RESUMO
OBJECTIVES: Placental abruption (PA) is associated with adverse maternal and neonatal outcomes and has an etiological mechanism that is not yet fully understood. The prediction of PA, which has been the subject of numerous studies, remains a challenge. In particular, there is evidence that PA can be considered a chronic process. So, this study aimed to show inflammatory biomarkers based on complete blood count parameters may be used to predict PA. STUDY DESIGN: A sample of 110 cases (pregnant women with PA) and 110 controls (healthy pregnant women with spontaneous labor) were required the study. The present case-control study included a total of 220 pregnant women. Inflammatory makers were used to evaluate the PA prediction RESULTS: Increases in body mass index, mean corpuscular volume and paletelet lymphocyte ratio are considered protective factors, while increases in neutrophil, the systemic inflammatory response index, neutrophil lymphocyte ratio and the pan-immune inflammation score are considered risk factors. Each 1 unit increase in neutrophil count increases the risk of a PA diagnosis by 1.81 times. CONCLUSION: Recent studies indicate a strong heterogeneity of clinical courses leading to PA in premature and term births. In the present study, our results showed that, inflammation is associated with PA.
Assuntos
Descolamento Prematuro da Placenta , Biomarcadores , Primeiro Trimestre da Gravidez , Humanos , Feminino , Gravidez , Estudos de Casos e Controles , Adulto , Descolamento Prematuro da Placenta/sangue , Descolamento Prematuro da Placenta/diagnóstico , Descolamento Prematuro da Placenta/imunologia , Biomarcadores/sangue , Primeiro Trimestre da Gravidez/sangue , Primeiro Trimestre da Gravidez/imunologia , Inflamação/sangue , Inflamação/diagnóstico , Inflamação/imunologia , Contagem de Células Sanguíneas , Neutrófilos/imunologia , Prognóstico , Valor Preditivo dos Testes , Fatores de Risco , Adulto JovemRESUMO
Placental abruption is the separation of the placenta from the lining of the uterus before childbirth. It is an infrequent perinatal complication with serious after-effects and a marked risk of maternal and fetal mortality. Despite the fact that numerous placental abruption risk factors are known, the pathophysiology of this issue is multifactorial and not entirely clear. The aim of this review was to examine the current state of knowledge concerning the molecular changes on the maternal-fetal interface occurring in placental abruption. Only original research articles describing studies published in English until the 15 March 2021 were considered eligible. Reviews, book chapters, case studies, conference papers and opinions were excluded. The systematic literature search of PubMed/MEDLINE and Scopus databases identified 708 articles, 22 of which were analyzed. The available evidence indicates that the disruption of the immunological processes on the maternal-fetal interface plays a crucial role in the pathophysiology of placental abruption. The features of chronic non-infectious inflammation and augmented immunological cytotoxic response were found to be present in placental abruption samples in the reviewed studies. Various molecules participate in this process, with only a few being examined. More advanced research is needed to fully explain this complicated process.
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Descolamento Prematuro da Placenta/metabolismo , Placenta/metabolismo , Trombina/metabolismo , Descolamento Prematuro da Placenta/imunologia , Feminino , Humanos , GravidezRESUMO
Antiphospholipid syndrome (APS) is associated with a risk of obstetrical complications, affecting both the mother and the fetus. Obstetrical APS is defined by a history of three consecutive spontaneous miscarriages before 10 weeks of gestation (WG), an intra-uterine fetal death after 10 WG, or a premature birth before 34 WG because of severe pre-eclampsia, eclampsia or placental adverse outcomes (intrauterine growth retardation, oligohydramnios). Pregnancy in women with a diagnosis of obstetric APS is at increased risk for placental abruption, HELLP (Hemolysis, Elevated Liver enzymes, Low Platelet count) syndrome and thrombosis that may be part of a catastrophic antiphospholipid syndrome (CAPS). A previous thrombosis and the presence of a lupus anticoagulant are risk factors for pregnancy failure. A multidisciplinary approach, associating the internist, the anesthesiologist and the obstetrician, is recommended for these high-risk pregnancies. Preconception counseling is proposed to identify pregnancy contraindications, and to define and adapt the treatment prior and during the upcoming pregnancy. Heparin and low-dose aspirin are the main treatments. The choice between therapeutic or prophylactic doses of heparin will depend on the patient's medical history. The anticoagulant therapeutic window for delivery should be as narrow as possible and adapted to maternal thrombotic risk. There is a persistent maternal risk in the postpartum period (thrombosis, HELLP syndrome, CAPS) justifying an antithrombotic coverage during this period. We suggest a monthly clinical and biological monitoring which can be more frequent towards the end of pregnancy. The persistence of notches at the Doppler-ultrasound evaluation seems to be the best predictor for a higher risk of placental vascular complications. Treatment optimization and multidisciplinary antenatal care improve the prognosis of pregnancies in women with obstetric APS, leading to a favorable outcome most of the time.
