ArticleClinical and experimental immunology2011
Activation of coagulation in bullous pemphigoid and other eosinophil-related inflammatory skin diseases.
Article in Clinical and experimental immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Risk of Incident Venous Thromboembolism Among Patients With Bullous Pemphigoid or Pemphigus Vulgaris: A Nationwide Cohort Study With Meta-Analysis.Journal of the American Heart Association · 2023Pooled it
- Corticosteroid-Sparing Control of Bullous Pemphigoid with Dupilumab and Tripterygium Glycosides: A Real-World Cohort with Longitudinal Transcriptomics.Journal of inflammation research · 2026Article
- Venous thromboembolism in bullous pemphigoid: current evidence from an updated systematic review.Dermatology reports · 2025Article
- Laboratory and clinical haemostatic aberrations in primary dermatologic disease: A review.Thrombosis journal · 2024Review
- Causal association between circulating blood cell traits and pulmonary embolism: a mendelian randomization study.Thrombosis journal · 2024Article
- IL-27 as a novel biomarker for pruritus in nodular prurigo and bullous pemphigoid.Frontiers in immunology · 2024Article
- Beyond the Surface: Investigating the Relationship Between Autoimmune Blistering Disorders and Venous Thromboembolism.Journal of the American Heart Association · 2023Article
- Concomitant use of dupilumab with glucocorticoid in bullous pemphigoid reduces disease severity: A preliminary study.Immunity, inflammation and disease · 2023Article
- Bullous pemphigoid: The role of type 2 inflammation in its pathogenesis and the prospect of targeted therapy.Frontiers in immunology · 2023Review
- Clinical Patterns, Survival, Comorbidities, and Treatment Regimens in 149 Patients With Pemphigus in Tuscany (Italy): A 12-Year Hospital-Based Study.Frontiers in immunology · 2022Article
- Relationship between bullous pemphigoid and metabolic syndrome: a 12-year case-control study conducted in China.Therapeutic advances in chronic disease · 2022Article
- Emerging Biomarkers and Therapeutic Strategies for Refractory Bullous Pemphigoid.Frontiers in immunology · 2021Review
- Bullous Pemphigoid: Trigger and Predisposing Factors.Biomolecules · 2020Review
- Resolution in bullous pemphigoid.Seminars in immunopathology · 2019Review
- Elevated plasma D-dimer levels in dermatomyositis patients with cutaneous manifestations.Scientific reports · 2019Article
- New Insights Into the Pathogenesis of Bullous Pemphigoid: 2019 Update.Frontiers in immunology · 2019Review
- Coagulation and Skin Autoimmunity.Frontiers in immunology · 2019Review
- Dermatitis Herpetiformis: Novel Perspectives.Frontiers in immunology · 2019Review
- Review
- BP180 Is Critical in the Autoimmunity of Bullous Pemphigoid.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bullous pemphigoid (BP) is a skin disease caused by autoantibodies to hemidesmosomal proteins BP180 and BP230, with eosinophils participating in blister formation. Tissue factor (TF), the initiator of coagulation, is embodied within the eosinophil granules and exposed upon activation. We evaluated the coagulation activation in patients with BP (63), chronic urticaria (CU; 20), atopic dermatitis (AD; 14), cutaneous drug reactions (CDRs; six), psoriasis (20), dermatitis herpetiformis (DH; four) and primary cutaneous T cell lymphoma (CTCL; five), and in 40 healthy controls. Prothrombin fragment F1+2 and d-dimer (coagulation markers) were measured by enzyme-linked immunosorbent assay (ELISA) in all plasma samples and BP blister fluid. Skin TF expression was evaluated immunohistochemically in the patients and 20 controls. F1+2 and d-dimer levels were higher in BP plasma than in control plasma (P = 0·0001 for both), and dramatically high in blister fluid; both correlated positively with disease severity, esinophil counts and anti-BP180 antibodies (P = 0·006-0·0001). Plasma F1+2 and d-dimer levels were higher in the CU, AD and CDR patients than in controls (P = 0·0001 for all), but normal in the psoriasis, DH and CTCL patients. Skin TF was expressed in the BP (P = 0·0001), CU (P = 0·0001), AD (P = 0·001) and CDR patients (P = 0·01), but not in the psoriasis, DH or CTCL patients. Co-localization confocal microscopy studies confirmed eosinophils as the source of TF in 10 BP patients. The coagulation cascade is activated in BP and other eosinophil-mediated skin disorders, but not in non-eosinophil driven conditions. This hypercoagulability may contribute to inflammation, tissue damage and, possibly, thrombotic risk.
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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.