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Antiphospholipid syndrome significantly increases the risk of thrombotic events.

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Multiple peer-reviewed studies and systematic reviews establish that antiphospholipid syndrome is an autoimmune, hypercoagulable condition strongly linked to an increased risk of thrombotic events in both arteries and veins.

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Efficacy of aspirin for the primary prevention of thrombosis in patients with antiphospholipid antibodies: an international and collaborative meta-analysis.. 2014. https://doi.org/10.1016/j.autrev.2013.10.014

We performed a meta-analysis to determine whether aspirin has a significant protective effect on risk of first thrombosis among patients with antiphospholipid antibodies (aPL+). Observational and interventional studies identified from the Medline, Embase and Cochrane databases were selected if they assessed the incidence of first thrombosis in aPL+ patients treated with aspirin versus those without. Pooled effect estimates were obtained using a random-effects model. Of 1211 citation retrieved, 11 primary studies (10 observational and 1 interventional) met inclusion criteria, including a total of 1208 patients and 139 thrombotic events. The pooled odds ratio (OR) for the risk of first thrombosis in patients treated with aspirin (n=601) was 0.50 (95%CI: 0.27 to 0.93) compared to those without aspirin (n=607), with significant heterogeneity across studies (I(2)=46%, p=0.05). Subgroup analysis showed a protective effect of aspirin against arterial (OR: 0.48 [95%CI: 0.28-0.82]) but not venous (OR: 0.58 [95% CI: 0.32-1.06]) thrombosis, as well as in retrospective (OR: 0.23 [0.13-0.42]) but not prospective studies (OR: 0.91 [0.52-1.59]). Subgroup analysis according to underlying disease revealed a significant protective effect of aspirin for asymptomatic aPL+ individuals (OR: 0.50 [0.25-0.99]), for systemic lupus erythematosus (SLE) (OR: 0.55 [0.31-0.98]) and obstetrical antiphospholipid syndrome (APS) (OR: 0.25 [0.10-0.62]). This meta-analysis shows that the risk of first thrombotic event is significantly decreased by low dose aspirin among asymptomatic aPL individuals, patients with SLE or obstetrical APS. Importantly, no significant risk reduction was observed when considering only prospective studies or those with the best methodological quality.

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Genetic determinants of arterial thrombosis in primary antiphospholipid syndrome: a systematic review.. 2026. https://doi.org/10.3389/fimmu.2026.1761613

<h4>Background</h4>Primary Antiphospholipid Syndrome (PAPS) is a systemic autoimmune disorder characterized by arterial and/or venous thrombosis and obstetric morbidity. Arterial thrombosis, although less frequent than venous events, is associated with substantial morbidity and mortality. Alongside environmental and acquired factors, several genetic polymorphisms affecting coagulation, endothelial function, fibrinolysis, and platelet activation have been investigated in relation to thrombotic risk. Clarifying their contribution may help refine hypotheses for risk stratification.<h4>Objectives</h4>To systematically review the available evidence on genetic polymorphisms associated with arterial thrombosis in PAPS and to evaluate their reported associations with arterial thrombotic manifestations.<h4>Search methods</h4>Electronic searches were conducted in MEDLINE, the Cochrane Library, ClinicalTrials.gov, the GWAS Catalog, the Genetic Association Database, and Google Scholar for studies published up to November 2024.<h4>Selection criteria</h4>Case-control, cohort, and genome-wide association studies were included if they assessed genetic variants in confirmed PAPS with arterial thrombosis. Comparators included healthy controls, patients with other autoimmune diseases, or APS without arterial events.<h4>Data collection and analysis</h4>Two reviewers independently screened studies, extracted data, and assessed risk of bias using the Cochrane and ROBINS-I tools. Due to substantial heterogeneity in study design, populations, and outcome definitions, meta-analysis was not feasible, and results were summarized narratively.<h4>Main results</h4>Eighteen studies published between 1994 and 2023 were identified, of which seventeen contributed to the genetic association synthesis. Variants in platelet membrane glycoproteins (GPIa 807T, GPIbα Kozak TC, and combined GPIa 807T plus GPIIb/IIIa PlA2) were the most frequently reported positive associations with arterial thrombosis. PAI-1 (4G) and MTHFR (C677T) showed inconsistent and weak associations, while the EPCR (PROCR) H1 haplotype was negatively associated with arterial thrombosis in isolated analyses. Classical thrombophilic mutations, including Factor V Leiden and Prothrombin G20210A, did not show consistent associations with arterial events. Overall certainty of evidence was low to very low.<h4>Conclusions</h4>The currently reviewed evidence indicates that inherited susceptibility to arterial thrombosis in PAPS is more frequently linked to platelet-related, endothelial, and fibrinolytic pathways than to classical coagulation gene mutations. These associations are based on small, heterogeneous, and largely non-replicated studies and should be considered hypothesis-generating.<h4>Systematic review registration</h4>https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42024603974, identifier CRD42024603974.