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Síndrome Antifosfolipídica/complicações , Complicações na Gravidez/imunologia , Aborto Espontâneo/imunologia , Descolamento Prematuro da Placenta/imunologia , Anti-Inflamatórios não Esteroides/uso terapêutico , Anticoagulantes/uso terapêutico , Síndrome Antifosfolipídica/diagnóstico , Síndrome Antifosfolipídica/tratamento farmacológico , Quimioterapia Combinada , Eclampsia/imunologia , Feminino , Morte Fetal/imunologia , Retardo do Crescimento Fetal/imunologia , Seguimentos , Síndrome HELLP/imunologia , Heparina/uso terapêutico , Humanos , Oligo-Hidrâmnio/imunologia , Pré-Eclâmpsia/imunologia , Gravidez , Nascimento Prematuro/etiologia , Prognóstico , Medição de Risco , Fatores de Risco , Resultado do TratamentoRESUMO
INTRODUCTION: Placental abruption is a serious condition that increases perinatal morbidity and mortality. Clinical prevention and treatment options are limited, especially in human preterm deliveries. Knowledge of the mechanisms that keep the placenta in place during pregnancy is critical for developing strategies for the prevention of abruption. Failure of physiological transformation of spiral arteries has been described as a major contributing factor of the placental abruption development. Baboons (Papio spp.) share striking similarities with humans in regard to placental structure, utero-placental blood flow, and fetal development; however, the mode of trophoblast invasion is shallow in baboons. This fact prompted the hypothesis that the incidence of placental abruption will be increased in baboons compared to humans. MATERIAL AND METHODS: Baboon placentas were collected between 2002 and 2008. Two independent veterinary pathologists evaluated the slides. A certified physician pathologist performed additional histology. RESULTS: Placental abruption was diagnosed in 22 baboons among 2423 live births during the study period (0.9% prevalence). The most common clinical presentations were fetal demise and vaginal bleeding. The most common pathological findings were intraplacental hemorrhages with or without hematoma formation (86.4%). Other findings consisted of neutrophil infiltration (50%), decidual necrosis (22.7%), decidual vascular congestion and inflammation, villous congestion and retroplacental hemorrhage/hematoma (each 18.2%). These pathologic findings were the same for term and preterm deliveries. CONCLUSION: This is the first systematic study of placental abruption in non-human primates, analyzing a large colony of baboons. Despite differences in trophoblast invasion, the clinical features observed in placental abruption affecting baboons resembled those reported in humans. The cluster of placental pathological findings in baboons also agreed with clinical reports, but the prevalence of these findings differed between baboons and humans. We discuss a mechanism of anti-abruption forces that offset shallow trophoblast invasion observed in baboons.
Assuntos
Descolamento Prematuro da Placenta/patologia , Descolamento Prematuro da Placenta/fisiopatologia , Modelos Animais de Doenças , Doenças dos Macacos/patologia , Doenças dos Macacos/fisiopatologia , Papio , Descolamento Prematuro da Placenta/epidemiologia , Descolamento Prematuro da Placenta/imunologia , Animais , Animais de Laboratório , Feminino , Morte Fetal/etiologia , Hematoma/etiologia , Hemorragia/etiologia , Doenças dos Macacos/epidemiologia , Doenças dos Macacos/imunologia , Infiltração de Neutrófilos , Placenta/irrigação sanguínea , Placenta/imunologia , Placenta/patologia , Placentação , Gravidez , Prevalência , Fatores de Risco , Texas , Hemorragia Uterina/etiologiaRESUMO
PROBLEM: Women with antiphospholipid antibodies (aPL) such as lupus anticoagulant, anticardiolipin antibodies, and anti-ß(2) glycoprotein-1 antibodies are at high risk of late pregnancy complications, such as severe pre-eclampsia, placental insufficiency, and fetal loss. It has been observed that aPL consists of a heterogeneous group of antibodies targeting several phospholipid-binding plasma proteins, including also anti-prothrombin (anti-PT), anti-protein S (anti-PS), and anti-protein C (anti-PC) antibodies. Their potential role in late pregnancy complications is not known. The aim of this work was to investigate the association between those autoantibodies and histories for adverse pregnancy outcome. METHOD OF STUDY: Anti-PT, anti-PS, and anti-PC antibodies were evaluated in 163 patients with previous severe pre-eclampsia, fetal death, and/or placental abruption and in as many women with previous uneventful pregnancies, negative for aPL. RESULTS: The prevalence of anti-PT antibodies was higher in cases than in controls (OR, 95% CI: 10.92, 4.52-26.38). The highest prevalence was observed in subjects with fetal death. CONCLUSION: Anti-PT antibodies appear to be associated with adverse pregnancy outcome, irrespectively of aPL.
