Risk factors for perinatal mortality in patients admitted to the hospital with the diagnosis of placental abruption.

OBJECTIVE: Placental abruption is a clinical term used when premature separation of the placenta from the uterine wall occurs prior to delivery of the fetus. Hypertension, substance abuse, smoking, intrauterine infection and recent trauma are risk factors for placental abruption. In this study, we sought for clinical factors that increase the risk for perinatal mortality in patients admitted to the hospital with the clinical diagnosis of placental abruption. MATERIALS AND METHODS: We identified all placental abruption cases managed over the past 6 years at our Center. Those with singleton pregnancies and a diagnosis of abruption based on strict clinical criteria were selected. Eleven clinical variables that had potential for increasing the risk for perinatal mortality were selected, logistic regression analysis was used to identify variables associated with perinatal death. RESULTS: Sixty-one patients were included in the study with 16 ending in perinatal death (26.2%). Ethnicity, maternal age, gravidity, parity, use of tobacco, use of cocaine, hypertension, asthma, diabetes, hepatitis C, sickle cell disease and abnormalities of amniotic fluid volume were not the main factors for perinatal mortality. Gestational age at delivery, birthweight and history of recent trauma were significantly associated with perinatal mortality. The perinatal mortality rate was 42% in patients who delivered prior to 30 weeks of gestation compared to 15% in patients who delivered after 30 weeks of gestation (p < 0.05). A three-fold increase in severe trauma was reported in the group of patients with perinatal mortality than in the group with perinatal survivors (25% versus 7%, respectively, p < 0.05). CONCLUSIONS: In patients admitted to hospital for placental abruption delivery prior to 30 weeks of gestation and a history of abdominal trauma are independent risk factors for perinatal death.

Thrombin regulates monocyte chemoattractant protein-1 expression in human first trimester and term decidual cells.

OBJECTIVE: Excess decidual macrophage infiltration has been linked to preeclampsia and a failure of endovascular trophoblast invasion. Severe preeclampsia with shallow placentation has also been linked to acquired and inherited maternal thrombophilias and recurrent decidual hemorrhage, which generates thrombin from decidual cell-expressed tissue factor. Therefore, the current study evaluated whether thrombin affects monocyte chemoattractant protein-1 (MCP-1) expression in stromal cells that are derived from cycling and gestational endometrium. STUDY DESIGN: Stromal cells that are isolated from cycling endometrium and first trimester and term decidua were grown to confluence, treated for 7 days with 10(-8) mol/L estradiol (E2) + 10(-7) mol/L medroxyprogesterone acetate (MPA), then switched to a serum-free medium that contained the corresponding steroids +/- thrombin. MCP-1 protein release was measured by enzyme-linked immunosorbent assay and Western blot; MCP-1 messenger RNA levels were assessed by real-time quantitative reverse transcription-polymerase chain reaction. RESULTS: Secreted MCP-1 levels were not significantly different in stromal or decidual cell cultures that were incubated with E2 or with E2 + MPA. Thrombin increased immunoreactive MCP-1 expression in a dose-response fashion in first trimester and term decidual cells but not in endometrial stromal cells. Thrombin-induced MCP-1 protein output was unaffected by MPA but was abrogated by incubation with the thrombin inhibitor, hirudin. Unexpectedly, thrombin-enhanced MCP-1 protein expression was unaccompanied by corresponding changes in steady state MCP-1 messenger RNA levels, which suggests its effects were posttranslational. CONCLUSION: MCP-1 protein expression is up regulated by thrombin in decidual cells across gestation, but not in stromal cells from predecidualized cycling endometrium.

Regulation of monocyte chemoattractant protein-1 expression by tumor necrosis factor-alpha and interleukin-1beta in first trimester human decidual cells: implications for preeclampsia.

The current study describes a statistically significant increase in macrophages (CD68-positive cells) in the decidua of preeclamptic patients. To elucidate the regulation of this monocyte infiltration, expression of monocyte chemoattractant protein-1 (MCP-1) was assessed in leukocyte-free first trimester decidual cells. Confluent decidual cells were primed for 7 days in either estradiol or estradiol plus medroxyprogesterone acetate to mimic the decidualizing steroidal milieu of the luteal phase and early pregnancy. The medium was exchanged for a serum-free defined medium containing corresponding steroids +/- tumor necrosis factor (TNF)-alpha or interleukin (IL)-1beta. After 24 hours, enzyme-linked immunosorbent assay measurements indicated that the addition of medroxyprogesterone acetate did not affect MCP-1 output, whereas 10 ng/ml of TNF-alpha or IL-1beta increased output by 83.5-fold +/- 20.6 and 103.1-fold +/- 14.7, respectively (mean +/- SEM, n = 8, P < 0.05). Concentration-response comparisons revealed that even 0.01 ng/ml of TNF-alpha or IL-1beta elevated MCP-1 output by more than 15-fold. Western blotting confirmed the enzyme-linked immunosorbent assay results, and quantitative reverse transcriptase-polymerase chain reaction confirmed corresponding effects on MCP-1 mRNA levels. The current study demonstrates that TNF-alpha and IL-1beta enhance MCP-1 in first trimester decidua. This finding suggests a mechanism by which recruitment of excess macrophages to the decidua impairs endovascular trophoblast invasion, the primary placental defect of preeclampsia.

Combined serum and ultrasound screening for detection of fetal aneuploidy.

Experience gathered over the last decade from high-risk centers provide strong evidence that mid-trimester sonographic markers are sensitive for Down syndrome prediction. More recent data indicate that combining mid trimester sonography with traditional serum markers significantly improves diagnostic accuracy over either group of markers by themselves.