Objective A limited number of platelet function studies in intrauterine growth restriction (IUGR) have yielded conflicting results. We sought to evaluate platelet reactivity in IUGR using a novel platelet aggregation assay.Study Design Pregnancies with IUGR were recruited from 24 weeks' gestation (estimated fetal weight < 10th centile) and had platelet function testing performed after diagnosis. A modification of light transmission aggregometry created dose-response curves of platelet reactivity in response to multiple agonists at differing concentrations. Findings were compared with healthy third trimester controls. IUGR cases with a subsequent normal birth weight were analyzed separately.Results In this study, 33 pregnancies retained their IUGR diagnosis at birth, demonstrating significantly reduced platelet reactivity in response to all agonists (arachidonic acid, adenosine diphosphate, collagen, thrombin receptor-activating peptide, and epinephrine) when compared with 36 healthy pregnancy controls (p < 0.0001). Similar results were obtained for cases demonstrating an increasing in utero growth trajectory. When IUGR preceded preeclampsia or gestational hypertension, platelet function was significantly reduced compared with normotensive IUGR.Conclusion Using this comprehensive platelet assay, we have demonstrated a functional impairment of platelets in IUGR. This may reflect platelet-derived placental growth factor release. Further evaluation of platelet function may aid in the development of future platelet-targeted therapies for uteroplacental disease.

Objective: Spontaneous platelet aggregation has not been adequately assessed as a potential risk factor for adverse outcomes in pregnancy. Therefore the objective of this study was to assess spontaneous platelet aggregation (SPA), measured via a novel functional assay, as a risk factor for hypertensive disease and intra-uterine growth restriction (IUGR).Study design: This was a prospective longitudinal study. Spontaneous platelet aggregation was assessed as a marker of platelet reactivity using a modification of light transmission aggregometry. Platelet reactivity was assessed in four groups: non-pregnant healthy female volunteers (n = 30), longitudinally in normal uncomplicated pregnancy (n = 50), hypertensive disorder (n = 40) and IUGR (n = 30). The mean percentage SPA was plotted and compared across all groups.Results: Spontaneous platelet aggregation was significantly reduced in the first trimester compared to the non-pregnant group (p-value = 0.003). The mean aggregation for the hypertensive group was 1.9%, (95% CI -0.08 to 4.02) and for the IUGR group was 1.6%, (95% CI -0.6 to 3.72). Platelet aggregation in the hypertensive group was significantly reduced compared to the normal pregnant group (p < 0.05). Spontaneous platelet aggregation was also reduced in the IUGR group compared to normal pregnancy (p < 0.05).Conclusion: This study demonstrates that a reduction of spontaneous platelet aggregation may be a novel risk factor for adverse pregnancy outcomes such as pre-eclampsia and IUGR. The most clinically significant finding is that SPA is significantly lower in pregnancies complicated by hypertension and IUGR compared to those who had a normal pregnancy outcome. Further studies should be carried out to asses if spontaneous platelet aggregation may be a clinically useful tool for the prediction of preeclampsia and IUGR. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

OBJECTIVE:The aim of this study was to characterize platelet function in pregnant patients with a history of unexplained recurrent miscarriage (RM) in the third trimester of a subsequent viable pregnancy, a time at which platelet dysfunction may be associated with an increased obstetric risk.STUDY DESIGN:A prospective study was performed comparing 30 viable pregnancies that had reached at least 28 weeks' gestation amongst patients who had a background history of unexplained RM, with 30 healthy pregnant controls at a similar gestational age. Platelet function was determined by means of platelet aggregation in response to 5 different agonists at multiple concentrations.RESULTS:Amongst the 30 RM patients with ongoing viable pregnancies, we demonstrated significantly reduced platelet aggregation compared to the pregnant controls in the third trimester. For three out of five agonists, we demonstrated statistically significantly decreased platelet aggregation and for all five agonists we demonstrated significantly decreased platelet aggregation in the postnatal period. There were no obvious differences in obstetric outcomes.CONCLUSION:This study shows that women with a history of unexplained RM have reduced platelet function after 28 weeks' gestation in their subsequent pregnancies compared to healthy pregnant controls, but without this difference leading to any obvious increase in adverse obstetric risk.