Assuntos
Descolamento Prematuro da Placenta/etiologia , Anticorpos Antifosfolipídeos/sangue , Morte Fetal/etiologia , Pré-Eclâmpsia/imunologia , Protrombina/imunologia , Descolamento Prematuro da Placenta/imunologia , Adulto , Autoanticorpos/sangue , Feminino , Morte Fetal/imunologia , Humanos , Gravidez , Complicações Cardiovasculares na Gravidez/etiologia , Complicações Cardiovasculares na Gravidez/imunologia , Resultado da Gravidez , Proteína C/imunologia , Proteína S/imunologiaRESUMO
OBJECTIVE: To estimate the relationship between thyroid antibodies and placental abruption. METHODS: This cohort study assesses thyroperoxidase and thyroglobulin antibodies in relation to placental abruption among 10,062 women with singleton viable pregnancies (from the First and Second Trimester Risk of Aneuploidy [FaSTER] trial). A thyroperoxidase antibody cutoff of 50 international units/mL is used for comparison with published data from another cohort. RESULTS: Women with elevated thyroperoxidase antibody levels in the first and second trimesters have a higher rate of placental abruption than antibody-negative women. This relationship is less strong in the first trimester (1.51% compared with 0.83%; odds ratio [OR], 1.83; 95% confidence interval [CI], 0.99-3.37) than in the second trimester (1.78% compared with 0.82%; OR, 2.20; 95% CI, 1.21-3.99). A similar, but weaker, relationship is present for thyroglobulin antibodies. Sixty-four of 782 thyroperoxidase antibody-positive pregnancies without abruption become negative by the second trimester; one pregnancy with abruption becomes antibody-positive. Odds ratios for pregnancies with both thyroperoxidase and thyroglobulin antibody elevations are also higher (first trimester: OR, 2.10; 95% CI, 0.91-4.86; second trimester: OR, 2.73; 95% CI, 1.17-6.33). CONCLUSION: The present data confirm an association between thyroid antibody elevations and placental abruption described in a recent report. These findings, however, do not provide support for recommending routine testing for thyroid antibodies during pregnancy. LEVEL OF EVIDENCE: II.
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Descolamento Prematuro da Placenta/imunologia , Iodeto Peroxidase/imunologia , Tireoglobulina/imunologia , Adulto , Estudos de Coortes , Feminino , Humanos , Gravidez , Segundo Trimestre da Gravidez , Adulto JovemRESUMO
This study was undertaken to determine the presence of thyroid autoantibodies and associated pregnancy complications from 49 pregnant women with thyroid disease. There were 31 (63%) women with Graves' disease (GD) and 18 (37%) with primary hypothyroidism (PHT). A total of 26 (53.1%) women, 19 (61%) with GD and seven (39%) with PHT, had positive antibodies. Six had thyroid peroxidase antibodies (TPO), one with thyroglobulin antibody (TG) and eight had TSH receptor antibodies (TR). Two had a mixture of antibodies involving TG/TPO (one GD vs one PHT), four with TG/TPO/TR (all had GD) and five with TPO/TR (four with GD vs one with PHT). There were associations in women with positive thyroid antibodies and pre-eclampsia (15.4%), abruptio placenta (4%), caesarean deliveries (31%), postpartum thyroiditis (19.2%) and abnormal neonatal thyroid function (15.4%). Women with positive thyroid antibodies in pregnancy need close care during and after pregnancy, as they can develop complications affecting both mother and fetus.
