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760: Siglec-6 is overexpressed in preeclamptic placentas
Poster Session V
Academic Issues, Antepartum Fetal Assessment, Genetics, Hypertension, Medical-Surgical Complications, Ultrasound-Imaging
administered beyond 24 weeks. Maternal composite morbidity that included HELLP syndrome, pulmonary edema, eclampsia, and renal insufficiency, and perinatal outcome were analyzed. RESULTS: Median prolongation was 7 days (range 2-55). There were no maternal death or eclampsia, but overall maternal morbidity rate was 43%, and the main severe complication observed was HELLP syndrome (27%). Overall perinatal survival rate was 42%. There were no perinatal survivors in those expectantly managed at ⬍ 24 weeks. Severe FGR complicated 17 of 52 fetuses (33%) and none of them survived. For those expectantly managed at 24-246/7, 25-256/7 weeks, the perinatal survival rates were 50% and 57%, respectively; but rate of RDS was very high (81%) (see table). After exclusion of fetuses with severe FGR, perinatal survival rates in women expectantly managed at 24-246/7 and 25-256/7 weeks were 60% and 100%, respectively. CONCLUSIONS: Perinatal outcome in severe preeclampsia in the midtrimester is dependent on GA and/or the presence of severe FGR. Given the high maternal morbidity and the extremely low perinatal survival rate, expectant management should not be offered before 24 weeks; in addition if a severe FGR is present, this threshold should be set at 25 weeks.
www.AJOG.org
shows a scatterplot of each patient’s SVRI versus CI. The groups segregate based on their hemodynamics. CONCLUSIONS: Our results suggest that severities of pre-eclampsia appear to have distinct hemodynamic profiles. Future studies will assess the hemodynamic changes as measures of disease severity and progression.
Table. Perinatal outcome stratified by gestational age at start of expectant management
GA (wks) ⬍23
N 5
Severe FGR, n (%)
Fetal death, n (%)
Neonatal death, n (%)
410 [120-510]
1/4* (25)
5 (100)
0 (0)
242/7 [233/7- 254/7]
490 [319 -700]
3/7 (43)
9 [4-18]
256/7 [24 4/7- 265/7]
586 [475-750]
3/18 (17)
7 [2-55]
262/7 [252/7- 332/7]
560 [155-1495]
10/23 (43)
7 [2-55]
256/7 [174/7- 332/7]
550 [120-1495]
17/52 (33)
Days gained
Delivery GA (wks)
Weight, g
4 [4-6]
23 [174/7- 23]
4 [2-18]
Discharged alive, n(%) 0 (0)
RDS, n (%) NA
.......................................................................................................................................................................................... 23-26/7
7
6 (86)
1 (14)
0 (0)
1 (100)
.......................................................................................................................................................................................... 24-246/7
18
8 (44)
1 (6)
9 (50)
9/10 (90)
.......................................................................................................................................................................................... 25-256/7
23
8 (35)
2 (9)
13 (57)
11/15 (73)
.......................................................................................................................................................................................... Total
53
27 (51)
4 (8)
22 (42)
21/26 (81)
..........................................................................................................................................................................................
Data are expressed as median (and range) or as percentage. *: No reference before 20 weeks GA
759 Electrical cardiometry in pre-eclampsia Jessica Selander1, Thomas Archer1, D. Yvette LaCoursiere1 1
UCSD Medical Center, San Diego, CA
OBJECTIVE: Hemodynamic changes occurring in pre-eclampsia ap-
pear hyperdynamic. This study aimed to assess the impact of mild and severe pre-eclampsia on hemodynamics as measured by the Aesculon® Electrical Cardiometry monitor. We hypothesized that mild preeclamptics demonstrate lower systemic vascular resistance index (SVRI) and higher cardiac index (CI) compared to normotensive pregnant women and severe pre-eclamptics; and severe pre-eclamptics demonstrate higher SVRI with lower CI compared to normotensives women and mild pre-eclamptics. STUDY DESIGN: This was a cross-sectional study of normotensive and pre-eclamptic women at 24 weeks gestation through term presenting to Labor and Delivery (June 2009-May 2010). Mild pre-eclampsia was defined as BP ⬎ 140/90mmHg and protein ⬎ 300mg on a 24 hour urine. Severe pre-eclampsia was defined as BP ⬎ 160/110 and protein ⬎ 5grams on a 24 hour urine. Primary outcomes were SVRI and CI. The control group was healthy singletons, BP ⬍ 140/90, and negative protineuria. Exclusion criteria were labor onset, induction or augmentation; and administration of IV, PO, or neuraxial medications. Analysis was performed with descriptive statistics and Kruskal-Wallis. RESULTS: 37 women were enrolled (20 normotensives, 9 mild and 8 severe pre-eclamptics). Between the groups, there was no statistical difference in age, parity, BMI, DMII, or hematocrit. SVRI and CI were statistically different across the three groups (p⫽0.003 and 0.006, respectively). Mild pre-eclamptics compared to normotensives had a higher CI (p⫽0.004) and a trend toward a lower SVRI (p⫽0.083). Severe pre-eclamptics had a higher SVRI compared to normotensives (p⫽ ⬍0.003). Compared to mild pre-eclamptics, severe pre-eclamptics had a higher SVRI (p⫽ 0.008) and lower CI (p⫽0.005). Figure 1
S298
760 Siglec-6 is overexpressed in preeclamptic placentas Jill Uyenishi1, Kristen Rumer1, Camille Hoffman1, Virginia Winn1 1
