Antiphospholipid Syndrome And Pregnancy Pdf


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Professional Reference articles are designed for health professionals to use. You may find the Antiphospholipid Syndrome Hughes' Syndrome article more useful, or one of our other health articles. NICE has issued rapid update guidelines in relation to many of these. This guidance is changing frequently.

Antiphospholipid Syndrome

Purely obstetric APS oAPS is an APS clinical presentation characterized by precisely defined morbidities occurring during pregnancy in women with no history of thrombosis. This causes aberrant placental angiogenesis and vasculogenesis. This study focuses on a subgroup of patients included in the NOH-APS cohort: those with an oAPS diagnosis who were treated for a new pregnancy during the 18 months individual observational period after diagnosis.

The time window for recruitment was January 1 to January 1 Clinical follow up started on July 1 and ended on September 1 None of the observed treated pregnant oAPS women was lost to follow up.

Briefly, all women fulfilled one of the following inclusion criteria: 1 three unexplained consecutive spontaneous abortions before the 10 week of gestation that could not be accounted for by maternal anatomic or hormonal abnormalities, or paternal or maternal chromosomal causes the recurrent embryo loss subgroup ; or 2 one unexplained death of a morphologically normal fetus fetal loss at or after the 10 week of gestation, with the normal morphology of the fetus confirmed by ultrasound scan or direct examination of the fetus fetal loss subgroup.

The exclusion criteria were: a history of thrombotic events at least one clinical episode of venous, arterial, or small-vessel thrombosis in any tissue or organ other than the placenta confirmed by objective validated criteria, ie.

We also excluded women whose pregnancy losses could be explained by infectious, metabolic, anatomic or hormonal factors. Patients were classified as primary aborters no previous successful pregnancy or secondary aborters. Complete thrombophilia screening tests were systematically performed, leading to the definition of subgroups.

Pregnant oAPS women were regularly followed by obstetricians involved in the NOHA network, as needed, and were systematically evaluated once a month by internists and hematologists in our outpatient department of hematology, with no loss to follow up. Any initial missing values for clinical characteristics could be obtained during the subsequent consultations and with the help of the network obstetricians and general practitioners.

This clinical investigation was conducted in accordance with the Declaration of Helsinki of as revised in All the women gave their informed consent to participate. Compliance to LMWH treatment was monitored by self-declaration of the patients and their partners, and systematic examination of the subcutaneous injection sites at each medical examination.

Platelet counts were checked on the day before the first LMWH injection, twice a week during the first three weeks, and then once a month. Abruptio placenta was defined according to classical clinical prenatal signs and symptoms: vaginal bleeding accompanied by non-reassuring fetal status or uterine hypertonicity, or sonographic visualization of abruption, and evidence of retroplacental clots during examination of the delivered placenta.

Cases were confirmed by histopathological diagnosis. Birthweights were assessed by birthweight percentile charts customized for maternal age, pre-pregnancy body mass index, parity, gestational age at delivery, and sex. We used blood samples collected for platelet monitoring under LMWH treatment. EDTA-anticoagulated blood samples were obtained by clean venipuncture: the first one the day before LMWH starting, the second one the 4 day of LMWH treatment, four hours after subcutaneous injection; both at The calculated interassay coefficients of variation for sFlt-1 and PlGF were 4.

In order to minimize interassay variations, plasmas obtained from a given patient before and during LMWH treatment were assayed at the same time using the same standard curve paired testing. We had no missing blood sample; 2. Complete biological results were obtained for all study subjects.

Quantitative data are presented as the median, interquartile range IQR and minimum-maximum values. Qualitative data are presented as values and percentages. All analyses were based on pregnancy outcomes that occurred during the first pregnancy after oAPS diagnosis, treated as described above. The goodness-of-fit of the model was assessed by the Hosmer-Lemeshow test. Discrimination was assessed using computing receiver operating characteristic ROC curves and calculating the area under the curve AUC.

The study design was based on our recruitment capacities assessed over a year period, thus no sample size calculation was performed. Most of the patients were non-overweight Caucasian European women, under 35 years of age, with no positive family history of venous or arterial thrombotic disease or significant pregnancy loss Online Supplementary Table S1.

Primary oAPS and fetal death were the main clinical presentation and the main criterion, respectively. Table 1. Pregnancy outcomes of the antiphospholipid syndromes APS women who initiated a new pregnancy during the 18 months individual observational period after obstetric APS diagnosis.