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Autoanticorpos/sangue , Hipertireoidismo/imunologia , Hipotireoidismo/imunologia , Imunoglobulinas Estimuladoras da Glândula Tireoide/sangue , Complicações na Gravidez/imunologia , Descolamento Prematuro da Placenta/epidemiologia , Descolamento Prematuro da Placenta/imunologia , Adulto , Cesárea/estatística & dados numéricos , Feminino , Humanos , Hipertireoidismo/epidemiologia , Hipotireoidismo/epidemiologia , Iodeto Peroxidase/imunologia , Pré-Eclâmpsia/epidemiologia , Pré-Eclâmpsia/imunologia , Gravidez , Complicações na Gravidez/epidemiologia , Receptores da Tireotropina/imunologia , Estudos Soroepidemiológicos , Tireoglobulina/imunologia , Tireoidite/epidemiologia , Tireoidite/imunologia , Adulto JovemRESUMO
OBJECTIVE: To estimate the prevalence of antithyroid peroxidase antibodies in the general obstetric population and to compare pregnancy outcomes in women who are antithyroid peroxidase-antibody positive with those who are antithyroid peroxidase-antibody negative. METHODS: Between November 2000 and April 2003, all women who presented for prenatal care underwent thyroid screening. Serum samples from women without clinical hypothyroidism who had been screened in the first 20 weeks of gestation and delivered a singleton newborn weighing 500 g or more were analyzed for concentrations of antithyroid peroxidase antibodies. Serum thyroid peroxidase antibody levels were determined using a chemiluminescent immunoassay. Pregnancy outcomes in women with positive antithyroid peroxidase antibodies (more than 50 international units/mL) were compared with those with negative levels. RESULTS: Serum samples from 17,298 women were tested. Of these, 1,012 (6%) women were identified with positive antithyroid peroxidase antibodies. Women who were antithyroid peroxidase-antibody positive were older, heavier, and more often parous than women with negative antithyroid peroxidase antibodies. Rate of placental abruption was threefold higher in women with antithyroid peroxidase antibodies (1.0% compared with 0.3%, odds ratio 3.4, 95% confidence interval 1.7-6.7) after adjustment for differences in maternal demographics. Seven of the 10 abruptions associated with antithyroid peroxidase antibody occurred in women with normal thyroid-stimulating hormone and free thyroxine levels. CONCLUSION: Antithyroid peroxidase antibodies are present in 6% of the general obstetric population and are associated with a threefold increase in the rate of placental abruption. However, this increase in placental abruption does not currently warrant routine antithyroid antibody screening during pregnancy. LEVEL OF EVIDENCE: II.
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Descolamento Prematuro da Placenta/imunologia , Autoanticorpos/imunologia , Iodeto Peroxidase/imunologia , Adulto , Feminino , Humanos , Gravidez , Resultado da Gravidez , Adulto JovemRESUMO
Women pregnant with a male fetus often generate cellular and humoral immune responses against male-specific minor histocompatibility (HY) antigens-however, the importance of these responses for pregnancy outcome is unclear. Epidemiologic studies have shown that the birth of a boy compared with a girl prior to a series of miscarriages significantly reduces the chance of a subsequent live birth and pregnancies with boys have an increased risk of placental abruption. This paper aims to review the current knowledge about the impact of anti-HY immunity on pregnancy outcome in terms of miscarriage and placental abruption. Our knowledge primarily comes from studies of the impact on pregnancy outcome of HLA class II alleles known to restrict CD4 T cell mediated anti-HY responses among 358 secondary recurrent miscarriage (SRM) patients and 203 of their children born prior to the miscarriages and investigation of these HLA alleles in 8 patients with recurrent severe placental abruptions. The chance of a subsequent live birth in SRM patients with firstborn boys compared to firstborn girls was significantly lower in women with HY-restricting HLA class II alleles [OR: 0.17 (0.1-0.4), p=0.0001]. Most patients with recurrent placental abruptions had firstborn boys and significantly more of these patients carried HLA haplotypes with HY-restricting class II alleles compared with controls (p=0.009). These findings are strongly indicative of aberrant maternal immune reactions against fetal HY antigens playing a role in recurrent miscarriage and placental abruption. We propose pathogenetic pathways for these conditions that in our view best explain the findings.
