from 117 pregnancies). Pregnant women were divided into four groups according to the onset of labor and the time of placental detachment in term labors. The samples were analyzed by the Western blot method. Statistical analysis was performed using the Shapiro-Wilk procedure. The Mann-Whitney test and Student's t-test were applied to compare the differences between parametric data. RESULTS: The average relative amount of RCAS1 observed in those patients with retained placental tissue was statistically significantly higher than in the patients with placental abruption. CONCLUSION: The differences observed in placental RCAS1 levels confirm the participation of this protein in the inhibition of maternal immune response during gestation. The present results also indicate that RCAS1 participates in the changes in the maternal immune system that take place during parturition and reinforce its potential involvement in the mechanism of placental abruption.
Attempts to define a pre-eclampsia susceptibility profile have been hampered by the wide clinical spectrum of the condition and the complex genetics underlying it. Genes that modulate blood pressure, fluid homeostasis and placental vascular development have been considered plausible candidates. Among these are the angiotensinogen (AGT) gene variant Met235Threo, which has been associated with pre-eclampsia and the endothelial nitric oxide synthase (eNOS) polymorphism Glu298Asp, which has been associated with both pre-eclampsia and abruptio placentae, a condition that often co-exists with pre-eclampsia. The aim of this study was to investigate a potential association between these gene variants and pre-eclampsia with and without abruptio placentae in a South African patient group. Fifty primigravidas with early onset, severe pre-eclampsia, 50 women presenting primarily with abruptio placentae (whether associated with pre-eclampsia or not) and a control panel of 50 healthy pregnant women constituted the study groups. The Met235Threo and Glu298Asp variants were characterised by polymerase chain reaction and restriction enzyme analysis. No association was demonstrated between the M235T variant of the AGT gene and pre-eclampsia or abruptio placentae. In contrast, the combined frequency of the eNOS variant genotypes (GT and TT) was significantly higher in the abruptio placentae group (49%) than the control group (21%) (p=0.006). Furthermore, in the pre-eclampsia patients who subsequently developed abruptio placentae, the eNOS GT genotype emerged as a major risk factor for the development of abruptio placentae (p<0.0001). These data suggest that the presence of a Glu298Asp eNOS variant may pre-dispose a pre-eclamptic woman to develop abruptio placentae or that it is a marker for predisposition.