Objective: This study was designed to evaluate platelet aggregation in pregnant women with a history of unexplained recurrent miscarriage (RM) and to compare platelet function in such patients who go on to have either another subsequent miscarriage or a successful pregnancy.Study design: A prospective longitudinal study was performed to evaluate platelet function in a cohort of patients with a history of unexplained RM. Platelet reactivity testing was performed at 4-7 weeks gestation, to compare platelet aggregation between those with a subsequent miscarriage and those who had successful live birth outcomes. Platelet aggregation was calculated using a modified assay of light transmission aggregometry with multiple agonists at different concentrations.Results: In a cohort of 39 patients with a history of RM, 30 had a successful pregnancy outcome while nine had a subsequent miscarriage again. Women with subsequent miscarriage had reduced platelet aggregation in response to adenosine diphosphate (P value 0.0012) and thrombin receptor activating peptide (P value 0.0334) when compared to those with successful pregnancies. Women with subsequent miscarriages also had a trend towards reduced platelet aggregation in response to epinephrine (P value 0.0568).Conclusion: Patients with a background history of unexplained RM demonstrate reduced platelet function if they have a subsequent miscarriage compared to those who go on to have a successful pregnancy. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

ObjectivePlatelets play an important role in the pathophysiology of uteroplacental disease and platelet reactivity may be an important marker of uteroplacental disease activity. However, platelet reactivity has not been evaluated comprehensively in normal pregnancy. We sought to evaluate platelet reactivity using a number of agonists at defined time points in pregnancy using a novel platelet assay and compare these with a nonpregnant cohort.DesignProspective longitudinal study.SettingOutpatient department of a large tertiary referral centre.SampleEighty participants with 30 nonpregnant women and 50 pregnant women assessed longitudinally.MethodsThis was a prospective cohort study performed longitudinally throughout uncomplicated singleton pregnancies with participants recruited before 15weeks of gestation. They were controlled for a number of factors known to affect platelet reactivity. Blood samples were obtained in each trimester. Thirty nonpregnant healthy female volunteers also had a platelet assay performed. A modification of standard light transmission aggregometry was used to assess platelet function, with light absorbance measured following the addition of five different agonists at submaximal concentrations. Dose-response curves were plotted for each agonist for the nonpregnant cohort and in each trimester for the pregnant cohort.Main outcome measuresDose-response curves and median effective concentration.ResultsWhen compared with the nonpregnant controls a significant reduction was demonstrated in platelet reactivity to collagen during the first trimester of pregnancy (P<0.0001). Platelet aggregation increased significantly from the first to third trimesters in response to collagen and arachidonic acid.ConclusionPlatelet reactivity varies according to pregnancy state, gestational age and agonist. The finding that platelet reactivity is reduced in the first trimester of pregnancy may be useful for the interpretation of further studies examining the role of platelet reactivity in the first trimester of pregnancies that develop uteroplacental disease.

Platelet function in pregnancies complicated by intra-uterine growth restriction (IUGR) is not well understood. We sought to evaluate platelet function in response to multiple concentrations of multiple agonists in pregnancies complicated by IUGR using a novel platelet function assay. Cases of intrauterine growth restricted singleton pregnancies were recruited following ultrasound diagnosis between 24–40 weeks gestation (estimated fetal weight <10th centile for gestational age) in a tertiary referral centre. A modification of standard light transmission aggregometry was used to assess platelet reactivity. Several agonists were assessed at incremental concentrations to characterise the response to multiple receptors. The findings were compared to healthy controls matched for gestational age with normal fetal weight. A total of 24 pregnancies complicated with IUGR and 36 healthy controls were recruited. Platelet reactivity in response to the agonists Arachidonic acid, Adenosine-diphosphate, Epinephrine and Thrombin-receptor activating protein was significantly reduced in the IUGR cohort. There was a nonsignificant trend to decreased reactivity in response to collagen (Table 1). In pregnancies complicated by IUGR there is a significant decrease in platelet function compared to healthy pregnant controls. This may reveal valuable insights into the patho-physiology of the disease, and may represent an inadequate growth factor response in IUGR. Further evaluation of the role of platelets may and aid in the development of future interventions for IUGR.