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Aborto Habitual/imunologia , Antígeno H-Y/imunologia , Isoanticorpos/imunologia , Gravidez/imunologia , Aborto Habitual/genética , Descolamento Prematuro da Placenta/genética , Descolamento Prematuro da Placenta/imunologia , Feminino , Antígenos de Histocompatibilidade Classe II/genética , Antígenos de Histocompatibilidade Classe II/imunologia , Humanos , Masculino , Resultado da Gravidez/genéticaRESUMO
BACKGROUND: A clinical subtype of purely obstetrical antiphospholipid antibody (aPL-Ab) syndrome (APS) requires three or more unexplained consecutive embryonic losses before the 10th week of gestation associated with persistently positive lupus anticoagulant (LAC), and/or anticardiolipin IgG or IgM, and/or anti-beta2-glycoprotein I (abeta2GpI) IgG or IgM. Although this diagnostic classification of APS appeared to be the most sensitive, the APS-associated serological criteria are still debated. PATIENTS/METHODS: We prospectively observed the second pregnancy of 284 women with a previous embryonic loss, both with and without aPL-Ab. RESULTS: aPL-Ab-positive women were more prone to pregnancy loss, embryonic loss, pre-eclampsia, placental abruption and intrauterine fetal growth restriction. Type IIa aPL-Ab positivity (LAC present alone) was associated with the highest risk of recurrent embryonic loss and intrauterine growth restriction. Type I aPL-Ab positivity (combinations of aPL-Ab type positivity) was associated with the strongest risks of late complications, pre-eclampsia and placental abruption. Finally, abeta2GpI-M positivities were not clinically relevant in these women. CONCLUSION: Patients with a first unexplained pregnancy loss before the 10th week of gestation who are also positive for aPL-Abs have a higher risk of various complications in their second pregnancy. In this study, measurement of abeta2GpI-M had a questionable prognostic value.
Assuntos
Aborto Espontâneo/imunologia , Anticorpos Antifosfolipídeos/sangue , Síndrome Antifosfolipídica/imunologia , Complicações na Gravidez/imunologia , Descolamento Prematuro da Placenta/imunologia , Adulto , Anticorpos Anticardiolipina/sangue , Síndrome Antifosfolipídica/complicações , Estudos de Casos e Controles , Distribuição de Qui-Quadrado , Perda do Embrião/imunologia , Feminino , Retardo do Crescimento Fetal/imunologia , Idade Gestacional , Humanos , Modelos Logísticos , Inibidor de Coagulação do Lúpus/sangue , Razão de Chances , Pré-Eclâmpsia/imunologia , Gravidez , Estudos Prospectivos , Medição de Risco , Fatores de Risco , Adulto Jovem , beta 2-Glicoproteína I/imunologiaRESUMO
PROBLEM: The coexistence of immune and decidual cells is related to the development of a resistance to immune-mediated apoptosis in both ectopic and eutopic decidua. This unique feature of endometrial cells seems to be linked with the expression of metallothionein (MT), an inhibitor of apoptosis. METHOD OF STUDY: The MT immunoreactivity level was assessed in 82 eutopic (CC) and ectopic (cesarean scar deciduosis - CSD) decidual tissue samples obtained from patients during cesarean sections at term and from patients on whom cesarean sections were performed on account of placental abruption (PA). RESULT: Statistically, significantly higher levels of MT immunoreactivity were found in eutopic and ectopic decidua sampled during cesarean sections performed on patients with advanced labor when compared to the levels found in tissues sampled during cesarean sections on patients without labor. No differences were observed in the MT immunoreactivity levels in decidual tissue samples derived from patients who had undergone cesarean sections on account of PA with respect to the progression of labor at the time of the surgical procedure. Statistically, the decidual MT immunoreactivity levels were significantly higher in the PA than the CC subgroups and in the PA than the CSD subgroups correlating with the stage of labor. CONCLUSION: MT in decidual cells seems to be responsible for the proper coexistence between decidual cells and activated immune cells that infiltrate both eutopic and ectopic decidua during cesarean section and PA.