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Management of thrombotic and obstetric antiphospholipid syndrome: a systematic literature review informing the EULAR recommendations for the management of antiphospholipid syndrome in adults. 2019. https://doi.org/10.1136/rmdopen-2019-000924

Objective To perform a systematic literature review (SLR) informing the European Lmmendations for the management of antiphospholipid syndrome (APS) in adults. Methods A SLR through January 2018 was performed. Research questions were constructed using the Patient, Intervention, Comparator, Outcome (PICO) format. We included data from articles that reported on each relevant intervention. Summary effect estimates were calculated for direct comparison studies that matched the PICO question exactly, and for studies with the relevant intervention and comparator. When meta-analyses were available, we used these estimates. Results From 7534 retrieved articles (+15 from hand searches), 188 articles were included in the review. In individuals with high-risk antiphospholipid antibody (aPL) profile without prior thrombotic or obstetric APS, two meta-analyses showed a protective effect of low-dose aspirin (LDA) against thrombosis. Two randomised controlled trials (RCTs) and three cohort studies showed no additional benefit of treatment with vitamin K antagonists at target international normalised ratio (INR) 3–4 versus INR 2–3 in patients with venous thrombosis. In patients with arterial thrombosis, two RCTs and two cohort studies showed no difference in risk of recurrent thrombosis between the two target INR groups. One open-label trial showed higher rates of thrombosis recurrences in triple aPL-positive patients treated with rivaroxaban than those treated with warfarin. RCTs and cohort studies showed that combination treatment with LDA and heparin was more effective than LDA alone in several types of obstetric APS. SLR results were limited by the indirect evidence and the heterogeneity of patient groups for some treatments, and only a few high-quality RCTs. Conclusion Well-designed studies of homogeneous APS patient populations are needed.

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Remnant cholesterol predicts risk of recurrent thrombosis beyond LDL-cholesterol in patients with antiphospholipid syndrome. 2025. https://doi.org/10.1186/s12916-025-04063-5

Antiphospholipid syndrome (APS) is notably linked to thrombotic events, particularly cardiovascular disease (CVD). The role of remnant cholesterol (RC) in predicting CVD risk is established, yet its relationship with thrombotic risk in APS patients remains to be elucidated. This study aims to assess the association between RC and recurrent thrombotic risk in patients with APS. A prospective analysis was conducted based on a cohort of APS patients who met the 2006 Sydney revised classification criteria. Thrombotic risks associated with varying levels of RC were evaluated using Kaplan–Meier survival analysis and Cox proportional hazards regression models. Mendelian randomization (MR) was applied to examine the causal link between RC and different types of thrombotic events. A total of 325 patients with APS were enrolled in this study. Over a median follow-up of 35 months, 51 patients experienced thrombotic events, including 24 venous, 19 arterial, and 16 microvascular incidents. Patients with RC levels above 0.60 mmol/L exhibited significantly higher risks, with multivariable-adjusted hazard ratio (and 95% confidence interval) for all-cause, venous, arterial thrombosis, and microvascular disease being 5.05 (2.23–11.41), 6.34 (1.71–23.54), 3.79 (1.00–14.32), and 4.36 (1.08–17.58), respectively. Notably, elevated RC remained a significant thrombotic risk factor even in patients with normal conventional lipid profiles. MR analysis revealed a significant causal association between RC and arterial thrombosis, but not venous thrombosis. Elevated RC is linked to a substantial increase in the risk of thrombotic events in APS patients. These findings suggest that RC could be a valuable marker for thrombotic risk in this population and a potential target for therapeutic intervention. A more than 5-fold increase in thrombotic risk, including arterial, venous, and microvascular events, is linked to individuals with RC levels >0.60 mmol/L in APS. Elevated RC remains a significant risk factor even in patients with normal conventional lipid indices (LDL-C, TC, TG, and non-HDL-C). Through MR analysis, there was a significant causal relationship between RC and AT in the general population, but not with VT, suggesting the complexity of the pathogenesis of VT in patients with APS. Patients with APS treated with hydroxychloroquine have lower RC levels, and hydroxychloroquine may have the potential to reduce RC. A more than 5-fold increase in thrombotic risk, including arterial, venous, and microvascular events, is linked to individuals with RC levels >0.60 mmol/L in APS. Elevated RC remains a significant risk factor even in patients with normal conventional lipid indices (LDL-C, TC, TG, and non-HDL-C). Through MR analysis, there was a significant causal relationship between RC and AT in the general population, but not with VT, suggesting the complexity of the pathogenesis of VT in patients with APS. Patients with APS treated with hydroxychloroquine have lower RC levels, and hydroxychloroquine may have the potential to reduce RC.