Aim We sought to determine subsequent pregnancy outcomes in a cohort of women with a history of unexplained recurrent miscarriage (RM) as compared to healthy pregnancy controls. Study design This was a prospective cohort study of women attending a dedicated RM clinic in the Rotunda Hospital in 2011. Inclusion criteria included women with a history of three consecutive first trimester losses that were unexplained in the past, no medical intervention and singleton pregnancies only. The inclusion criteria for the healthy controls included no history of stillbirth, intrauterine growth restriction, preeclampsia or preterm labour. Results Of the 42 women with RM recruited to the study nine (23%) experienced further first trimester miscarriages, one molar and one ectopic pregnancy. The remaining RM cohort with ongoing pregnancies (n = 31) were compared to healthy controls (n = 31) matched for age and BMI. The only statistical difference between the two groups was the earlier mean gestational delivery of the RM group (38 + 2 vs 39 + 4 weeks, p = 0.004) attributed to earlier induction due to their past history. Otherwise there was no significant difference with respect to pregnancy complications, delivery and neonatal outcomes. All of RM patients achieved successful term deliveries with a 74% vaginal delivery rate and a mean birthweight of 3.23 kg. Conclusion This study re-iterates the reassuring prognosis for women with a history of unexplained RM who undergo supportive care at a dedicated clinic. The majority delivered appropriately grown fetuses at term which was comparable to healthy controls.

Objective To evaluate platelet aggregation in patients with a history of recurrent miscarriage (RM) during a subsequent successful pregnancy and compare them to healthy pregnant controls. Study design A prospective longitudinal study was performed to compare platelet function in 30 patients with a history of three consecutive unexplained first trimester pregnancy losses and 30 healthy age-matched pregnant controls. Exclusion criteria included the use of anti-platelet medications such as aspirin and medical conditions that can affect platelet function. Light transmission aggregometry was used to assay platelet agonists at different times and concentrations to create dose-response curves. Results In contrast, to the increased platelet aggregation response seen in healthy controls, platelet reactivity in patients with RM peaked at 12–14 weeks gestation, highlighted by the increased aggregation response to epinephrine (p = 0.0008) and collagen (p < 0.0001) and then decreased in the third trimester in response to epinephrine (p < 0.0001), arachidonic acid (p < 0.0001) and Thrombin Receptor Activating Peptide (p < 0.0001). Conclusion Patients with a history of recurrent miscarriage have significantly different platelet function when compared to healthy controls, in particular during the first trimester. Knowledge of which patients have impaired platelet function may allow for more targeted therapy in the setting of recurrent miscarriage.

To determine abnormalities in reactivity of platelets in cases of pre-eclampsia and gestational hypertension using a novel platelet function assay. Thirty patients diagnosed with either pre-eclamspia or gestational hypertension were recruited. Inclusion criteria were singleton pregnancies between 24+0 and 39+6 with either pre-eclampsia or gestational hypertension as defined by ACOG criteria. Exclusion criteria included diabetes, clotting disorders, aspirin usage or BMI>30. All patients were in the third trimester of pregnancy and the values obtained were compared to patients (N=30) who were in the third trimester of uncomplicated normal pregnancy not affected by either pre-eclamspia or gestational hypertension. A 30ml whole blood sample was drawn according to a strict protocol to maintain platelet integrity. A platelet function assay was performed on each sample within 30 minutes of blood draw. A modification of standard light transmission aggregometry was used to assess platelet function, with light absorbance measured following addition of 5 different agonists at maximal and sub-maximal concentrations. Since platelets have multiple receptors it is necessary to study more than one receptor with the various agonists. The percentage aggregation response for each concentration of each agonist was calculated. Platelet reactivity differed significantly between the two groups of patients for each agonist. Platelet aggregation to arachidonic acid (p<0.0042), epinephrine (p<0.00001) and collagen (p<0.00001) was less reactive in pre-eclamptic and gestational hypertension than in uncomplicated third trimester patients. This pattern of platelet aggregation was not repeated for the agonists TRAP and ADP. We have demonstrated a significant reduction in platelet reactivity in patients with both pre-eclampsia and gestational hypertension compared to patients with uncomplicated pregnancies in the third trimester. These data may be of value when designing interventions for prevention or treatment of pre-eclampsia.