Assuntos
Descolamento Prematuro da Placenta/metabolismo , Decídua/imunologia , Endométrio/metabolismo , Trabalho de Parto , Metalotioneína/metabolismo , Placenta/metabolismo , Descolamento Prematuro da Placenta/imunologia , Adulto , Cesárea , Decídua/citologia , Decídua/metabolismo , Endométrio/imunologia , Feminino , Humanos , Trabalho de Parto/imunologia , Metalotioneína/imunologia , Placenta/imunologia , GravidezRESUMO
OBJECTIVE: The objective of the study was to determine whether placental abruption is associated with an increased incidence of histologic chorioamnionitis among singleton gestations and whether this association is dependent on its severity. STUDY DESIGN: Data were derived from the New Jersey-Placental Abruption Study, an ongoing, multicenter, case-control study conducted in New Jersey since August 2002. Subjects were women with a clinical diagnosis of abruption, and controls were matched to cases based on parity and maternal race/ethnicity. Two perinatal pathologists, blinded to the case-control status, performed all histologic examination based on standardized protocol. The association between chorioamnionitis and abruption was quantified based on odds ratio (OR) with 95% confidence interval (CI), after adjustment for potential confounders, and all analyses were stratified based on preterm birth (less than 37 weeks) status. RESULTS: At preterm gestations (n = 141), chorioamnionitis was present in 30.8% and 12.5% of abruption cases and controls, respectively (OR 3.6, 95% CI 1.7 to 10.5). At term gestations (n = 205), the corresponding rates were 34.6% and 20.4%, respectively (OR 2.8, 95% CI 1.3 to 6.1). Severe chorioamnionitis was 7.2 (95% CI 1.6 to 20.1) and 18.3 (95% CI 2.2 to 150.4) times more common in abruption patients at preterm and term gestations, respectively. CONCLUSION: Histologic chorioamnionitis is associated with placental abruption. The association was strongest in the presence of severe chorioamnionitis at term and, to a lesser extent, at preterm gestations. These observations suggest that the histologic findings in abruption are accompanied by severe inflammation, in both preterm and term gestations.
Assuntos
Descolamento Prematuro da Placenta/imunologia , Corioamnionite/patologia , Ruptura Prematura de Membranas Fetais/imunologia , Infiltração de Neutrófilos , Descolamento Prematuro da Placenta/etiologia , Adulto , Estudos de Casos e Controles , Corioamnionite/imunologia , Feminino , Humanos , Placenta/patologia , Doenças Placentárias/imunologia , Gravidez , Nascimento Prematuro/imunologia , Estudos Prospectivos , Fatores de RiscoRESUMO
PROBLEM: RCAS1 is a protein responsible for the suppression of cytotoxic immune response during gestation. The present study evaluates the immunoreactivity level of RCAS1 with respect to immune cell status during placental abruption (PA) and retained placental tissue (RPT). METHOD OF STUDY: RCAS1, CD3, CD56, CD69 and CD25 immunoreactivity was assessed by immunohistochemistry in 66 decidual samples derived from PA and from RPT. RESULTS: RCAS1 immunoreactivity was statistically significantly higher in decidual tissue samples derived from patients with RPT than in those derived from patients with PA. A statistically significantly lower number of CD56(+) and CD3(+) cells and immunoreactivity level of CD69 were found in patients with RPT, compared to those with PA. CONCLUSION: Placental abruption seems to be associated with excessive accumulation and activity of CD3(+) and CD56(+) cells in decidua, which processes might, in turn, result from an insufficient RCAS1 decidual level.
Assuntos
Descolamento Prematuro da Placenta/metabolismo , Antígenos de Neoplasias/metabolismo , Decídua/imunologia , Sistema Imunitário/metabolismo , Descolamento Prematuro da Placenta/imunologia , Feminino , Humanos , Sistema Imunitário/citologia , Placenta Retida/imunologia , Placenta Retida/metabolismo , GravidezRESUMO
PROBLEM: Placental abruption is a potential life-threatening condition for both the fetus and the mother, being significantly more common in pregnancies with male fetuses. The pathogenesis of placental abruption remains unknown. However, some recent reports point toward a maternal immune response against the fetus as a possible mechanism. No data exist concerning special characteristics of patients suffering recurrent placental abruptions. METHOD OF STUDY: Identification of all patients with recurrent placental abruption in a retrospective review of 881 consecutive Caucasian women seen in our tertiary centre for recurrent pregnancy losses between 1986 and 2005. The HLA, DRB1, DRB3, 4, 5 and DQB1 genotypes of patients were compared with relevant controls. RESULTS: Eight patients were identified with recurrent placental abruption. The patients had a total of 22 abruptions; 18 (82%) in which the fetus died. Seven patients (88%) had first-born boys, and 15 abruptions (68%) involved male fetuses. All patients with a first-born boy, except one, had HLA-class II alleles known to restrict CD4+ T-cell responses against male-specific minor histocompatibility (HY)-antigens (HLA-DRB1*15, HLA-DRB3*0301 and HLA-DQB1*05). Haplotypes with these HLA-alleles constituted 64% of the patients' haplotypes compared to 28% of those of the controls (p=0.009). Furthermore, 43% of the patients were homozygous for these haplotypes compared to 5% of controls (p=0.023). CONCLUSION: We have found that recurrent placental abruption is exclusively almost preceded by the birth of a boy and the majority of patients have HLA-class II known to restrict CD4 T-cell reactions against HY-antigens. This indicates that maternal immunological responses against HY-antigens play a role in recurrent placental abruption.
