Introduction: Six years after the US Food and Drug Administration approval of the broadspectrum antibiotic ofloxacin (OFLX), the chiral switching of this racemic mixture resulted in a drug composed of the l-optical isomer levofloxacin (LVFX).Since both fluoroquinolones (FQs) were introduced to the pharmaceutical market, they have been widely prescribed by physicians, with careful administration during pregnancy and breastfeeding.Therefore, the role of the influx and efflux placental transporters in the concentrations of these drugs that permeate through human placental barrier model was investigated in this study.Methods: The contribution of major carriers on the transplacental flux of OFLX and LVFX uptake into choriocarcinoma BeWo cells was evaluated in the presence vs absence of wellknown inhibitors.Results: Our results reveal that neither the influx transporters such as organic cation transporters, organic anion transporters, and monocarboxylate transporters nor the efflux transporters such as P-glycoprotein or breast cancer resistance protein significantly affected the transport of OFLX.In contrast, multiple transporters revealed pronounced involvement in the transfer of the levorotatory enantiomer in and out of the in vitro placental barrier.These data suggest a non-carrier-mediated mechanism of transport of the racemic mixture, while LVFX is subjected to major influx and efflux passage through the placental brush border membranes. Conclusion:This study provides underlying insights to elucidate the governing factors that influence the flux of these FQs through organ barriers, in view of the controversial safety profile of these drugs in pregnant population.

the chiral switching of this racemic mixture resulted in a drug composed of the l -optical isomer levofloxacin (LVFX). Since both fluoroquinolones (FQs) were introduced to the pharmaceutical market, they have been widely prescribed by physicians, with careful administration during pregnancy and breastfeeding. Therefore, the role of the influx and efflux placental transporters in the concentrations of these drugs that permeate through human placental barrier model was investigated in this study. Methods: The contribution of major carriers on the transplacental flux of OFLX and LVFX uptake into choriocarcinoma BeWo cells was evaluated in the presence vs absence of well-known inhibitors. Results: Our results reveal that neither the influx transporters such as organic cation transporters, organic anion transporters, and monocarboxylate transporters nor the efflux transporters such as P-glycoprotein or breast cancer resistance protein significantly affected the transport of OFLX. In contrast, multiple transporters revealed pronounced involvement in the transfer of the levorotatory enantiomer in and out of the in vitro placental barrier. These data suggest a non-carrier-mediated mechanism of transport of the racemic mixture, while LVFX is subjected to major influx and efflux passage through the placental brush border membranes. Conclusion: This study provides underlying insights to elucidate the governing factors that influence the flux of these FQs through organ barriers, in view of the controversial safety profile of these drugs in pregnant population.

INTRODUCTION:Research in animal models and preliminary clinical studies in humans support the use of pravastatin for the prevention of preeclampsia. However, its use during pregnancy is still controversial due to limited data about its effect on the human placenta and fetus.METHODS:In the present study, human placental cotyledons were perfused in the absence or presence of pravastatin in the maternal reservoir (PraM). In addition, placental explants were treated with pravastatin for 5, 24 and 72 h under normoxia and hypoxia. We monitored the secretion of placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng), endothelial nitric oxide synthase (eNOS) expression and activation and the fetal vasoconstriction response to angiotensin-II.RESULTS:The concentrations of PlGF, sFlt-1 and sEng were not significantly altered by pravastatin in PraM cotyledons and in placental explants compared to control. Under hypoxic conditions, pravastatin decreased sFlt-1 concentrations. eNOS expression was significantly increased in PraM cotyledons but not in pravastatin-treated placental explants cultured under normoxia or hypoxia. eNOS phosphorylation was not significantly affected by pravastatin. The feto-placental vascular tone and the fetal vasoconstriction response to angiotensin-II, did not change following exposure of the maternal circulation to pravastatin.CONCLUSION:We found that pravastatin does not alter the essential physiological functions of the placenta investigated in the study. The relevance of the study lays in the fact that it expands the current knowledge obtained thus far regarding the effect of the drug on the normal human placenta. This data is reassuring and important for clinicians that consider the treatment of high-risk patients with pravastatin, a treatment that exposes some normal pregnancies to the drug.