University of Colorado Denver, Aurora, CO
OBJECTIVE: Preeclampsia (PE), characterized by the onset of hyper-
tension and proteinuria in the second half of pregnancy, affects ⬃5% of pregnancies. The placenta is thought to play a central role in the pathogenesis of PE, a disorder unique to human pregnancy. Sialic acid binding immunoglobulin-like lectin (Siglec)-6 is a transmembrane receptor that binds leptin. Interestingly, Siglec-6 is expressed exclusively in human placenta and is not found in other mammalian placentas including non-human primates. Recent data has shown increased Siglec-6 RNA in preterm preeclamptic placentas. Further, Siglec-6 is expressed by both invasive and syntial trophoblasts but not by maternal decidual cells (Winn 2009). In this study we determined the protein levels of Siglec-6 in the basal plate (BP) and chorionic villi (CV) of preterm PE placentas compared to preterm labor (PTL) controls. Determining if and where Siglec-6 protein is aberrantly expressed will be important for ultimately understanding its potential function in PE pathogenesis. STUDY DESIGN: BP and CV were collected from placentas within 30 minutes of delivery from pregnancies complicated by PE (n⫽12; 24-37 wks) or PTL (n⫽12; 24-37 wks) with IRB approval. Subjects were excluded for known fetal anomalies or infection. Siglec-6 levels were quantified by immunoblotting using actin as a protein loading control. Student’s t-test was used for statistical analysis with significance set at a p value ⬍ 0.05. RESULTS: Siglec-6 expression was significantly increased in both the BP (2-fold) and CV (3-fold) of PE placentas compared to controls. While the increase in Siglec-6 was consistent across the gestational window in CV, the increase in the BP was most dramatic before 32 weeks gestation. CONCLUSIONS: PE placentas have increased Siglec-6 compared to controls. The aberrant expression in the BP suggests Siglec-6 may play a role in or reflect impaired cytotrophoblast invasion seen in PE placentas. The increased expression in the CV warrants further study of Siglec-6 as a potential PE biomarker.
American Journal of Obstetrics & Gynecology Supplement to JANUARY 2011
Academic Issues, Antepartum Fetal Assessment, Genetics, Hypertension, Medical-Surgical Complications, Ultrasound-Imaging
administered beyond 24 weeks. Maternal composite morbidity that included HELLP syndrome, pulmonary edema, eclampsia, and renal insufficiency, and perinatal outcome were analyzed. RESULTS: Median prolongation was 7 days (range 2-55). There were no maternal death or eclampsia, but overall maternal morbidity rate was 43%, and the main severe complication observed was HELLP syndrome (27%). Overall perinatal survival rate was 42%. There were no perinatal survivors in those expectantly managed at ⬍ 24 weeks. Severe FGR complicated 17 of 52 fetuses (33%) and none of them survived. For those expectantly managed at 24-246/7, 25-256/7 weeks, the perinatal survival rates were 50% and 57%, respectively; but rate of RDS was very high (81%) (see table). After exclusion of fetuses with severe FGR, perinatal survival rates in women expectantly managed at 24-246/7 and 25-256/7 weeks were 60% and 100%, respectively. CONCLUSIONS: Perinatal outcome in severe preeclampsia in the midtrimester is dependent on GA and/or the presence of severe FGR. Given the high maternal morbidity and the extremely low perinatal survival rate, expectant management should not be offered before 24 weeks; in addition if a severe FGR is present, this threshold should be set at 25 weeks.
www.AJOG.org
shows a scatterplot of each patient’s SVRI versus CI. The groups segregate based on their hemodynamics. CONCLUSIONS: Our results suggest that severities of pre-eclampsia appear to have distinct hemodynamic profiles. Future studies will assess the hemodynamic changes as measures of disease severity and progression.
Table. Perinatal outcome stratified by gestational age at start of expectant management
GA (wks) ⬍23
N 5
Severe FGR, n (%)
Fetal death, n (%)
Neonatal death, n (%)
410 [120-510]
1/4* (25)
5 (100)
0 (0)
242/7 [233/7- 254/7]
490 [319 -700]
3/7 (43)
9 [4-18]
256/7 [24 4/7- 265/7]
586 [475-750]
3/18 (17)
7 [2-55]
262/7 [252/7- 332/7]
560 [155-1495]
10/23 (43)
7 [2-55]
256/7 [174/7- 332/7]
550 [120-1495]
17/52 (33)
Days gained
Delivery GA (wks)
Weight, g
4 [4-6]
23 [174/7- 23]
4 [2-18]
Discharged alive, n(%) 0 (0)
RDS, n (%) NA
.......................................................................................................................................................................................... 23-26/7
7
6 (86)
1 (14)
0 (0)
1 (100)
.......................................................................................................................................................................................... 24-246/7
18
8 (44)
1 (6)
9 (50)
9/10 (90)
.......................................................................................................................................................................................... 25-256/7
23
8 (35)
2 (9)
13 (57)
11/15 (73)
.......................................................................................................................................................................................... Total
53
27 (51)
4 (8)
22 (42)
21/26 (81)
..........................................................................................................................................................................................
