Background: Inflammation is associated with many disorders of preterm infants including periventricular leukomalacia, chronic lung disease, and necrotizing enterocolitis. Activated protein c (APC) has shown positive immunomodulatory effects. Objectives: We aimed to study neutrophil and monocyte function in response to lipopolysaccharide (LPS) and APC stimulation ex vivo in preterm infants Methods: Peripheral blood was taken on day 1, 3, and 7 and stimulated with LPS in the absence or presence of APC. Expression of toll-like receptor 4 (TLR4) and CD11b and reactive oxygen intermediate (ROI) release from neutrophils and monocytes was examined by flow cytometry. Results: LPS induced neutrophil ROI in adults and preterm infants and was significantly reduced by APC. Baseline and LPS-induced monocyte ROI production in preterm neonates was increased compared to adult and term controls. Neutrophil TLR4 baseline expression was higher in term controls compared to preterm infants. Conclusion: Increased systemic ROI release in preterm infants may mediate tissue damage, ROI was reduced by APC. However, due to the high risk of hemorrhage further examination of APC mutant forms with anti-inflammatory but decreased anticoagulant properties is merited.

Traditionally, the assessment of endometrial receptivity at transvaginal ultrasound scan has been based on the thickness and the morphological appearance of the endometrium. The objective of this study was to prospectively evaluate endometrial thickness (ET), endometrial morphology and uterine artery Doppler parameters prior to assisted reproduction treatment (ART) in the prediction of pregnancy outcome. This was a prospective cohort study. ET, morphology and uterine artery Doppler (UtAD) pulsatility index (PI) and resistance index (RI) were measured in the mid-luteal stage of the menstrual cycle ultrasonographically, timed with urinary luteinizing hormone testing. A total of 50 women were included in the analysis. The clinical pregnancy rate (CPR) per embryo transfer was 42.0% (n = 21/50). Twenty nine women (58.0%) had an unsuccessful outcome. There were no differences in mean +/- SD endometrial thickness (ET) (10.0 +/- 1.8 mm vs. 10.5 +/- 2.4; p = 0.43), or endometrial morphology (100% (n = 21) vs 100% (n = 29); p = 1.00) between the pregnant and not pregnant groups. Similarly, there were no differences in mean +/- SD UtAD PI (2.17 +/- 0.83 vs. 2.07 +/- 0.81; p = 0.67 or mean +/- SD UtAD RI (0.84 +/- 0.10 vs. 0.81 +/- 0.10; p = 0.30). Ultrasonographic endometrial assessment did not differentiate between those who would have a subsequent clinical pregnancy.

Introduction Diffuse chorionic hemosiderosis (DCH) is an abnormality of the placental membranes characterized by the deposition of iron pigment. It is usually secondary to recurrent venous bleeding in early pregnancy. In many papers, it is associated with pre-term delivery. Fetal vascular malperfusion (FVM) is an abnormality of the feto-placental circulation that may be seen at any stage of gestation, but most often in the third trimester. It may be graded as low grade (LGFVM) or high grade (HGFVM). No link has been identified in the placental literature between DCH and FVM, but we have noted the 2 co-existing in placentas submitted for analysis. This study explored a possible association of these 2 entities. Methods Laboratory records were searched for singleton cases coded as DCH based on diagnosis on H&E stain over a 6-year period. Of 4478 placentas reported, 66 cases were coded as DCH (1.5%). These were classified as showing HGFVM, LGFVM, or no FVM. Controls (n = 132) were gestational age-matched cases without DCH. Cord length, coiling, insertion, or other abnormalities were noted. Membranes were classified as normal or circumvallate. Results were analyzed using Graphpad. Results Gestation ranged between 16 and 41 weeks gestation. 14/66 (21%) cases of DCH showed HGFVM and 2/66 (3%) showed LGFVM. 16/132 (12%) controls showed HGFVM and 21/132 (15.9%) had LGFVM. Where FVM is present, high-grade FVM is significantly associated with DCH versus controls ( P < .0031 Fischer’s Test). Discussion HGFVM occurs significantly more often in placentas with DCH than in controls. Both FVM and DCH are associated with adverse perinatal outcomes, and a possible relationship between the 2 remains to be clarified.