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Increased risk of thrombosis in antiphospholipid syndrome patients treated with direct oral anticoagulants. Results from an international patient-level data meta-analysis.. 2018. https://doi.org/10.1016/j.autrev.2018.04.009

<h4>Background</h4>Direct oral anticoagulants (DOACs) are widely used for secondary prevention of venous thromboembolism (VTE) but their clinical efficacy and safety are not established in Antiphospholipid Syndrome (APS) patients. There is only one randomized controlled trial published while others are still ongoing. Many non-randomized studies have been published in this field with conflicting opinions.<h4>Purpose of review</h4>We conducted a systematic review using MEDLINE, EMBASE and Cochrane databases from 2000 until March 2018 regarding APS patients treated with DOACs. We performed a patient-level data meta-analysis to a) estimate the prevalence of recurrent thrombosis in APS patients treated with DOACs in the literature, and b) identify variables associated with recurrent thrombosis.<h4>Results</h4>We identified 47 studies corresponding to 447 APS patients treated with DOACs. Three commercially available DOACs were analyzed: rivaroxaban (n = 290), dabigatran etexilate (n = 144) and apixaban (n = 13). A total of 73 out of 447 patients (16%) experienced a recurrent thrombosis while on DOACs with a mean duration until thrombosis of 12.5 months. Rates of recurrent thromboses were 16.9% and 15% in APS patients receiving either anti-Xa inhibitors or dabigatran respectively. Triple positivity (positivity for all three antiphospholipid antibodies) was associated with a four-fold increased risk of recurrent thrombosis (56% vs 23%; OR = 4.3 [95%CI; 2.3-7.7], p < 0.0001) as well as a higher number of clinical criteria for APS classification. In patients treated with anti-Xa inhibitors, history of arterial thrombosis was associated with a higher risk of recurrent thrombosis (32% vs 14%; OR = 2.8 [95%CI; 1.4-5.7], p = 0.006). In conclusion, DOACs are not effective in all APS patients and should not be used routinely in these patients. Randomized controlled trials assessing clinical efficacy and safety as primary endpoints are underway. In the meantime, a registry of APS patients on DOACs could be proposed to establish in which APS subgroups DOACs would be a safe alternative to warfarin.

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Arterial thrombosis in antiphospholipid syndrome (APS): Clinical approach and treatment. A systematic review.. 2021. https://doi.org/10.1016/j.blre.2020.100788

Thrombotic Antiphospholipid Syndrome (APS) is a condition affecting young individuals in whom a thromboembolic event occurs in the presence of circulating antiphospholipid antibodies (aPL). An extensive body of literature has covered the most common clinical presentation of the syndrome, venous thromboembolism. Arterial thrombosis in APS, a lesser clinical expression, is less studied. This review will concentrate on the body of literature concerning pathogenesis, clinical presentation and management of arterial thrombosis in APS.

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Antiphospholipid syndrome in pregnancy: a comprehensive literature review.. 2025. https://doi.org/10.1186/s12884-025-07471-w