The first randomized pilot clinical study investigating the use of pravastatin for the prevention of preeclampsia in high-risk patients has provided encouraging preliminary safety and pharmacokinetic data, justifying continued research in this field. Still, the ability of pravastatin to attenuate the fetal peripheral vasoconstriction responses to acute hypoxic stress in sheep, via increased nitric oxide (NO) bioavailability, may raise concerns about its use during pregnancy. The aim of this study was to investigate the effect of pravastatin on endothelial nitric oxide synthase (eNOS) expression, NO production and the feto-placental vasoconstriction response to angiotensin-II. In the present study we used the ex-vivo human placental perfusion model and cultures of placental explants. Placental cotyledons were perfused for 5 h in the absence or presence of pravastatin in the maternal reservoir (PraM). Placental explants were treated with various concentrations of pravastatin for 24-72 h under normoxia (21% O2) or reduced O2 conditions (hypoxia; 1% O2). eNOS expression was significantly increased in PraM cotyledons but not in pravastatin-treated placental explants cultured under normoxia or hypoxia. eNOS phosphorylation and NO production were not significantly affected by pravastatin. The feto-placental vascular tone and fetal vasoconstriction response to angiotensin-II (Figure), did not change following exposure of the maternal circulation to pravastatin. The present study focused on the effect of pravastatin treatment on eNOS expression and function in the normal human placenta. The results suggest that maternal treatment with pravastatin may not impair the fetal vascular tone.

Accumulating evidence supports the concept of increased thrombin generation, placental vascular lesions, and inflammation as crucial points in the development of the great obstetrical syndromes [preeclampsia, intrauterine growth restriction (IUGR), preterm labor (PTL), preterm prelabor rupture of membranes (PROM), fetal demise and recurrent abortions]. In light of this, the role of heparins for primary or secondary prevention of these syndromes is becoming more and more apparent, mainly due to the antithrombotic and anti-inflammatory effects of heparins. There is agreement regarding the use of heparin in the prevention of gestational complications in patients with antiphospholipid syndrome, while its use for other obstetrical complications is under debate. In the present review we will describe the physiologic role of heparins on coagulation and inflammation and we will discuss current evidence regarding the use of heparins for the prevention/treatment of obstetrical syndromes.

Background: Symptoms of both depression and Post Traumatic Stress Disorder (PTSD) are prevalent among first-time mothers following birth. However, the direction of the association between the two types or symptoms is unclear.Methods: Ninety six first-time mothers giving birth via vaginal delivery (N=38), emergency C-Section (N=27) and planned C-Section (N=21) were assessed for depression and PTSD twice: Six weeks postpartum and six-weeks later.Results: Cross-lagged Structural Equation Modeling (SEM) analyses revealed a prospective effect of depressive symptoms on PTSD symptoms. No moderating factors were identified.Limitations: A relatively modest sample size and only two assessment waves.Conclusions: An early detection and intervention with symptoms of post-partum depression might also prevent the development of PTSD symptoms. (C) 2015 Elsevier B.V. All rights reserved.

To investigate whether patients with a history of recurrent pregnancy loss (RPL) have an increased risk for future maternal cardiovascular (CV) morbidity. A population-based study compared the incidence of long-term CV morbidity in a cohort of women with and without a diagnosis of RPL. Deliveries occurred since the year 1988, with a mean follow-up duration of 11.2 years. We excluded from the study women with known CV disease and congenital cardiovascular malformations, chronic hypertension and multiple pregnancies. CV morbidity was divided into 4 categories according to severity and type including simple and complex CV events (eg, angina pectoris and congestive heart failure, respectively), and invasive and noninvasive cardiac procedures (eg, insertion of a stent and a treadmill stress test, respectively). Kaplan-Meier survival curve was used to estimate cumulative incidence of CV hospitalizations. Cox proportional hazards models were used to estimate the adjusted hazard ratios (HR) for CV morbidity. During the study period 99,285 parturient met the inclusion criteria; 6.7% (n=6690) occurred in patients with a history of RPL. During the follow-up period patients with RPL had higher rates of cardiovascular morbidity including cardiac invasive and noninvasive diagnostic procedures, simple as well as complex cardiovascular events, and hospitalizations due to cardiovascular causes (table). Using a Kaplan-Meier survival curve, patients with a previous diagnosis of RPL had a significantly higher cumulative incidence of cardiovascular hospitalizations (Figure). Using a Cox proportional hazards model, adjusted for confounders such as preeclampsia, diabetes mellitus, and obesity, a history of RPL remained independently associated with CV hospitalizations (adjusted HR, 1.7; 95% CI, 1.5-1.8; P=0.001). Recurrent pregnancy loss is an independent risk factor for long term maternal cardiovascular complications and for hospitalizations due to a cardiovascular cause.Tabled 1View Large Image Figure ViewerDownload Hi-res image Download (PPT) Open table in a new tab