Background An amendment to the 1962 Coroner's Act in the Republic of Ireland mandated that all stillbirths and neonatal deaths were to be reported to the local coroner's office. In response to this, the bereavement team and department of anatomic pathology modified the pathway for placental examination following stillbirth and reporting deaths to the coroner. This paper is a review of the effect of this practice. Methods This study is a review of all cases of stillbirths for 9 months following the amendment of the Coroner's Act. A descriptive, exploratory design was used involving a retrospective chart review. Results Twenty-nine cases of stillbirth occurred during the study period. In cases where a placental examination was performed (n = 22), a cause of death was identified in the placenta or cord for seventeen (68%) of these cases. Seven cases had a consented autopsy with six cases confirming the initial diagnosis made at the time of gross placental examination. In one case, the cause of the stillbirth remained unexplained following placental examination and a full autopsy. No new information was gained from the autopsy in these seven cases. A further two cases had an autopsy directed by the coroner; the cause of death in these cases will be decided by the coroner. Conclusions The introduction of the pathway has improved the care provided to bereaved parents by providing parents with timely information about the potential cause of stillbirth and thereby reduces the need for an autopsy examination.

Introduction Stillbirth remains an often unpredictable and devastating pregnancy outcome, and despite thorough investigation, the number of stillbirths attributable to unexplained causes remains high. Placental examination has become increasingly important where access to perinatal autopsy is limited. We aimed to examine the causes of stillbirth in normally formed infants over 30 years and whether a declining autopsy rate has affected our ability to determine a cause for stillbirths. Material and methods All cases of normally formed singleton infants weighing >= 500 g that died prior to the onset of labor from 1989 to 2018 were examined. Trends for specific causes and uptake of perinatal autopsy were analyzed individually. Results In all, 229 641 infants were delivered, with 840 stillbirths giving a rate of 3.66/1000. The rate of stillbirth declined from 4.84/1000 in 1989 to 2.51 in 2018 (P < .001). There was no difference in the rate of stillbirth between nulliparous and multiparous women (4.25 vs 3.66 per 1000,P = .026). Deaths from placental abruption fell (1.13/1000 in 1989 to 0 in 2018,P < .001) and the relative contribution of placental abruption to the incidence of stillbirth also fell, from 23.3% (7/30) in 1989 to 0.0% (0/19) in 2018 (P < .001). Stillbirth attributed to infection remained static (0.31/1000 in 1989 to 0.13 in 2018,P = .131), while a specific causal organism was found in 79.2% (42/53) of cases. Unexplained stillbirths decreased from 2.58/1000 (16/6200) in 1989 to 0.13 (1/7581) in 2018 (P < .001) despite a fall in the uptake of perinatal autopsy (96.7% [29/30] in 1989 to 36.8% (7/19) in 2018;P < .001). Placental disease emerged as a significant cause of stillbirth from 2004 onwards (89.5% [17/19] in 2018). Conclusions The present analysis is one of the largest single-center studies on stillbirth published to date. Stillbirth rates have fallen across the study period across parity. A decrease in deaths secondary to placental abruption contributed largely to this. Infection-related deaths are static; however, in one-fifth of cases a causative organism was not found. Despite a decreasing autopsy rate, the number of unexplained stillbirths continues to fall as the importance of placental pathology is increasingly recognized.

Stillbirth remains an often unpredictable and devastating pregnancy outcome, and despite thorough investigation, the number of stillbirths attributable to unexplained causes remains high. Placental examination has become increasingly important where access to perinatal autopsy is limited. We aimed to examine the causes of stillbirth in normally formed infants over 30 years and whether a declining autopsy rate has affected our ability to determine a cause for stillbirths. All cases of normally formed singleton infants weighing ≥500 g that died prior to the onset of labor from 1989 to 2018 were examined. Trends for specific causes and uptake of perinatal autopsy were analyzed individually. In all, 229 641 infants were delivered, with 840 stillbirths giving a rate of 3.66/1000. The rate of stillbirth declined from 4.84/1000 in 1989 to 2.51 in 2018 ( P  < .001). There was no difference in the rate of stillbirth between nulliparous and multiparous women (4.25 vs 3.66 per 1000, P  = .026). Deaths from placental abruption fell (1.13/1000 in 1989 to 0 in 2018, P  < .001) and the relative contribution of placental abruption to the incidence of stillbirth also fell, from 23.3% (7/30) in 1989 to 0.0% (0/19) in 2018 ( P  < .001). Stillbirth attributed to infection remained static (0.31/1000 in 1989 to 0.13 in 2018, P  = .131), while a specific causal organism was found in 79.2% (42/53) of cases. Unexplained stillbirths decreased from 2.58/1000 (16/6200) in 1989 to 0.13 (1/7581) in 2018 ( P  < .001) despite a fall in the uptake of perinatal autopsy (96.7% [29/30] in 1989 to 36.8% (7/19) in 2018; P  < .001). Placental disease emerged as a significant cause of stillbirth from 2004 onwards (89.5% [17/19] in 2018). The present analysis is one of the largest single-center studies on stillbirth published to date. Stillbirth rates have fallen across the study period across parity. A decrease in deaths secondary to placental abruption contributed largely to this. Infection-related deaths are static; however, in one-fifth of cases a causative organism was not found. Despite a decreasing autopsy rate, the number of unexplained stillbirths continues to fall as the importance of placental pathology is increasingly recognized.