Antiphospholipid syndrome (APS) is an autoimmune disorder associated with thrombotic events and adverse obstetric outcomes, particularly in its obstetric form (OAPS). Affecting approximately 0.5% of the population, APS is a leading contributor to recurrent pregnancy loss (RPL), preeclampsia (PE), and fetal growth restriction ((FGR). Despite advancements in understanding its pathophysiology and management, optimal treatment strategies for APS in pregnancy remain challenging and require systematic evaluation. This review synthesizes current evidence on APS mechanisms, diagnostic criteria, and therapeutic interventions, with a focus on maternal and fetal outcomes in OAPS. A comprehensive search of PubMed, was conducted to identify studies exploring APS pathogenesis, diagnostic standards, and treatment efficacy in obstetric settings. Inclusion criteria prioritized randomized controlled trials, cohort studies, and systematic reviews with a clear focus on APS and pregnancy. The review confirmed that APS current accepted pathogenesis is governed by a "two-hit" model, where antiphospholipid antibodies (aPLs) initiate endothelial damage, culminating in thrombosis and placental insufficiency. Epidemiological analysis underscores the prevalence and severity of APS in obstetric contexts, with lupus anticoagulant (LA) emerging as a significant predictor of adverse outcomes. Evidence supports the use of low-dose aspirin (LDA) and heparin to reduce miscarriage rates, while adjunctive treatments, such as hydroxychloroquine (HCQ), have shown promise in improving live birth rates and reducing preterm delivery in high-risk cases. Emerging therapies, including tumoral necrosis factor (TNF-alpha) inhibitors and nitric oxide modulators, may offer additional benefits in refractory cases. APS remains a critical determinant of adverse pregnancy outcomes, necessitating precise diagnostic criteria and tailored management approaches. This systematic review emphasizes the importance of individualized therapeutic regimens to optimize maternal and fetal health in OAPS and highlights areas for future research, particularly regarding novel pharmacological approaches. Further studies are essential to refine treatment protocols and improve clinical guidelines for managing APS in pregnancy.

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Thrombocytopenia in antiphospholipid syndrome: predictors, prognostic implications, and thrombotic risk in a large cohort study.. 2025. https://doi.org/10.1016/j.thromres.2025.109544

BACKGROUND Antiphospholipid syndrome (APS) is a multifaceted autoimmune disorder associated with thrombosis and pregnancy morbidity. Thrombocytopenia, a frequent manifestation of APS, presents unique clinical challenges due to its dual association with thrombotic and hemorrhagic risks. This study investigates the incidence, characteristics, and predictors of thrombocytopenia in a large cohort of antiphospholipid antibodies (aPL)-positive patients and its association with other clinical manifestations. METHODS We conducted a multicenter retrospective cohort study from 2014 to 2024 involving 211 aPL-positive patients at San Giovanni Bosco and San Luigi Gonzaga Hospital, Turin, Italy. Data on demographic, laboratory, and clinical features were collected every six months or at the occurrence of new clinical events. Thrombocytopenia definitions excluded other etiologies. Laboratory and clinical evaluations included thrombosis risk factors, autoantibody profiles, and treatment regimens. RESULTS Thrombocytopenia occurred in 42 patients (20 %), with varying severity: mild (33 %), moderate (38 %), and severe (29 %). Severe cases primarily exhibited platelet counts below 20 × 10^9/L. Patients with thrombocytopenia demonstrated higher rates of thrombotic events, venous recurrences, deep vein thrombosis, pulmonary embolism, and catastrophic APS (CAPS). Renal involvement was more frequent, while inflammatory manifestations (pericarditis, pleuritis, and arthralgia) were less common. Patients with thrombocytopenia showed higher frequency of anti-β2 glycoprotein I antibodies IgG positivity and leukopenia. Therapeutic interventions included increased use of steroids, intravenous immunoglobulins, mycophenolate, and rituximab. Thrombocytopenia was more prevalent in systemic APS diagnoses (21 % vs. 3 %). CONCLUSION Thrombocytopenia in APS patients, particularly in severe cases, correlates with heightened thrombotic risk and systemic manifestations. These findings highlight the importance of customized strategies that balance thrombosis prevention with bleeding risk, especially in complex cases.

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Risk Factors for Recurrent Thrombosis in Patients with Antiphospholipid Syndrome—A Single-Centre Cohort Study. 2025. https://doi.org/10.1055/a-2646-9016