Implantation, trophoblast development and placentation are crucial processes in the establishment and development of normal pregnancy. Abnormalities of these processes can lead to pregnancy complications known as the great obstetrical syndromes: preeclampsia, intrauterine growth restriction, fetal demise, premature prelabor rupture of membranes, preterm labor, and recurrent pregnancy loss. There is mounting evidence regarding the physiological and therapeutic role of heparins in the establishment of normal gestation and as a modality for treatment and prevention of pregnancy complications. In this review, we will summarize the properties and the physiological contributions of heparins to the success of implantation, placentation and normal pregnancy.

BackgroundS100B is a brain damage biomarker. When measured immediately after birth, it reflects neonatal brain damage following asphyxia. In this study, we used feticide as a novel model of fetal brain damage. We examined whether such damage is reflected by a rise in S100B in maternal blood before delivery.MethodsEight pregnant women were recruited between January and July 2012. Maternal blood samples were drawn before and after feticide at predetermined time points (0, 15, 30, 60, 120, and 240min). S100B, lactate dehydrogenase, creatine kinase, and creatinine concentrations were measured by standard human ELISA and chemical analyzer.ResultsNo significant difference was noted between S100B levels before and after feticide, neither in non-specific cell death markers (lactate dehydrogenase and creatine kinase), which remained within normal range. S100B ranged between 0.015-0.04 mu g/L through all the predetermined time points.ConclusionNo statistically significant differences were demonstrated in S100B levels before and after feticide. (c) 2013 John Wiley & Sons, Ltd.

OBJECTIVE: We sought to investigate whether patients with a history of recurrent pregnancy loss (RPL) have an increased risk for future maternal atherosclerotic morbidity.STUDY DESIGN: A population-based study compared the incidence of long-term atherosclerotic morbidity (renal and cardiovascular) in a cohort of women with and without a diagnosis of RPL. Patients had a mean follow-up duration of more than a decade. Women with known atherosclerotic disease were excluded from the study. Cardiovascular morbidity was divided into 4 categories according to severity and type including simple and complex cardiovascular events and invasive and noninvasive cardiac procedures. Kaplan-Meier survival curves were used to estimate cumulative incidence of cardiovascular and renal hospitalizations. Cox proportional hazards models were used to estimate the adjusted hazard ratios for cardiovascular and renal morbidity.RESULTS: During the study period 99,285 patients were included; of these 6.7% (n = 6690) had a history of RPL. Patients with RPL had higher rates of renal and cardiovascular morbidity including cardiac invasive and noninvasive diagnostic procedures, simple as well as complex cardiovascular events, and hospitalizations due to cardiovascular causes. Using KaplanMeier survival curves, patients with a previous diagnosis of RPL had a significantly higher cumulative incidence of cardiovascular but not renal hospitalizations. Using a Cox proportional hazards model, adjusted for confounders such as preeclampsia, diabetes mellitus, obesity, and smoking, a history of RPL remained independently associated with cardiovascular hospitalizations (adjusted hazard ratio, 1.6; 95% confidence interval, 1.4-1.8; P = .001).CONCLUSION: RPL is an independent risk factor for long-term maternal cardiovascular complications.