CONTEXT.—:Fetal growth restriction is a risk factor for intrauterine fetal death. Currently, definitions of fetal growth restriction in stillborns are heterogeneous.OBJECTIVES.—:To develop a consensus definition for fetal growth restriction retrospectively diagnosed at fetal autopsy in intrauterine fetal death.DESIGN.—:A modified online Delphi survey in an international panel of experts in perinatal pathology, with feedback at group level and exclusion of nonresponders. The survey scoped all possible variables with an open question. Variables suggested by 2 or more experts were scored on a 5-point Likert scale. In subsequent rounds, inclusion of variables and thresholds were determined with a 70% level of agreement. In the final rounds, participants selected the consensus algorithm.RESULTS.—:Fifty-two experts participated in the first round; 88% (46 of 52) completed all rounds. The consensus definition included antenatal clinical diagnosis of fetal growth restriction OR a birth weight lower than third percentile OR at least 5 of 10 contributory variables (risk factors in the clinical antenatal history: birth weight lower than 10th percentile, body weight at time of autopsy lower than 10th percentile, brain weight lower than 10th percentile, foot length lower than 10th percentile, liver weight lower than 10th percentile, placental weight lower than 10th percentile, brain weight to liver weight ratio higher than 4, placental weight to birth weight ratio higher than 90th percentile, histologic or gross features of placental insufficiency/malperfusion). There was no consensus on some aspects, including how to correct for interval between fetal death and delivery.CONCLUSIONS.—:A consensus-based definition of fetal growth restriction in fetal death was determined with utility to improve management and outcomes of subsequent pregnancies.

We read with interest the article by Chandra et al1 on reproductive health after kidney transplantation and the reiteration that pregnancy management should be provided by a multidisciplinary team (nephrologist, a midwife, and an obstetrician). We would encourage extending the management team to include obstetric pathologists, and indeed wish to highlight a gap in our knowledge. There is an increased prevalence of preeclampsia and fetal growth restriction in pregnancies of women with renal transplants.2 Pathological lesions seen in these pregnancy complications include placental maternal vascular malperfusion and villitis of unknown etiology.3 One of the features of maternal vascular malperfusion is acute atherosis (Figure 1A), which is similar histologically to the vascular lesion seen in allograft rejections,4 while villitis of unknown etiology (Figure 1B), characterized by infiltration of the fetal villi by maternal T-lymphocytes, may also represent an alloimmune reaction.5 It is possible that immunosuppression may modify the maternal milieu and maternal–fetal interaction in early pregnancy such that placentation may be suboptimal leading to maternal vascular malperfusion; it may also dampen maternal immune response to decrease the prevalence of chronic inflammation, including villitis of unknown etiology and chronic deciduitis, in the placenta.FIGURE 1.: A, Acute atherosis showing fibrinoid necrosis of the arterial wall and presence of lipophages and perivascular lymphocytic infiltrate. B, Villitis of unknown etiology showing infiltration of the villous stroma by lymphocytes and histiocytes.There are no previous data on placental pathology in pregnancies of women with renal transplants and yet pathological examination of the placenta affords an opportunity to investigate the pathophysiology underlying the increased prevalence of these pregnancy complications in kidney-transplanted women and may inform management of these women. We could only locate few numbers of pregnancies where placentas were sent for pathological examination from our two centers. A prospective collection of placental pathology data from women with kidney transplants managed contemporaneously, possibly facilitated by national and transnational registries, such as the National Transplantation Pregnancy Registry in the United States, the UK Transplant Pregnancy Registry, the Australia and New Zealand Dialysis and Transplant registry, and the European Dialysis and Transplant Association registry, is needed to recruit sufficient numbers of placentas for a collaborative study. We would be keen to hear from other interested researchers on how to probe the pathophysiology of placental pathology in these pregnancies.