Platelet function has not been well characterised in pregnancy. We used a modification of light transmission aggregometry to prospectively assess SPA in normal and complicated pregnancies. The study was powered (80%) to detect a 6% change in platelet aggregation across the time-points and an 8% change for PET or IUGR. In 50 patients with normal pregnancy, platelet function was assessed in the three trimesters and post-natally. In 35 patients with pre-eclampsia (PET) and 18 patients with intra-uterine growth restriction (IUGR) platelet function was assessed in the third trimester. Comparisons between platelet function assays in the four time points of normal pregnancy were made using a mixed effects model with study participant as a random-effect, allowing for possible correlations between the repeated assessments. ANOVA was used to compare these assessments with the PET and IUGR groups. The results are presented as Bonferroni adjusted p-values. SPA increased significantly between the 1st and 2nd trimester (7% increase, p-value=0.0001); the 3rd trimester (9% increase, p-value=0.0020) and the post-natal assessment (15% increase, p-value=0.0002) in normal pregnancy. In contrast there was no increase in the platelet aggregation profile of patients with either PET or IUGR. We demonstrate for the first time a significant incremental increase in SPA with advancing gestational age in normal pregnancy. In contrast this increase in platelet aggregation does not occur in the third trimester in platelets from patients with either PET or IUGR. These results suggest that sequential analysis of SPA may be a novel marker for at risk pregnancies.

Forty patients diagnosed with either pre-eclamspia or gestational hypertension were recruited. Inclusion criteria were singleton pregnancies between 24+0 and 39+6 with either pre-eclampsia or gestational hypertension as defined by ACOG criteria. Exclusion criteria included diabetes, clotting disorders, aspirin usage or BMI >30. Patients were in the third trimester of pregnancy and the values obtained were compared to patients (N=30) who were in the third trimester of uncomplicated ‘normal’ pregnancy. A 30ml whole blood sample was drawn according to a strict protocol to maintain platelet integrity. A platelet function assay was performed on each sample within 30 minutes of blood draw. A modification of standard light transmission aggregometry was used to assess platelet function, with light absorbance measured following addition of 5 different agonists at maximal and sub-maximal concentrations. Since platelets have multiple receptors it is necessary to study more than one receptor with the various agonists. The percentage aggregation response for each concentration of each agonist was calculated. Platelet reactivity differed significantly between the two groups of patients for each agonist. Platelet aggregation to arachidonic acid (p<0.0042), epinephrine (p<0.00001) and collagen (p<0.00001) was less reactive in pre-eclamptic and gestational hypertension than in uncomplicated third trimester patients. This pattern of platelet aggregation was not repeated for the agonists TRAP and ADP. We have demonstrated a significant reduction in platelet reactivity in patients with both pre-eclampsia and gestational hypertension compared to patients with uncomplicated pregnancies in the third trimester. These data may be of value when designing interventions for prevention or treatment of pre-eclampsia.