maternal serum anti-genital mycoplasma antibodies, and preterm parturition Offer Erez, Ruthy Beer Weisel, Sari Prutchi Sagiv, Tal Rafaeli, Ilan Levi, Vered Klaitman, Barak ArichaTamir, Alona Kuzmina, Limor Besser, Orna Staretz-Chacham, Iris Shoham, Michela Quaranta, Gershon Holcberg, Moshe Mazor Soroka University Medical Center, School of Medicine, Faculty of Health Sciences, Ben Gurion University of the Negev, Department of Obstetrics and Gynecology, Beer Sheva, Israel, Soroka University Medical Center, School of Medicine, Faculty of Health Sciences, Ben Gurion University of the Negev, Department of Neonatology, Beer Sheva, Israel, Soroka University Medical Center, Promyco Diagnostics, Beer Sheva, Israel, Clalit Health Services, Mor Research Applications, Tel Aviv, Israel, Policlinico GB Rossi Azienda Ospedaliera, Obstetrics and Gynecology Departement, Verona, Italy OBJECTIVE: Genital mycoplasmas (GM) are the most prevalent intraamniotic microorganism in women with preterm parturition. In contrast, the relationship between cervical colonization with these microorganisms and preterm parturition is not well established. The aim of this study was to determine the association between maternal serum concentrations of anti GM antibodies (AB) and spontaneous preterm delivery (PTD). STUDY DESIGN: a prospective observational study was conducted including women with preterm parturition (n 131) and patients in labor at term (n 22) as controls. Maternal serum AGM-AB were determined by the PROMYCO kit a novel immunoassay. RESULTS: There was a positive correlation between maternal serum AGM-AB during the episode of preterm parturition and at delivery (r 0.92, p 0.0001). Median maternal serum AGM-AB was higher in women with a positive GM cervical culture than in those with a negative one (p 0.001). There was no correlation between gestational age at sample collection and maternal serum AGM-AB concentrations. Women with preterm parturition who delivered preterm and a positive cervical GM culture had a higher rate of elevated AGM-AB ( 75th percentile) than those with a sterile cervical culture (83.3% vs. 41.5%, p 0.012). Among women with preterm labor and a positive GM cervical culture, those who delivered preterm had a higher median AGM-AB than those who delivered at term (p 0.042). CONCLUSION: Maternal cervical colonization with GM is associated with elevated serum AGM-AB concentrations. In the presence of cervical colonization with genital mycoplasma, maternal serum concentrations of AGM-AB may assist in identifying those who will deliver preterm following an episode of preterm parturition. This is important, since our observation might contribute to a better identification of patients with cervical colonization with GM and preterm parturition that may benefit from antimicrobial treatment.

OBJECTIVE:The purpose of this study was to investigate whether a history of preterm delivery (PTD) poses a risk for subsequent maternal long-term cardiovascular morbidity. STUDY DESIGN:A population-based study compared the incidence of cardiovascular morbidity in a cohort of women who delivered preterm (<37 weeks' gestation) and those who gave birth at term at the same period. Deliveries occurred during the years 1988-1999 with follow up until 2010. Kaplan-Meier survival curves were used to estimate cumulative incidence of cardiovascular hospitalizations. Cox proportional hazards models were used to estimate the adjusted hazard ratios for cardiovascular hospitalizations. RESULTS:During the study period 47,908 women met the inclusion criteria; 12.5% of the patients (n = 5992) delivered preterm. During a follow-up period of >10 years, patients with PTD had higher rates of simple and complex cardiovascular events and higher rates of total cardiovascular-related hospitalizations. A linear association was found between the number of previous PTD and future risk for cardiovascular hospitalizations (5.5% for ≥2 PTDs; 5.0% for 1 PTD vs 3.5% in the comparison group; P < .001). The association remained significant for spontaneous vs induced PTD and for early (<34 weeks) and late (34 weeks to 36 weeks 6 days' gestation) PTD. In a Cox proportional hazards model that adjusted for pregnancy confounders such as labor induction, diabetes mellitus, preeclampsia, and obesity, PTD was associated independently with cardiovascular hospitalizations (adjusted hazard ratio, 1.4; 95% confidence interval, 1.2-1.6). CONCLUSION:PTD is an independent risk factor for long-term cardiovascular morbidity in a follow-up period of more than a decade.

Objective: Alpha-1 antitrypsin (AAT), a circulating anti-inflammatory molecule, rises four-to sixfold during acute phase responses and during pregnancy. AAT deficiency is linked with various pregnancy complications. The aim of this study is to determine plasma concentrations and activity of AAT and serum cytokine levels in blood samples from women undergoing spontaneous abortions as compared with elective abortions.Methods: A prospective case-control study consisted of patients with sporadic abortions (n = 15), recurrent spontaneous abortions (n = 14) and healthy pregnancies going through elective terminations (n = 11). Circulating AAT and cytokine levels were determined before dilatation and curettage.Results: AAT levels were lower in both recurrent and sporadic spontaneous abortion groups compared with healthy pregnancies (1.421 +/- 0.08, 1.569 +/- 0.14 and 3.224 +/- 0.45 mg/ml, respectively, p < 0.001). Reduced AAT levels correlated with elevated proinflammatory cytokines.Conclusions: AAT levels in patients with either sporadic or recurrent spontaneous abortions were lower than normal pregnancies, and were associated with an inflammatory profile. Future studies should examine larger cohort groups, effects of earlier time-points and the influence of antithrombotic therapy in such patients who are diagnosed with relatively low levels of circulating AAT, in an effort to improve pregnancy outcomes.