Introduction Endometrial injury or 'scratch' preceding an assisted reproductive therapy (ART) cycle has recently been shown not to improve livebirth rates among women undergoing ART. The objective of this study was to compare pregnancy outcomes in nulliparous women who underwent an accurately timed mid-luteal scratch biopsy prior to ART with those who did not. Methods This was a prospective cohort study. Women were recruited between October 2016 and February 2018 inclusive. Women who met the inclusion criteria and who did not undergo an endometrial scratch in the study period were used as a comparison group. Patients underwent a cycle of ART in the menstrual cycle following endometrial scratch. Results Ninety-eight women were eligible for participation in the study. There were no differences in rates of implantation (35.7% (n = 20/56) vs. 35.4% (n = 17/48); p = 1.00), clinical pregnancy (40.0% (n = 20/50) vs. 39.5% (n = 17/43); p = 1.00) or live birth (34.0% (n = 17/50) vs. 25.6% (n = 11/43); p = 0.50) per embryo transfer between those who underwent a scratch and those who did not. Conclusion Endometrial scratch is a simple, inexpensive and low-risk procedure. However, in this relatively small cohort study, no differences in rates of implantation, clinical pregnancy or live birth in women with primary infertility were determined between those who underwent a scratch and those who did not.

STUDY QUESTION Which transcriptomic alterations in mid-luteal endometrial scratch biopsies, taken prior to the assisted reproductive treatment (ART) treatment cycle are associated with unsuccessful pregnancy? SUMMARY ANSWER Dysregulated interleukin-17 (IL-17) pathway components are demonstrated in women who fail to become pregnant after ART. WHAT IS KNOWN ALREADY Implantation failure is now recognised as a critical factor in unexplained infertility and may be an important component of failed ART. STUDY DESIGN, SIZE, DURATION Using a prospective longitudinal study design, 29 nulliparous women with unexplained infertility undergoing ART were recruited between October 2016 and February 2018. Mid-luteal stage endometrium and matched serum samples were collected, and patients underwent a single embryo transfer in the subsequent cycle. RNA-seq analysis of endometrial biopsies was performed on the discovery cohort (n = 20). PARTICIPANTS/MATERIALS, SETTING, METHODS Gene set enrichment analysis of the differentially expressed genes (DEGs) was performed. Endometrium and serum were then prepared for IL-17A analysis by ELISA. MAIN RESULTS AND THE ROLE OF CHANCE There were 204 differentially expressed protein-coding genes identified in tissue from women who became pregnant (n = 9) compared with tissue from women who failed to become pregnant (n = 11) (false discovery rate; P < 0.05). Of the 204 DEGs, 166 were decreased while 38 were increased in the pregnant compared to the non-pregnant groups. Gene set enrichment analysis of the DEGs identified an over-representation of IL-17 and Pl3K-Akt signalling pathways. All the DEGs within the IL-17 signalling pathway (MMP3, MMP1, IL1β, LCN2, S100A9 and FOSL1) demonstrated decreased expression in the pregnant group. Serum IL-17 protein levels were increased in the non-pregnant discovery cohort (n = 11) and these findings were confirmed a validation cohort (n = 9). LIMITATIONS, REASONS FOR CAUTION Limitations of our study include the cohort size and the lack of aneuploidy data for the embryos; however, all embryos transferred were single good or top-quality blastocysts. WIDER IMPLICATIONS OF THE FINDINGS These findings demonstrate dysregulated IL-17 pathway components in women who fail to become pregnant after ART. Elevated serum levels of the pro-inflammatory cytokine IL-17 may predict failure of ART in women with unexplained infertility. Future trials of anti-IL-17 therapies in this cohort warrant further investigation. STUDY FUNDING/COMPETING INTEREST(S) Funding from the UCD Wellcome Institutional Strategic Support Fund, which was financed jointly by University College Dublin and the SFI-HRB-Wellcome Biomedical Research Partnership (ref 204844/Z/16/Z), is acknowledged. The authors have no competing interests. TRIAL REGISTRATION NUMBER NA.