OBJECTIVE: In countries at latitudes above 42 degrees north, endogenous production of vitamin D essentially ceases from November until March.As fetal bone development is entirely dependent on the maternal pool of vitamin D there are concerns about the implications of inadequate levels.We sought to examine the prevalence of hypovitaminosis D in pregnancy and to correlate maternal vitamin D to fetal anthropometry and birthweight.STUDY DESIGN: This is a prospective cohort study.Sixty healthy pregnant women had 25-hydroxy vitamin D (25[OH]D) measured in the early pregnancy(mean 14.3ϩ/Ϫ2.6weeks), at 28 weeks and in cord blood at delivery.Two specific subgroups were analysed in order to examine results in the context of known seasonal variation in 25[OH]D.Thirty women were recruited in early pregnancy in September/October and delivered in March/April (winter cohort).A further 30 women were recruited in March/April and delivered in September/October (summer cohort).Fetal anthropometry was assessed with ultrasound at 20 and 34 weeks and at delivery birthweight, length and head circumference were recorded.RESULTS: There was a high prevalence of both hypovitaminosis D and vitamin D deficiency with a marked seasonal variation observed, Table 1.Maternal 25[OH]D correlated with fetal 25[OH]D in cord blood (pϽ0.05).In the winter cohort, a positive correlation was found between first trimester (pϭ0.04) and cord (pϭ0.02)25[OH]D, and fetal femur length at 20 weeks.Additionally a positive correlation was noted between 25[OH]D at 28 weeks (pϭ0.02)and in cord blood (pϭ0.007), and fetal femur length at 34 weeks.No significant association was noted between maternal and fetal 25[OH]D and infant birthweight, length or head circumference.CONCLUSION: The prevalence of maternal hypovitaminosis D is particularly high in women who are pregnant during winter months in northern latitudes.This may have potential detrimental effects on fetal skeletal growth.These findings add to the growing body of evidence supporting routine vitamin D supplementation in pregnancy.

ObjectiveAbnormalities of platelet function have been implicated in a range of obstetric complications. However, little information is available on changes in platelet function throughout normal pregnancy. Our objective was to assess platelet aggregation using a range of agonists across a range of concentrations at defined time points in pregnancy.Study DesignA total of 50 healthy women with uncomplicated singleton pregnancies were recruited prior to15 weeks gestation. Maternal blood samples were obtained before 15, 24 weeks and 34 weeks gestation. A modification of standard light transmission aggregometry was used to assess platelet function, with light absorbance measured following addition of 5 different agonists at sub-maximal concentrations. Since platelets have multiple receptors it is necessary to study more than one receptor with the various agonists. The percentage aggregation response for each concentration of each agonist was calculated. To characterise maximal platelet aggregation in each trimester of pregnancy dose response curves were plotted for each agonist in each trimester.ResultsPlatelet aggregation in response to three of the agonists is significantly enhanced in the second and third trimesters (p<0.0001). Fig 1 demonstrates that platelet aggregation to arachidonic acid (AA), collagen and epinephrine in the first trimester followed similar trends and differed significantly to later gestations (p<0.0001). This pattern of platelet aggregation was not repeated for the agonists TRAP and ADP.ConclusionTabled 1 ObjectiveAbnormalities of platelet function have been implicated in a range of obstetric complications. However, little information is available on changes in platelet function throughout normal pregnancy. Our objective was to assess platelet aggregation using a range of agonists across a range of concentrations at defined time points in pregnancy. Abnormalities of platelet function have been implicated in a range of obstetric complications. However, little information is available on changes in platelet function throughout normal pregnancy. Our objective was to assess platelet aggregation using a range of agonists across a range of concentrations at defined time points in pregnancy. Study DesignA total of 50 healthy women with uncomplicated singleton pregnancies were recruited prior to15 weeks gestation. Maternal blood samples were obtained before 15, 24 weeks and 34 weeks gestation. A modification of standard light transmission aggregometry was used to assess platelet function, with light absorbance measured following addition of 5 different agonists at sub-maximal concentrations. Since platelets have multiple receptors it is necessary to study more than one receptor with the various agonists. The percentage aggregation response for each concentration of each agonist was calculated. To characterise maximal platelet aggregation in each trimester of pregnancy dose response curves were plotted for each agonist in each trimester. A total of 50 healthy women with uncomplicated singleton pregnancies were recruited prior to15 weeks gestation. Maternal blood samples were obtained before 15, 24 weeks and 34 weeks gestation. A modification of standard light transmission aggregometry was used to assess platelet function, with light absorbance measured following addition of 5 different agonists at sub-maximal concentrations. Since platelets have multiple receptors it is necessary to study more than one receptor with the various agonists. The percentage aggregation response for each concentration of each agonist was calculated. To characterise maximal platelet aggregation in each trimester of pregnancy dose response curves were plotted for each agonist in each trimester. ResultsPlatelet aggregation in response to three of the agonists is significantly enhanced in the second and third trimesters (p<0.0001). Fig 1 demonstrates that platelet aggregation to arachidonic acid (AA), collagen and epinephrine in the first trimester followed similar trends and differed significantly to later gestations (p<0.0001). This pattern of platelet aggregation was not repeated for the agonists TRAP and ADP. Platelet aggregation in response to three of the agonists is significantly enhanced in the second and third trimesters (p<0.0001). Fig 1 demonstrates that platelet aggregation to arachidonic acid (AA), collagen and epinephrine in the first trimester followed similar trends and differed significantly to later gestations (p<0.0001). This pattern of platelet aggregation was not repeated for the agonists TRAP and ADP. ConclusionTabled 1