Background Recurrent thrombosis poses a clinical challenge in patients with antiphospholipid syndrome (APS). There are limited data on risk factors due to its rarity. Aims This study aimed to study the association between cardiovascular (CV) and APS-related risk factors and recurrent thrombosis and evaluate the adjusted Global Anti-Phospholipid Syndrome Score (aGAPSS). Methods This retrospective cohort study comprised APS patients at Karolinska University Hospital, Sweden, from 2014 to 2020 with follow-up until the last medical visit or death. Multiple thrombotic events per patient were included. Cox proportional hazard model estimated hazard ratios (HRs) and 95% confidence intervals (CIs). Logistic regression and Poisson regression were conducted to further examine the relation between risk factors and recurrent thrombosis. Results The cohort included 250 patients (67% women and 62% primary APS) with a median age of 44.5 (35–59) years. Forty-nine recurrent thrombotic events occurred in 36 patients, yielding an incidence of 4.46 (95% CI 3.30–5.90) per 100 person-years. Thrombocytopenia was associated with recurrent thrombosis (HR 2.57 [95% CI 1.01–6.02]). Although CV risk factors were not consistently significant for recurrent thrombosis, chronic kidney disease (CKD) indicated an increased probability (OR 2.55 [95% CI 1.01–6.26]). For each point of aGAPSS, the HR for recurrent thrombosis increased by 10% (1.10 [95% CI 1.01–1.19]). Notably, inadequate anticoagulation triggered recurrence in almost a quarter of cases. Conclusion Thrombocytopenia was confirmed as a major risk factor for recurrent thrombosis. CKD warrants closer attention in future assessment. Although an increase in aGAPSS was associated with recurrent thrombosis, further evaluation is required. Improving anticoagulation treatment is essential to reduce recurrence.

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Direct Oral Anticoagulants Use in Antiphospholipid Syndrome: Are These Drugs an Effective and Safe Alternative to Warfarin? A Systematic Review of the Literature.. 2016. https://doi.org/10.1007/s11926-016-0623-7

<h4>Background</h4>The cornerstone of thrombotic antiphospholipid syndrome (APS) patients' management is to prevent recurrent thrombosis by long-term anticoagulation.<h4>Purpose of review</h4>The purpose of the review is to summarize available literature on direct oral anticoagulants (DOACs) use in APS patients through a systematic review and to determine factors associated with thrombosis recurrence.<h4>Recent findings</h4>The recent RAPS trial demonstrated that APS patients treated with rivaroxaban had a significant twofold-increased thrombin potential, suggesting a higher thrombotic risk, in comparison with warfarin users. Furthermore, several reports of APS patients treated with DOACs have raised safety issues. Our systematic review identified 122 published APS patients treated with DOACs; among them, 19 experienced a recurrent thrombosis while on DOACs. Of note, triple positivity (positivity of all three laboratory criteria for APS) was associated with a 3.5-fold increased risk for recurrent thrombosis. In conclusion, DOACs should be used with caution in APS patients and randomized control trials with clinical primary endpoints assessing clinical efficacy and safety are awaited to establish whether the prescription of DOACs could be a safe alternative to warfarin.

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Circulating Platelets in Thrombotic Antiphospholipid Syndrome Display High Procoagulant Activity and Surface Complement Deposition: Correlation with Thrombotic Risk. 2023. https://doi.org/10.1182/blood-2023-184601