Abstract Background/Aims To assess the association between placental morphology and neonatal and infant anthropometry, including analysis by sex. Study Design Data from the ROLO Kids [Randomized COntrol Trial of LOw Glycaemic Index in Pregnancy] study were analyzed including placental weight and morphology. Placental, anthropometric and skinfold measurements were recorded as markers of adiposity in 196 neonates and 215 infants at 6 months of age. Ratios including subscapular-to-triceps skinfold ratio and waist-to-height ratio were used as markers of central adiposity, while the sum of all skinfolds and subscapular plus triceps skinfolds were used as markers of general adiposity. Analysis was performed for total groups and by sex. Results On simple linear regression placental weight was associated with neonatal and infant anthropometric measurements. On multiple regression, the placental weight was associated with birth weight. In the neonatal period placental weight was associated with general adiposity in males only (sum of skinfolds (B 0.007, p < .001) and subscapular + triceps skinfolds a marker of general adiposity (B 0.004 p < .001)). At 6 months of age placental length was positively associated with central adiposity in the total group (B 0.006, p .036) and maximum cord diameter was inversely associated with infant central adiposity (B − 0.309 p .043) in males only. Conclusion The placental phenotype is associated with anthropometry at birth and this association persists to early infancy with a stronger relationship noted in this cohort amongst males. This suggests sexual dimorphism may play a role in the impact of the placenta on infant anthropometry.

Histological chorioamnionitis (HCA) is associated with preterm birth and adverse neonatal outcomes. We evaluated the rise in C-reactive protein (CRP) in preterm infants as a predictor of HCA severity and outcomes. Consecutive preterm infants, born January 2009 to January 2014 in the National Maternity Hospital, Dublin, under 32 weeks' gestation or <1.5 kg birthweight, were included. Histological chorioamnionitis was staged as maternal inflammatory response, foetal inflammatory response and non-HCA. Preterm infants (n = 518) were included with a mean gestational age 28.5 ± 2.8 weeks, birthweight 1.1 ± 0.3 kg, and 53.5% were male. Histological chorioamnionitis was found in 25.4%. Histological chorioamnionitis was present in 93.7% when CRP > 5 mg/L, 65.2% when CRP 1-5 mg/L and in 19.4% when CRP < 1 mg/L. When both the immature to total neutrophil (IT) ratio was >0.2 and the CRP > 1 mg/L the positive predictive value and negative predictive value for HCA were 92.5% and 84.9%, respectively. Histological chorioamnionitis was associated with more resuscitation and respiratory distress syndrome (both P < .001). A CRP > 10 mg/L was associated with a foetal inflammatory response and increased early-onset sepsis. Higher early CRP was a surrogate predictor of HCA and correlated with the severity of HCA. Higher CRP and HCA were associated with adverse early outcomes.

Aim Histological chorioamnionitis (HCA) is associated with preterm birth and adverse neonatal outcomes. We evaluated the rise in C-reactive protein (CRP) in preterm infants as a predictor of HCA severity and outcomes. Methods Consecutive preterm infants, born January 2009 to January 2014 in the National Maternity Hospital, Dublin, under 32 weeks' gestation or <1.5 kg birthweight, were included. Histological chorioamnionitis was staged as maternal inflammatory response, foetal inflammatory response and non-HCA. Results Preterm infants (n = 518) were included with a mean gestational age 28.5 +/- 2.8 weeks, birthweight 1.1 +/- 0.3 kg, and 53.5% were male. Histological chorioamnionitis was found in 25.4%. Histological chorioamnionitis was present in 93.7% when CRP > 5 mg/L, 65.2% when CRP 1-5 mg/L and in 19.4% when CRP < 1 mg/L. When both the immature to total neutrophil (IT) ratio was >0.2 and the CRP > 1 mg/L the positive predictive value and negative predictive value for HCA were 92.5% and 84.9%, respectively. Histological chorioamnionitis was associated with more resuscitation and respiratory distress syndrome (bothP < .001). A CRP > 10 mg/L was associated with a foetal inflammatory response and increased early-onset sepsis. Conclusion Higher early CRP was a surrogate predictor of HCA and correlated with the severity of HCA. Higher CRP and HCA were associated with adverse early outcomes.

