ArticleArthritis & rheumatology (Hoboken, N.J.)2024
Calprotectin Impairs Platelet Survival in Patients With Primary Antiphospholipid Syndrome.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Serum S100A8 as a potential biomarker for diagnosis of antiphospholipid syndrome and risk stratification among aPL carriers.Lupus science & medicine · 2026Article
- A review of the impact of isolated antiphospholipid antibody positivity on pregnancy outcomes and clinical management strategies.Frontiers in immunology · 2026Review
- Antiphospholipid Syndrome: An Antibody-Mediated Disease With Emerging Therapeutic Opportunities.Arthritis & rheumatology (Hoboken, N.J.) · 2025Review
- Pathophysiological Links Between Inflammatory Bowel Disease and Cardiovascular Disease: The Role of Dysbiosis and Emerging Biomarkers.Biomedicines · 2025Review
- Insights from the 2024 pediatric rheumatology basic/translational years in review.Pediatric rheumatology online journal · 2025Review
- Identification of shared biomarkers and potential therapeutic targets for antiphospholipid syndrome and recurrent miscarriage by integrated bioinformatics analysis and machine learning.Frontiers in medicine · 2025Article
- Targeting toll-like receptors: unveiling potential therapeutic strategies for deep vein thrombosis.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
24 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveWhile thrombosis and pregnancy loss are the best-known clinical features of antiphospholipid syndrome (APS), many patients also exhibit "extra-criteria" manifestations, such as thrombocytopenia. The mechanisms that drive APS thrombocytopenia are not completely understood, and no clinical biomarkers are available for predicting antiphospholipid antibody (aPL)-mediated thrombocytopenia. Calprotectin is a heterodimer of S100A8 and S100A9 that is abundant in the neutrophil cytoplasm and released upon proinflammatory neutrophil activation. Here, we sought to evaluate the presence, clinical associations, and potential mechanistic roles of circulating calprotectin in a cohort of primary APS and aPL-positive patients.
methodsLevels of circulating calprotectin were determined in plasma by the QUANTA Flash chemiluminescent assay. A viability dye-based platelet assay was used to assess the potential impact of calprotectin on aPL-mediated thrombocytopenia.
resultsCirculating calprotectin was measured in 112 patients with primary APS and 30 aPL-positive (without APS criteria manifestations or lupus) patients as compared to patients with lupus (without APS), patients with unprovoked venous thrombosis (without aPL), and healthy controls. Levels of calprotectin were higher in patients with primary APS and aPL-positive patients compared to healthy controls. After adjustment for age and sex, calprotectin level correlated positively with absolute neutrophil count (r = 0.41, P < 0.001), positively with C-reactive protein level (r = 0.34, P = 0.002), and negatively with platelet count (r = -0.24, P = 0.004). Mechanistically, we found that calprotectin provoked aPL-mediated thrombocytopenia by engaging platelet surface toll-like receptor 4 and activating the NLRP3-inflammasome, thereby reducing platelet viability in a caspase-1-dependent manner.
conclusionThese data suggest that calprotectin has the potential to be a functional biomarker and a new therapeutic target for APS thrombocytopenia.
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