Data are expressed as median (and range) or as percentage. *: No reference before 20 weeks GA
759 Electrical cardiometry in pre-eclampsia Jessica Selander1, Thomas Archer1, D. Yvette LaCoursiere1 1
UCSD Medical Center, San Diego, CA
OBJECTIVE: Hemodynamic changes occurring in pre-eclampsia ap-
pear hyperdynamic. This study aimed to assess the impact of mild and severe pre-eclampsia on hemodynamics as measured by the Aesculon® Electrical Cardiometry monitor. We hypothesized that mild preeclamptics demonstrate lower systemic vascular resistance index (SVRI) and higher cardiac index (CI) compared to normotensive pregnant women and severe pre-eclamptics; and severe pre-eclamptics demonstrate higher SVRI with lower CI compared to normotensives women and mild pre-eclamptics. STUDY DESIGN: This was a cross-sectional study of normotensive and pre-eclamptic women at 24 weeks gestation through term presenting to Labor and Delivery (June 2009-May 2010). Mild pre-eclampsia was defined as BP ⬎ 140/90mmHg and protein ⬎ 300mg on a 24 hour urine. Severe pre-eclampsia was defined as BP ⬎ 160/110 and protein ⬎ 5grams on a 24 hour urine. Primary outcomes were SVRI and CI. The control group was healthy singletons, BP ⬍ 140/90, and negative protineuria. Exclusion criteria were labor onset, induction or augmentation; and administration of IV, PO, or neuraxial medications. Analysis was performed with descriptive statistics and Kruskal-Wallis. RESULTS: 37 women were enrolled (20 normotensives, 9 mild and 8 severe pre-eclamptics). Between the groups, there was no statistical difference in age, parity, BMI, DMII, or hematocrit. SVRI and CI were statistically different across the three groups (p⫽0.003 and 0.006, respectively). Mild pre-eclamptics compared to normotensives had a higher CI (p⫽0.004) and a trend toward a lower SVRI (p⫽0.083). Severe pre-eclamptics had a higher SVRI compared to normotensives (p⫽ ⬍0.003). Compared to mild pre-eclamptics, severe pre-eclamptics had a higher SVRI (p⫽ 0.008) and lower CI (p⫽0.005). Figure 1
S298
760 Siglec-6 is overexpressed in preeclamptic placentas Jill Uyenishi1, Kristen Rumer1, Camille Hoffman1, Virginia Winn1 1
University of Colorado Denver, Aurora, CO
OBJECTIVE: Preeclampsia (PE), characterized by the onset of hyper-
tension and proteinuria in the second half of pregnancy, affects ⬃5% of pregnancies. The placenta is thought to play a central role in the pathogenesis of PE, a disorder unique to human pregnancy. Sialic acid binding immunoglobulin-like lectin (Siglec)-6 is a transmembrane receptor that binds leptin. Interestingly, Siglec-6 is expressed exclusively in human placenta and is not found in other mammalian placentas including non-human primates. Recent data has shown increased Siglec-6 RNA in preterm preeclamptic placentas. Further, Siglec-6 is expressed by both invasive and syntial trophoblasts but not by maternal decidual cells (Winn 2009). In this study we determined the protein levels of Siglec-6 in the basal plate (BP) and chorionic villi (CV) of preterm PE placentas compared to preterm labor (PTL) controls. Determining if and where Siglec-6 protein is aberrantly expressed will be important for ultimately understanding its potential function in PE pathogenesis. STUDY DESIGN: BP and CV were collected from placentas within 30 minutes of delivery from pregnancies complicated by PE (n⫽12; 24-37 wks) or PTL (n⫽12; 24-37 wks) with IRB approval. Subjects were excluded for known fetal anomalies or infection. Siglec-6 levels were quantified by immunoblotting using actin as a protein loading control. Student’s t-test was used for statistical analysis with significance set at a p value ⬍ 0.05. RESULTS: Siglec-6 expression was significantly increased in both the BP (2-fold) and CV (3-fold) of PE placentas compared to controls. While the increase in Siglec-6 was consistent across the gestational window in CV, the increase in the BP was most dramatic before 32 weeks gestation. CONCLUSIONS: PE placentas have increased Siglec-6 compared to controls. The aberrant expression in the BP suggests Siglec-6 may play a role in or reflect impaired cytotrophoblast invasion seen in PE placentas. The increased expression in the CV warrants further study of Siglec-6 as a potential PE biomarker.
American Journal of Obstetrics & Gynecology Supplement to JANUARY 2011