Background Antiphospholipid syndrome (APS) is characterized by circulating antiphospholipid antibodies (aPL) accompanied by arterial and/or venous thrombosis, and/or recurrent pregnancy loss. It commonly affects young women in whom it dramatically increases their risk of myocardial infarction, ischemic stroke, deep vein thrombosis and pulmonary embolism. Although the thrombotic risk associated with aPL is established, the underlying mechanisms are still incompletely defined and there are no definitive predictive biomarkers. As a result the management of APS involves indefinite anticoagulation. Increased activation of vascular cells, including platelets is considered to underlie the pathogenesis of APS, and may be mediated in some cases by complement. There is a considerable crosstalk between platelets and complement at various levels during thrombosis. First, activated complement proteins stimulate platelets through their cognate receptors on the platelet surface, and genetic deficiency of complement proteins in mice leads to decreased platelet responsiveness. Second, platelets secrete complement proteins into the medium upon activation. Third, agonist-stimulated platelets contribute to activation of both the classical and alternative pathways of the complement cascade. Hence, we sought to investigate the association between the complement-platelet axis and the prothrombotic pathology observed in APS. Methods Venous blood was drawn from patients with APS and healthy controls, and washed human platelets were prepared by differential centrifugation. Platelets either remained unstimulated or were treated with thrombin (0.1, 0.25, 0.5 U/ml) for 5 min and then labelled with FITC-PAC1, PE-anti-CD62P antibody, Alexa Fluor 488-anti-C4d conjugate, PE-Annexin V, Mitotracker Red, MitoSOX Red, Fluo4-AM, Rhod2-AM, Cell Event Green Caspase 3/7 detection reagent and FITC-IETD-FMK for 30 min in the dark, and then analyzed by flow cytometry to measure integrin activation, P-selectin expression (α-granule secretion), complement C4d binding, phosphatidylserine (PS) exposure, mitochondrial membrane potential, mitochondrial ROS, cytosolic calcium, mitochondrial calcium, caspase 3/7 activity (apoptosis) and caspase 8 activity (extrinsic apoptosis pathway), respectively. Platelet markers were correlated with complement binding and clinical characteristics of APS patients including number of thrombotic events and circulating levels of aPL. Results Thrombin-induced platelet integrin activation and P-selectin expression were identical in APS patients and healthy controls. However, platelets isolated from APS patients had significantly higher procoagulant activity (PS exposure) as well as complement C4d binding in both unstimulated and thrombin-stimulated states compared to healthy controls. There was a strong positive correlation between platelet PS exposure and C4d binding in APS patients, but not healthy individuals, suggesting a role for complement activation in formation of procoagulant platelets in APS. A subset of APS patients with high platelet procoagulant activity (PS exposure > mean + 2SD observed in healthy individuals) had lower mitochondrial membrane potential and increased mitochondrial calcium transients compared to healthy individuals, suggesting mitochondrial permeability transition pore (mPTP)-driven PS exposure. Another subset of APS patients with PS exposing platelets showed caspase activation indicating apoptosis. Platelet PS exposure and C4d binding correlated strongly with the number of thrombotic events as well as levels of circulating aPL, which identifies complement-induced procoagulant platelets as predictors and possible underlying mechanisms for thrombosis in APS. Conclusion Our preliminary studies suggest that PS-exposing platelets are generated in APS by multiple mechanisms including agonist-induced mPTP formation and apoptosis-associated caspase activation. Platelet PS exposure in APS is positively correlated with

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ClinicalTrials.gov: Observational Study to Evaluate the Effectiveness of DOACS for Secondary Thrombosis Prevention in Low-risk Thrombotic APS Patients. https://clinicaltrials.gov/study/NCT07372170

Observational Study to Evaluate the Effectiveness of DOACS for Secondary Thrombosis Prevention in Low-risk Thrombotic APS Patients This is an observational study designed to evaluate the effectiveness and safety of direct oral anticoagulants (DOACs) compared with vitamin K antagonists (VKAs) for the secondary prevention of thrombosis in patients with low-risk thrombotic antiphospholipid syndrome. Antiphospholipid syndrome is an autoimmune disorder associated with an increased risk of thrombotic events. Although VKAs have traditionally been the standard treatment, DOACs are increasingly used in clinical practice in selected patients, despite limited evidence in this setting. This study includes patients with previous venous thrombosis and a low-risk serological profile who are treated with either DOACs or VKAs according to routine clinical practice. The primary objective is to compare thrombotic recurrence and bleeding events between both treatment strategies. The results of this study will contribute to improving knowledge about the use of DOACs in patients with low-risk thrombotic antiphospholipid syndrome.

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The Association between Antiphospholipid Syndrome after Conventional Treatment and Preeclampsia. 2023. https://doi.org/10.31083/j.ceog5004070

Background: Despite conventional treatment, the prognosis of antiphospholipid syndrome (APS) pregnancy remains poor, and some pregnancies are still complicated by preeclampsia (PE). This study aimed to identify the relationship between conventionally-treated APS and the onset of PE. Methods: Relevant studies published up to April 2021 were searched on the PubMed, Cochrane Library, and Embase databases. Related data were extracted from the included studies, and we performed a meta-analysis. Review Manager 5.4 were used to calculate the pooled odds ratio (OR) and 95% confidence intervals (CIs). Results: This study screened 6 studies, including 1 cohort study and 5 case-control studies. Even after conventional treatment, the rate of PE in APS pregnancy is still significantly higher than in the control group. There was a higher pooled OR in the cohort study (OR: 8.37, 95% CI: 3.42–20.48) than the case-control studies (OR: 2.30, 95% CI: 1.12–4.74) in the subgroup analysis. Conclusions: APS pregnancy increases the risk of PE even after conventional treatment. Routine monitoring and standardized and better treatment methods should be developed to prevent the occurrence of PE.