ObjectiveWe have shown that the platelet phenotype in non-pregnant women who have had recurrent miscarriage is different to that of age and normal controls. We aimed to characterise platelet function in detail in pregnant patients with and without a history of recurrent miscarriageStudy DesignWe characterised platelet function in response to incremental concentrations of 5 different agonists in a prospective study of 41 pregnant patients with a history of recurrent miscarriage and 50 normal healthy pregnancies of similar gestation. Inclusion criteria were three or more consecutive first trimester miscarriages with a negative thrombophilia screen. Exclusion criteria included use of anti-platelet therapy, known pre-existing disorders of platelet function and multiple gestations. A fasting blood sample was obtained to measure platelet aggregation to multiple concentrations of five different agonists using a modification of light transmission aggregometry. The percentage aggregation response for each agonist was calculated.ResultsEleven of 41 patients with a history of recurrent miscarriage had a first trimester miscarriage. The remaining 30 patients had normal pregnancies. Platelet function from the 11 patients with miscarriage was compared to that from 50 normal healthy pregnant women in the first trimester and the 30 patients with on-going pregnancies with previous miscarriage. In the recurrent miscarriage group who suffered a first trimester loss there was a significant reduction in platelet aggregation in response to Arachidonic acid (p=0.004), Adenosine Diphosphate (p<0.0001), Epinephrine (p=0.0293) and TRAP (p<0.0001) when compared to those who had on-going pregnancies (Fig. 1).ConclusionPlatelet reactivity is significantly reduced in those continuing to experience recurrent first trimester miscarriage. This may be critical in modelling treatment interventions peri-conceptually. Our research findings also challenge the pharmacological basis for the empiric use of aspirin in patients with idiopathic recurrent miscarriage. ObjectiveWe have shown that the platelet phenotype in non-pregnant women who have had recurrent miscarriage is different to that of age and normal controls. We aimed to characterise platelet function in detail in pregnant patients with and without a history of recurrent miscarriage We have shown that the platelet phenotype in non-pregnant women who have had recurrent miscarriage is different to that of age and normal controls. We aimed to characterise platelet function in detail in pregnant patients with and without a history of recurrent miscarriage Study DesignWe characterised platelet function in response to incremental concentrations of 5 different agonists in a prospective study of 41 pregnant patients with a history of recurrent miscarriage and 50 normal healthy pregnancies of similar gestation. Inclusion criteria were three or more consecutive first trimester miscarriages with a negative thrombophilia screen. Exclusion criteria included use of anti-platelet therapy, known pre-existing disorders of platelet function and multiple gestations. A fasting blood sample was obtained to measure platelet aggregation to multiple concentrations of five different agonists using a modification of light transmission aggregometry. The percentage aggregation response for each agonist was calculated. We characterised platelet function in response to incremental concentrations of 5 different agonists in a prospective study of 41 pregnant patients with a history of recurrent miscarriage and 50 normal healthy pregnancies of similar gestation. Inclusion criteria were three or more consecutive first trimester miscarriages with a negative thrombophilia screen. Exclusion criteria included use of anti-platelet therapy, known pre-existing disorders of platelet function and multiple gestations. A fasting blood sample was obtained to measure platelet aggregation to multiple concentrations of five different agonists using a modification of light transmission aggregometry. The percentage aggregation response for each agonist was calculated. ResultsEleven of 41 patients with a history of recurrent miscarriage had a first trimester miscarriage. The remaining 30 patients had normal pregnancies. Platelet function from the 11 patients with miscarriage was compared to that from 50 normal healthy pregnant women in the first trimester and the 30 patients with on-going pregnancies with previous miscarriage. In the recurrent miscarriage group who suffered a first trimester loss there was a significant reduction in platelet aggregation in response to Arachidonic acid (p=0.004), Adenosine Diphosphate (p<0.0001), Epinephrine (p=0.0293) and TRAP (p<0.0001) when compared to those who had on-going pregnancies (Fig. 1). Eleven of 41 patients with a history of recurrent miscarriage had a first trimester miscarriage. The remaining 30 patients had normal pregnancies. Platelet function from the 11 patients with miscarriage was compared to that from 50 normal healthy pregnant women in the first trimester and the 30 patients with on-going pregnancies with previous miscarriage. In the recurrent miscarriage group who suffered a first trimester loss there was a significant reduction in platelet aggregation in response to Arachidonic acid (p=0.004), Adenosine Diphosphate (p<0.0001), Epinephrine (p=0.0293) and TRAP (p<0.0001) when compared to those who had on-going pregnancies (Fig. 1). ConclusionPlatelet reactivity is significantly reduced in those continuing to experience recurrent first trimester miscarriage. This may be critical in modelling treatment interventions peri-conceptually. Our research findings also challenge the pharmacological basis for the empiric use of aspirin in patients with idiopathic recurrent miscarriage. Platelet reactivity is significantly reduced in those continuing to experience recurrent first trimester miscarriage. This may be critical in modelling treatment interventions peri-conceptually. Our research findings also challenge the pharmacological basis for the empiric use of aspirin in patients with idiopathic recurrent miscarriage.