Assuntos
Descolamento Prematuro da Placenta/imunologia , Antígeno H-Y/imunologia , Antígenos HLA-DQ/imunologia , Antígenos HLA-DR/imunologia , Adulto , Linfócitos T CD4-Positivos/imunologia , Feminino , Antígenos HLA-DQ/genética , Cadeias beta de HLA-DQ , Antígenos HLA-DR/genética , Haplótipos , Humanos , Gravidez , Recidiva , Estudos RetrospectivosRESUMO
BACKGROUND: Clinicians widely regard placental abruption as an acute event, though accumulating data point towards abruption being the end-result of chronic processes early in pregnancy, and perhaps even extending to conception. The Collaborative Perinatal Project was a prospective cohort study performed from 1959 to 1966 in the United States. Since enrolled pregnancies were managed without the biases created by modern perinatal surveillance and interventions, the natural history of disease in these data is ideal to study obstetrical complications such as placental abruption. OBJECTIVE: We assessed the associations versus contributions of the clinical feature of early gestational vaginal bleeding and histologic lesions (chronic and acute) with placental abruption. STUDY DESIGN: Women enrolled in the Collaborative Perinatal Project (1959-1966) were used, restricting the analysis to those that delivered singleton births (n=46,364). Risks of placental abruption were compared between women with and without vaginal bleeding at <20 weeks gestation. We also examined the relationships between placental abruption and chronic and acute histologic lesions, including infarcts, decidual necrosis, presence of macrophages in the decidua, amnion or chorion, and neutrophil infiltration in the amnion, chorion, placental surface, and umbilical vein. RESULTS: Any episode of vaginal bleeding at <20 weeks in pregnancy conferred an increased risk of placental abruption (adjusted relative risk (RR) 1.6, 95% confidence interval (CI) 1.3, 1.8). The greatest risk occurred with bleeding in both the first two trimesters (RR 3.1, 95% CI 2.3, 4.1). The presence of histologic lesions in the placenta, cord and membranes similarly carried an increased risk of placental abruption, even in the absence of vaginal bleeding. The risk of abruption was, however, highest in the presence of both histologic lesions and vaginal bleeding early in pregnancy. CONCLUSION: Vaginal bleeding early in pregnancy and histologic lesions of the placenta, umbilical cord, and membranes are associated with increased risk of placental abruption in later pregnancy. However, the increased risk associated with placental lesions, especially chronic inflammatory lesions, even in the absence of early vaginal bleeding, suggests that prolonged inflammation may be implicated in placental abruption.
Assuntos
Descolamento Prematuro da Placenta/etiologia , Placenta/patologia , Hemorragia Uterina/complicações , Descolamento Prematuro da Placenta/imunologia , Adolescente , Adulto , Doença Crônica , Estudos de Coortes , Decídua/patologia , Feminino , Humanos , Inflamação , Gravidez , Estudos Retrospectivos , Fatores de Risco , Cordão Umbilical/patologia , Estados UnidosRESUMO
OBJECTIVES: RCAS1 is a membrane protein that plays a role in the maintenance of maternal immune tolerance during pregnancy. The work presented here demonstrates the results of RCAS1 expression in placenta in cases of placental abruption and patients with retained placental tissue during the third stage of labor. STUDY DESIGN: The placenta tissue samples were obtained during vaginal and cesarean delivery (derived from 117 pregnancies). Pregnant women were divided into four groups according to the onset of labor and the time of placental detachment in term labors. The samples were analyzed by the Western blot method. Statistical analysis was performed using the Shapiro-Wilk procedure. The Mann-Whitney test and Student's t-test were applied to compare the differences between parametric data. RESULTS: The average relative amount of RCAS1 observed in those patients with retained placental tissue was statistically significantly higher than in the patients with placental abruption. CONCLUSION: The differences observed in placental RCAS1 levels confirm the participation of this protein in the inhibition of maternal immune response during gestation. The present results also indicate that RCAS1 participates in the changes in the maternal immune system that take place during parturition and reinforce its potential involvement in the mechanism of placental abruption.