BACKGROUND:The weight of the delivered placenta gives a useful representation of placental function in utero. In the absence of Irish data, many pathologists rely on data from other populations, many of which are now 15 to 30 years old. The development of a population-specific nomogram would aid in the examination of placentas after delivery, allowing pathologists and medical scientists to more easily distinguish between placental physiological changes and pathology.AIMS:To record placental weights among women having a singleton delivery in Dublin and to establish median placental weights for each gestational age after 37 weeks.METHODS:Prospective cohort study in a Tertiary level University Hospital. All singleton pregnancies were included; stillbirths, multiple gestations, and cases with obstetric complications involving the placenta were excluded. The placentas were weighed both untrimmed and trimmed with standard scales. Demographic features including birth weight and maternal parity were also recorded.RESULTS:Four hundred thirty placentas were weighed over a 6-week period. A median term placental weight based on gestational age was established, with a range from the tenth to ninetieth centiles.CONCLUSION:The weight of the placenta is one of several measurements that are easy to acquire, and when recorded in a systematic fashion, provide information not just on an individual, but also on a population basis. Birth weights have increased over the last century, and this study provides national data helping distinction between placental physiology and pathology.

Objective To assess the effect of aspirin use in low-risk pregnancy on: (1) pregnancy-associated plasma protein-A (PAPP-A) and placental-like growth factor (PLGF); (2) urinary albumin-to-creatinine ratio (ACR) and blood pressure; (3) fetal growth parameters; and (4) placental histopathology. Study Design This secondary analysis from the T rial of low-dose aspirin with an E arly S creening T est for preeclampsia and growth restriction randomized controlled trial was based on low-risk nulliparous women randomized at 11 weeks to (1) aspirin 75 mg; (2) no aspirin; and (3) aspirin based on the preeclampsia Fetal Medicine Foundation screening test. At baseline, women underwent assessment of blood pressure, PAPP-A, PLGF, and ACR, repeated 9 to 10 weeks postaspirin, in addition to fetal growth assessment. Gross and histopathological placental analyses were performed in line with Amsterdam criteria. Results A total of 445 subjects were included (aspirin n = 163 [36.6%]; no aspirin n = 282 [63.4%]). Although the fetal-to-placental weight ratio was significantly greater in the aspirin group (7.5 [±1.3] vs. 7.3 [±1.4], p = 0.045), as was change in ultrasound assessed estimated fetal weight from second to third trimesters (1,624.5 g [±235.1] vs. 1,606.2 [±189.4], p = 0.042), this was invalidated by the lack of a difference in birth weight. Aspirin did not significantly impact on change in serum or urine preeclampsia biomarkers, maternal blood pressure, or placental histopathology. Conclusion Aspirin use in low-risk pregnancy does not appear to impact on preeclampsia biomarkers, fetal growth, or placental pathology.

To evaluate the impact of low dose aspirin (LDA) use in low-risk pregnancy on; (i) placental biomarkers PAPP-A and PLGF, (ii) systemic markers albumin creatinine ratio (ACR) and blood pressure, (iii) fetal growth parameters and (iv) placental histopathology. This was a secondary analysis including data from the primary site of the TEST RCT where 546 low-risk nulliparous women were randomised at 11-weeks to; (i) routine aspirin 75mg from 11 to 36-weeks; (ii) no aspirin; and (iii) aspirin based upon the preeclampsia Fetal Medicine Foundation screening test. At baseline women underwent assessment of blood pressure, PAPP-A, PLGF and ACR. These were repeated at 20-22 weeks (9-10 weeks post LDA commencement) in addition to ultrasound assessment of fetal growth, which was repeated again at 32-weeks. Gross and histopathological placental analysis were performed including assessment of fetalplacental weight ratio, cord coiling, fetal and maternal vascular malperfusion, maturation defects and villitis. Aspirin and non-aspirin groups were compared using logistic regression. 445 subjects were included (LDA n=163 no LDA=282), with the LDA group comprising n=13 from the screen positive arm and 150 from the routine LDA arm. As rates of smoking and weight differed at baseline, these were controlled for in analyses. LDA was associated with a significant increase in abdominal circumference (p=0.04) and femur length (p=0.01) at 20-22 weeks (p=0.04), which was not persistent at 32-weeks (p=0.60). There was no difference in birthweight 3520.3g (507.6) vs. 3470.7g (523.0) p=0.70 [Table 1]. Although there was an increased fetal placental weight in the aspirin group (7.5 vs. 7.3), this did not reach significance p=0.05. There was no difference between groups in relation to blood pressure, serum and urine biomarkers or histopathological placental findings. Low dose aspirin appears to promote fetal growth in low-risk nulliparous women between the first and second trimester, which is not evident thereafter. Our study did not demonstrate an impact of aspirin on placental or systemic biomarkers assessed.