In the APS group, 3. Fetal karyotype investigations on early loss before ten weeks through genomic hybridization on miscarriage tissue was only available in The same test performed on fetal death was available for all cases and showed a 5. An additional 5. Neonatal death before 28 days was reported in 3.

PMCs were diagnosed in No treatment had to be stopped or replaced for safety reasons. There were no cases of heparin-induced thrombocytopenia. Treatment-associated variations of PlGF and of sFlt1 concentrations were respectively lower and higher in women who developed PMCs than in those who did not Table 2 and Figure 2.

Table 2. Figure 1. Spearman coefficient of rank correlation 0. Figure 2. We systematically looked for any associations between each of the five APS markers, the aPLAbs, and the angiogenic factors basal concentrations, treatment-associated variations and ratio of the treatment-associated variations.

Assuming that the fixed dose of 40 mg enoxaparin may not fit all women, we looked for any correlations between basal concentrations of angiogenic factors and their releases, and BMI values: no significant association could be evidenced data not shown. No significant associations between BMI values and PMCs, severe PMCs, pregnancy loss before ten weeks, fetal death, stillbirth and neonatal death in patients receiving enoxaparin were observed data not shown.

Risk factors for PMCs are shown in Table 3. PMCs are pathologies arising after the 19 completed WG; therefore, risk factors for PMCs were investigated in the subgroup of women with an ongoing pregnancy during the 20 gestational week. Looking for any cut-off values, 1. Table 3. These associations persisted after adjustment for prior fetal death and age.

The 1. The study of risk factors for difficult pregnancies within the whole cohort, ie. An abnormal karyotype also strongly predicted fetal death. Deaths occurring after nine completed weeks, ie. Multivariate analysis also confirmed prior fetal death to predict for recurrence; familial thromboembolism and familial atherothrombosis to independently increase the risk of stillbirth and maternal tobacco smoking or triple positivity for aPLAbs to enhance the risk of neonatal death.

The AUC was 0. With this observational study we describe for the first time the early systemic blood variations of two angiogenic factors: PlGF, an agonist of placenta development, and sFlt1, a PlGF antagonist, in newly pregnant oAPS women clinically defined on the basis of previous pregnancy loss and receiving the LMWH-LDA treatment. As a consequence, the categorization of the PlGF:sFlt1 ratio values into quartiles allowed a decrease of risks to be described as values jumped from the lower to the higher quartiles.

Interestingly, a negative predictive value for the risk of PMCs and of severe PMCs were obtained, which may help to rule out the ulterior development of these still abnormally prevalent syndromes in conventionally-treated oAPS women. The range of renal manifestations associated with APS has been broadened. Heparin displaces natural sFlt1 stores from vascular smooth muscle cells and vessel walls in vitro, a phenomenon which is regulated by heparanase.

Furthermore, our findings are consistent with available studies demonstrating a deleterious association between an angiogenic imbalance and pregnancy complications in which a dysfunctional placental organ is thought to play a key pathophysiological role.

The similar risk profiles for preeclampsia, abruptio placenta and fetal growth restriction provide compelling evidence to suggest that these conditions may share common pathophysiological mechanisms. Given this, heparin injections may serve as a truly dynamic sensitization test for assessing active mediators poorly accessible to plasma exploration in usual conditions. Figure 3. Overall, prognostic values were only seen in non-embryonic losses, ie. Isolated recurrent early, embryonic loss defines a subgroup of oAPS patients which differ from other oAPS, with a better overall prognosis.

It has been proposed that patients experiencing recurrent implantation failure possess a selection mechanism that inappropriately rejects good quality embryos, recurrent embryo loss being caused by failure of natural embryo quality control. The strength of this study includes a homogeneous and well characterized group of women receiving a single type of treatment during pregnancy, an accurate phenotyping of the various PMCs, and measurements performed in a single laboratory by personnel blinded to the outcomes.

Limitations include the single-center design, the overall low number of PMCs, the retrospective study of frozen samples, the absence of any control group allowing analysis of the aPlAb-dependence and the LMWH-LDA treatment-dependence of the variations in angiogenic factors.

Confirmation would lead to the non-selection of conventionally-treated patients with an overall good prognosis in the very first trials testing new therapeutic developments. We thank all the study participants, the patients who agreed to join us in this long-term adventure.

We thank the NOHA network of gynecologists, obstetricians and general practitioners who actively contributed to this study. We also thank M.