Assuntos
Descolamento Prematuro da Placenta/metabolismo , Antígenos de Neoplasias/metabolismo , Terceira Fase do Trabalho de Parto/metabolismo , Placenta Retida/metabolismo , Placenta/metabolismo , Descolamento Prematuro da Placenta/imunologia , Actinas/metabolismo , Adulto , Feminino , Humanos , Terceira Fase do Trabalho de Parto/imunologia , Placenta/imunologia , Placenta Retida/imunologia , Gravidez , Distribuições Estatísticas , Estatísticas não ParamétricasAssuntos
Descolamento Prematuro da Placenta/etiologia , Anticorpos Anticardiolipina , Síndrome Antifosfolipídica/complicações , Descolamento Prematuro da Placenta/imunologia , Descolamento Prematuro da Placenta/patologia , Adulto , Anticorpos Anticardiolipina/sangue , Síndrome Antifosfolipídica/imunologia , Síndrome Antifosfolipídica/patologia , Feminino , Humanos , Idade Materna , Gravidez , Gravidez de Alto RiscoRESUMO
Placental abruption is an unpredictable severe complication in pregnancy. In order to investigate the possibility that the activation of the fetal nonadaptive immune system may be involved in the pathogenesis of this disease, IL-6 release from cord blood monocytes was examined by intracellular cytokine staining and flow cytometric analysis. Our results demonstrate that preterm placental abruption (n = 15) in contrast to uncontrollable preterm labor (n = 33) is associated with significantly (P < 0.001) increased release of IL-6 from the fetal monocytes. The same holds true for rhesus disease (n = 9, P < 0.001) that is characterized by a maternal production of antibodies against the rhesus-D antigen expressed by the fetal erythrocytes. This suggests that during rhesus disease, IL-6 release of monocytes is induced by antibody-mediated cross-linking of these cells to the erythrocytes in the fetal circulation. Hence, this assumption favors the idea that also in case of placental abruption, an increased maternal antibody production against paternal antigens leads to an elevated IL-6 release by the fetal monocytes. To elucidate this potential mechanism, the presence of anti-HLA-antibodies was assessed in the maternal circulation of patients with placental abruption (n = 17) and patients with uncontrollable preterm labor (n = 29). The percentage of women producing anti-paternal HLA-antibodies was significantly (P < 0.01) increased in the group of women with preterm placental abruption (47%) in comparison to women with uncontrollable preterm labor (14%). Therefore, our results suggest that an increased humoral immune response of the mother against the fetus may be decisively involved in the pathogenesis of placental abruption.
Assuntos
Descolamento Prematuro da Placenta/etiologia , Feto/imunologia , Antígenos HLA/imunologia , Descolamento Prematuro da Placenta/imunologia , Descolamento Prematuro da Placenta/fisiopatologia , Anticorpos/sangue , Feminino , Sangue Fetal/citologia , Sangue Fetal/imunologia , Humanos , Imunidade , Monócitos/imunologia , Trabalho de Parto Prematuro/etiologia , Trabalho de Parto Prematuro/imunologia , Trabalho de Parto Prematuro/fisiopatologia , Gravidez , Fatores de TempoRESUMO
During pregnancy the fetus represents a semi-allograft. Both membrane-bound and soluble forms of the nonclassic human leukocyte antigen (HLA)-G protect the fetus from maternal immune attack. To assess the relevance of soluble HLA-G (sHLA-G) levels in the maternal circulation for the occurrence of characteristic pregnancy disorders, we analyzed sHLA-G plasma levels of women with normal and pathological pregnancies. Compared to normal pregnancy, significantly increased sHLA-G levels were detected in women delivered preterm because of intrauterine activation (uncontrollable labor, rupture of fetal membranes, cervical insufficiency) and women with Hemolysis, Elevated Liver enzymes, Low Platelet count (HELLP) syndrome. Contrary to these disorders, the sHLA-G levels in women with placental abruption were more than three times lower than in normal pregnancy (p < .0001). Nonparametric discriminant analysis showed that women with sHLA-G levels below 9.95 ng/mL had a relative risk of 7.12 for the development of placental abruption during further course of pregnancy. These results suggest that the occurrence of pregnancy-associated diseases is strongly influenced by maternal sHLA-G plasma levels.