ReviewJournal of thrombosis and haemostasis : JTH2021
Antiphospholipid syndrome: Complement activation, complement gene mutations, and therapeutic implications.
Review in Journal of thrombosis and haemostasis : JTH, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 93 citations in OpenAlex.
- Autoimmune-associated thrombosis: mechanisms, population burden, and prevention strategies.The Lancet regional health. Europe · 2026Review
- Antiphospholipid antibodies and cardiovascular thrombosis.Nature reviews. Cardiology · 2026Review
- BRD3OS Dysregulation in Antiphospholipid Syndrome: Integrative Network and RNA Structural Analysis of m6A-Related Candidate Regions.Biomolecules · 2026Article
- Chromogenic factor X-guided warfarin monitoring in lupus anticoagulant-positive primary antiphospholipid syndrome with adrenal hemorrhage and progressive deep vein thrombosis: a case report.Journal of medical case reports · 2026Article
- The evolving landscape of complement therapeutics in rheumatology.Annals of the rheumatic diseases · 2026Review
- C4b-binding protein as an antigenic target in the pathogenesis of antiphosphatidylethanolamine autoantibodies.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Translational immunothrombosis in autoimmune Heparin-Induced thrombocytopenia: targeting the FcγRIIa-Syk-BTK and complement pathways.Clinical and experimental medicine · 2026Review
- Complement activation and altered fibrin clot properties in obstetric antiphospholipid syndrome: impact on thromboembolism and pregnancy.Clinical rheumatology · 2026Article
- Pulmonary Embolism in Antiphospholipid Syndrome (APS)-Where Are We and Where Are We Going?International journal of molecular sciences · 2026Review
- Autoantibody repertoire in lupus nephritis: from pathogenic mechanisms to clinical integration for precision decision-making.Frontiers in immunology · 2026Review
- The role of neutrophil extracellular traps in antiphospholipid syndrome.Frontiers in immunology · 2026Review
- The efferocytosis-related genes of SLC26A6, TYRO3, and PDK4 have been identified as predictors of prognosis in hepatocellular carcinoma and are associated with the immune status.International journal of medical sciences · 2026Article
- Antiphospholipid Syndrome: An Antibody-Mediated Disease With Emerging Therapeutic Opportunities.Arthritis & rheumatology (Hoboken, N.J.) · 2025Review
- Article
- Complement activation in secondary thrombotic microangiopathies.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Review
- Activated Complement System's Impact in Antiphospholipid Syndrome Thrombosis: From Pathophysiology to Treatment.Journal of clinical medicine · 2025Review
- Mechanism of hydroxychloroquine in the treatment of obstetric antiphospholipid syndrome by inhibiting NETs-induced trophoblast pyroptosis.Molecular biology reports · 2025Article
- Prevalence and Risk Factors of Acute Ischemic Stroke in Patients with Antiphospholipid Syndrome: A Retrospective Monocenter Analysis.Journal of cardiovascular development and disease · 2025Article
- Understanding the structure of βBlood vessels, thrombosis & hemostasis · 2025Review
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Antiphospholipid syndrome (APS) is an acquired thromboinflammatory disorder characterized by the presence of antiphospholipid antibodies as well as an increased frequency of venous or arterial thrombosis and/or obstetrical morbidity. The spectrum of disease varies from asymptomatic to a severe form characterized by widespread thrombosis and multiorgan failure, termed catastrophic APS (CAPS). CAPS affects only about ∼1% of APS patients, often presents as a thrombotic microangiopathy and has a fulminant course with >40% mortality, despite the best available therapy. Animal models have implicated complement in the pathophysiology of thrombosis in APS, with more recent data from human studies confirming the interaction between the coagulation and complement pathways. Activation of the complement cascade via antiphospholipid antibodies can cause cellular injury and promote coagulation via multiple mechanisms. Finally, analogous to classic complement-mediated diseases such as atypical hemolytic uremic syndrome, a subset of patients with APS may be at increased risk for development of CAPS because of the presence of germline variants in genes crucial for complement regulation. Together, these data make complement inhibition an attractive and potentially lifesaving therapy to mitigate morbidity and mortality in severe thrombotic APS and CAPS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.