Objective: To evaluate the effect of magnesium sulfate (MgSO4) on placental expression levels of vascular endothelial growth factor (VEGF). Materials and methods: Cotyledons of term normotensive and preeclamptic placentas were dually perfused for 6 h, with MgSO4 (6-7 mg%) in the maternal reservoir [normotensive (n = 3); preeclamptic (n = 4)] and with the control medium (without MgSO4) [normotensive (n = 3); preeclamptic (n = 6)]. After perfusion, placental tissue samples were collected from four different placental compartments (amnion, chorion, placental villous and decidua). The collected placental tissues were homogenized and examined for VEGF by ELISA. Statistical significance was determined using a two-way analysis of variance. Results: After perfusion with control medium, significantly lower levels of VEGF were detected in the chorion and placental villous compartments of preeclamptic placentas (70 +/- 24 pg/g protein and 29 +/- 11 pg/g protein; respectively), as compared with normotensive placentas (172 +/- 80 pg/g protein and 51 +/- 17 pg/g protein; respectively; p < 0.05). Exposure of preeclamptic placentas to MgSO4 resulted in decreased VEGF levels by the amnion (57 +/- 26 pg/g protein), as compared with the control group (153 +/- 62 pg/g protein) (p < 0.05). On the other hand, MgSO4 significantly increased VEGF levels by the placental villous and the decidua (58 +/- 15 pg/g protein, 70 +/- 29 pg/g protein; respectively), as compared with the control group (29 +/- 11 pg/g protein, 33 +/- 14 pg/g protein; respectively) (p < 0.01, p < 0.05; respectively). Exposure to MgSO4 did not affect VEGF levels in normotensive placentas. Conclusion: Reduced levels of VEGF are expressed by some placental compartments in preeclampsia compared with normotensive pregnancy. Perfusion with MgSO4 affects VEGF expression differently by preeclamptic and normotensive placentas. Increased production of placental VEGF in preeclampsia may play a role in the therapeutic action of MgSO4.

OBJECTIVE: Drugs of abuse affect pregnancy outcomes, however, the mechanisms in which cannabis exerts its effects are not well understood. The aim of this study was to examine the influence of short-term (1-2 hours) exposure to cannabidiol, a major phytocannabinoid, on human placental breast cancer resistance protein function.STUDY DESIGN: The in vitro effect of short-term exposure to cannabidoil on breast cancer resistance protein in BeWo and Jar cells (MCF7/P-gp cells were used for comparison) was tested with mitoxantrone uptake, and nicardipine was used as positive control. The ex vivo perfused cotyledon system was used for testing the effect of cannabidoil on glyburide transport across the placenta. Glyburide (200 ng/mL) was introduced to maternal and fetal compartments through a recirculating 2 hour perfusion, and its transplacental transport was tested with (n = 8) or without (n = 8) cannabidoil.RESULTS: (1) Cannabidoil inhibition of breast cancer resistance protein-dependent mitoxantrone efflux was concentration dependent and of a noncell type specific nature (P < .0001); (2) In the cotyledon perfusion assay, the administration of cannabidoil to the maternal perfusion media increased the female/male ratio of glyburide concentrations (1.3 +/- 0.1 vs 0.8 +/- 0.1 at 120 minutes of perfusion, P < .001).CONCLUSION: (1) Placental breast cancer resistance protein function is inhibited following even a short-term exposure to cannabidoil; (2) the ex vivo perfusion assay emphasize this effect by increased placental penetration of glyburide to the fetal compartment; and (3) these findings suggest that marijuana consumption enhances placental barrier permeability to xenobiotics and could endanger the developing fetus. Thus, the safety of drugs that are breast cancer resistance protein substrates is questionable during cannabis consumption by pregnant women.