Tailland, D. Dupaigne, C. Ferrer, S. Ripart, A. Cornille, F. Masia, L. Boileau, F. Grojean, R. Arnaud and A. Sotto for their assistance with patient management. Meyzonnier, N. Best, A. Megzari, R. Jacquet, S. Granier, B. Lafont, C. Masseguin, H. Obert, H.

Blood ; 3 : — Among women with pure obstetric APS, late pregnancy complications are more frequent in cases of prior fetal loss. Late pregnancy complications are more frequent among women treated for pure obstetric APS than among nontreated controls. The incidence of pregnancy outcomes for women with the purely obstetric form of antiphospholipid syndrome APS treated with prophylactic low-molecular-weight heparin LMWH plus low-dose aspirin LDA has not been documented. We observed women without a history of thrombosis who had experienced 3 consecutive spontaneous abortions before the 10th week of gestation or 1 fetal loss at or beyond the 10th week. Among APS women, prior fetal loss was a risk factor for fetal loss, preeclampsia PE , premature birth, and the occurrence of any placenta-mediated complication.

PDF version. ABSTRACT : This retrospective review of hospital records analysed pregnancy outcome with 2 different treatments for women with recurrent miscarriage diagnosed with antiphospholipid syndrome in the index pregnancy. Of 64 women, 29 had received aspirin and 35 aspirin plus heparin. Pregnancy-induced hypertension, prematurity, intrauterine growth restriction and neonatal death were considered as maternal and fetal complications. There were no significant differences in antenatal and maternal complications between the groups. However, there were significant differences in mean anticardiolipin IgG antibody levels.


To learn the principles of management of APS in pregnancy. on two or more occasions at least 12 weeks apart detected according to the guidelines of the.


Read terms. Diagnosis requires that at least one clinical and one laboratory criterion are met. Antiphospholipid antibodies are a diverse group of antibodies with specificity for binding to negatively charged phospholipids on cell surfaces. Despite the prevalence and clinical significance of APS, there is controversy about the indications for and types of antiphospholipid tests that should be performed in order to diagnose the condition.

Antiphospholipid syndrome is associated with various conditions, including arterial and venous thromboses, autoimmune thrombocytopenia, fetal loss, preeclampsia, intrauterine growth restriction, placental insufficiency, and preterm delivery. Diagnosis of antiphospholipid syndrome is based on a combination of clinical history and laboratory testing. Initial diagnosis requires testing for lupus anticoagulant and anticardiolipin antibodies; patients should be diagnosed if lupus anticoagulant is present or if medium to high levels i. Positive test results must be confirmed by a second test after several weeks.

Published studies are primarily clinical and epidemiological research but also basic. CiteScore measures average citations received per document published. Read more. SRJ is a prestige metric based on the idea that not all citations are the same.

Systemic Autoimmune Diseases

Antiphospholipid antibody syndrome commonly called antiphospholipid syndrome or APS is an autoimmune disease present mostly in young women. Those with APS make abnormal proteins called antiphospholipid autoantibodies in the blood. This causes blood to flow improperly and can lead to dangerous clotting in arteries and veins, problems for a developing fetus and pregnancy miscarriage. People with this disorder may otherwise be healthy, or they also may suffer from an underlying disease, most frequently systemic lupus erythematosus commonly called lupus or SLE. APS affects women five times more commonly than men. It is typically diagnosed between the ages of 30 and

Marchetti, M. Cohen, P. Antiphospholipid syndrome APS is an acquired thrombophilia with clinical manifestations associated with the presence of antiphospholipid antibodies aPL in patient plasma. Obstetrical APS is a complex entity that may affect both mother and fetus throughout the entire pregnancy with high morbidity. Clinical complications are as various as recurrent fetal losses, stillbirth, intrauterine growth restriction IUGR , and preeclampsia. Pathogenesis of aPL targets trophoblastic cells directly, mainly via proapoptotic, proinflammatory mechanisms, and uncontrolled immunomodulatory responses. APS pregnancies should be a major field in obstetrical research, and new therapeutics are still in progress.

Hughes Syndrome pp Cite as. Antiphospholipid syndrome APS predominantly affects young women and there has been a growing awareness of this condition amongst obstetricians and gynecologists over the last decade. In this chapter we discuss the association between APS and recurrent pregnancy loss, and present some of the dilemmas in the management of on-going pregnancies in women with APS. Knowledge of the pathogenesis of adverse pregnancy outcome in APS is incomplete and some of the numerous hypotheses and areas of research in this rapidly evolving field are outlined. Unable to display preview. Download preview PDF.

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