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Clinical Interpretation of Platelet Activation Marker sCLEC-2 in Antiphospholipid Syndrome.. 2026. https://doi.org/10.1002/jcla.70230

<h4>Background</h4>Soluble C-type lectin-like receptor 2 (sCLEC-2) has emerged as a biomarker of platelet activation and thrombus formation. Antiphospholipid syndrome (APS) is characterized by arterial and venous thrombosis and pregnancy complications, driven in part by platelet activation. However, the clinical utility of sCLEC-2 and the sCLEC-2/D-dimer ratio in APS remains unclear.<h4>Methods</h4>Plasma samples from 19 patients with primary APS, 30 with SLE-associated APS, 10 with SLE without APS, 40 with other collagen diseases, and 40 healthy controls (n = 139) were analyzed. Plasma sCLEC-2 levels and D-dimer levels were quantified by immunoassay. Antiphospholipid antibodies (anti-cardiolipin antibodies and anti-β<sub>2</sub>-glycoprotein I antibodies IgG/IgM) were measured by ELISA kits. Group comparisons and correlations were evaluated.<h4>Results</h4>Using the upper limit of the 95% CI of healthy controls as a cutoff, sCLEC-2 positivity was observed in 100% of non-APS autoimmune disease patients, and 98.0% of APS patients. sCLEC-2, D-dimer, and the sCLEC-2/D-dimer ratio were significantly higher in non-APS and APS groups compared with controls (p < 0.001). A slight but significant difference in the sCLEC-2 and the ratio was observed between the non-APS and APS groups. However, no significant differences were found among APS subgroups stratified by thrombosis type. sCLEC-2 showed no correlation with any of four major antiphospholipid antibody titers.<h4>Conclusion</h4>Although we observed raised sCLEC-2 and sCLEC-2/D-dimer ratio among APS and non-APS groups and modest differences between the two groups, clinical interpretation of the findings requires a prospective study evaluating dynamic changes of sCLEC-2 in the clinical course.

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Antiphospholipid syndrome. https://en.wikipedia.org/wiki/Antiphospholipid_syndrome

Antiphospholipid syndrome, or antiphospholipid antibody syndrome (APS or APLS), is an autoimmune, hypercoagulable state caused by antiphospholipid antibodies Antiphospholipid syndrome, or antiphospholipid antibody syndrome (APS or APLS), is an autoimmune, hypercoagulable state caused by antiphospholipid antibodies. APS can lead to blood clots (thrombosis) in both arteries and veins, pregnancy-related complications, and other symptoms like low platelets, kidney disease, heart disease, and rash. Although the exact etiology of APS is still not clear, gene Antiphospholipid syndrome, or antiphospholipid antibody syndrome (APS or APLS), is an autoimmune, hypercoagulable state caused by antiphospholipid antibodies. APS can lead to blood clots (thrombosis) in both arteries and veins, pregnancy-related complications, and other symptoms like low platelets, kidney disease, heart disease, and rash. Although the exact etiology of APS is still not clear, genetics is believed to play a key role in the development of the disease. Diagnosis is made based on symptoms and testing, but sometimes research criteria are used to aid in diagnosis. The research criteria for definite APS requires one clinical event (i.e. thrombosis or pregnancy complication) and two positive blood test results spaced at least three months apart that detect lupus anticoagulant, anti-apolipoprotein antibodies, and/or anti-cardiolipin antibodies. Antiphospholipid syndrome can be primary or secondary. Primary antiphospholipid syndrome occurs in the absence of any other related disease. Secondary antiphospholipid syndrome occurs with other autoimmune diseases, such as systemic lupus erythematosus. In rare cases, APS leads to rapid organ failure due to generalized thrombosis; this is termed "catastrophic antiphospholipid syndrome" (CAPS or Asherson syndrome) and is associated with a high risk of death. Antiphospholipid syndrome often requires treatment with anticoagulant medication to reduce the risk of further episodes of thrombosis and improve the prognosis of pregnancy. The anticoagulant medication used for treatment may differ depending on the circumstance, such as pregnancy.

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66th annual scientific meeting : 37th annual scientific meeting, Association of Rheumatology Health Professionals ; October 24-29, 2002, New Orleans, Louisiana, Ernest N. Morial Convention Center. https://archive.org/details/66thannualscient00hobo

Spondylitis-Seronegative Arthritis Antiphospholipid Antibodies and Pregnancy Antiphospholipid Syndrome Difficult … We have previously reported that the risk of thrombotic manifestations in French Canadian … '») showed new thrombotic events; 3 (5.4 "’ll) died. New thrombotic events were obseiAed

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