Objectives. Marijuana is the most commonly used illicit drug during pregnancy. Due to high lipophilicity, cannabinoids can easily penetrate physiological barriers like the human placenta and jeopardize the developing fetus. We evaluated the impact of cannabidiol (CBD), a major non-psychoactive cannabinoid, on P-glycoprotein (P-gp) and Breast Cancer Resistance Protein (BCRP) expression, and P-gp function in a placental model, BeWo and Jar choriocarcinoma cell lines (using P-gp induced MCF7 cells (MCF7/P-gp) for comparison).Study design. Following the establishment of the basal expression of these transporters in the membrane fraction of all three cell lines, P-gp and BCRP protein and mRNA levels were determined following chronic (24-72 h) exposure to CBD, by Western Blot and qPCR. CBD impact on P-gp efflux function was examined by uptake of specific P-gp fluorescent substrates (calcein-AM, DiOC2(3) and rhodamine123( rh123)). Cyclosporine A (CsA) served as a positive control.Results. Chronic exposure to CBD resulted in significant changes in the protein and mRNA levels of both transporters. While P-gp was down-regulated, BCRP levels were up-regulated in the choriocarcinoma cell lines. CBD had a remarkably different influence on P-gp and BCRP expression in MCF7/P-gp cells, demonstrating that these are cell type specific effects. P-gp dependent efflux (of calcein, DiOC2(3) and rh123) was inhibited upon short-termexposure to CBD.Conclusions. Our study shows that CBD might alter P-gp and BCRP expression in the human placenta, and inhibit P-gp efflux function. We conclude that marijuana use during pregnancy may reduce placental protective functions and change its morphological and physiological characteristics.

ObjectiveTo investigate the perinatal outcomes of women that had a placenta accreta in a previous pregnancy.Study DesignWe retrospectively compared all subsequent singleton cesarean deliveries (CD) of women with a previous placenta accreta, with CD of women with no such history, during the years 1988-2011.ResultsOut of 34,567 singleton CD that occurred during the study period, 0.1% (n=30) were of women with a previous placenta accreta. Recurrent placenta accreta occurred in 23.3% (7/30) of patients with placenta accreta in their previous pregnancy. Previous placenta accreta was significantly associated with uterine rupture, peripartum hysterectomy and the need for blood transfusions. Nevertheless, increased risk for adverse perinatal outcomes such as low Apgar scores at 5 minutes and perinatal mortality was not found in these patients (table).Tabled 1Selected pregnancy and perinatal outcomes of patients with and without a previous placenta accreteConclusionA pregnancy following a previous placenta accreta is at increased risk for adverse maternal outcomes such as recurrent accreta, uterine rupture and peripartum hysterectomy. However, adverse perinatal outcomes are not demonstrated. ObjectiveTo investigate the perinatal outcomes of women that had a placenta accreta in a previous pregnancy. To investigate the perinatal outcomes of women that had a placenta accreta in a previous pregnancy. Study DesignWe retrospectively compared all subsequent singleton cesarean deliveries (CD) of women with a previous placenta accreta, with CD of women with no such history, during the years 1988-2011. We retrospectively compared all subsequent singleton cesarean deliveries (CD) of women with a previous placenta accreta, with CD of women with no such history, during the years 1988-2011. ResultsOut of 34,567 singleton CD that occurred during the study period, 0.1% (n=30) were of women with a previous placenta accreta. Recurrent placenta accreta occurred in 23.3% (7/30) of patients with placenta accreta in their previous pregnancy. Previous placenta accreta was significantly associated with uterine rupture, peripartum hysterectomy and the need for blood transfusions. Nevertheless, increased risk for adverse perinatal outcomes such as low Apgar scores at 5 minutes and perinatal mortality was not found in these patients (table).Tabled 1Selected pregnancy and perinatal outcomes of patients with and without a previous placenta accrete Out of 34,567 singleton CD that occurred during the study period, 0.1% (n=30) were of women with a previous placenta accreta. Recurrent placenta accreta occurred in 23.3% (7/30) of patients with placenta accreta in their previous pregnancy. Previous placenta accreta was significantly associated with uterine rupture, peripartum hysterectomy and the need for blood transfusions. Nevertheless, increased risk for adverse perinatal outcomes such as low Apgar scores at 5 minutes and perinatal mortality was not found in these patients (table). ConclusionA pregnancy following a previous placenta accreta is at increased risk for adverse maternal outcomes such as recurrent accreta, uterine rupture and peripartum hysterectomy. However, adverse perinatal outcomes are not demonstrated. A pregnancy following a previous placenta accreta is at increased risk for adverse maternal outcomes such as recurrent accreta, uterine rupture and peripartum hysterectomy. However, adverse perinatal outcomes are not demonstrated.