Platelet function in pregnancies complicated by intra-uterine growth restriction (IUGR) is not well understood. We sought to evaluate platelet function in response to multiple concentrations of multiple agonists in pregnancies complicated by IUGR using a novel platelet function assay. Cases of intrauterine growth restricted singleton pregnancies were recruited following ultrasound diagnosis between 24–40 weeks gestation (estimated fetal weight <10th centile for gestational age) in a tertiary referral centre. A modification of standard light transmission aggregometry was used to assess platelet reactivity. Several agonists were assessed at incremental concentrations to characterise the response to multiple receptors. The findings were compared to healthy controls matched for gestational age with normal fetal weight. A total of 24 pregnancies complicated with IUGR and 36 healthy controls were recruited. Platelet reactivity in response to the agonists Arachidonic acid, Adenosine-diphosphate, Epinephrine and Thrombin-receptor activating protein was significantly reduced in the IUGR cohort. There was a nonsignificant trend to decreased reactivity in response to collagen (Table 1). Abstract PF.04 Table 1 Concentration of EC50 for each agonist Agonist EC50 P value Normal pregnancy IUGR Arachidonic acid 0.064 0.283 <0.0001 Adenosine-diphosphate 21 54 0.0007 Collagen 0.052 0.427 0.0973 Epinephrine 231.4 3839 0.0015 Thrombin-receptor activating protein 10.27 71.54 <0.0001 In pregnancies complicated by IUGR there is a significant decrease in platelet function compared to healthy pregnant controls. This may reveal valuable insights into the patho-physiology of the disease, and may represent an inadequate growth factor response in IUGR. Further evaluation of the role of platelets may and aid in the development of future interventions for IUGR.