ArticleInternational journal of molecular sciences2022
IgA Antiphospholipid Antibodies in Antiphospholipid Syndrome and Systemic Lupus Erythematosus.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Anti-phospholipid antibodies as a risk factor for renal injury in patients with systemic lupus erythematosus: a comprehensive analysis.Frontiers in immunology · 2026Pooled it
- Association of IgA antiphospholipid antibodies with hypercoagulability and inflammation in antiphospholipid syndrome.Journal of thrombosis and thrombolysis · 2026Observational
- Systemic lupus erythematosus-associated autoantibodies in sickle cell disease: Spontaneous emergence in a patient and in transgenic sickle mice.British journal of haematology · 2025Article
- High Prevalence of aCL-IgA and aβ2GPI-IgA in Drug-Free Schizophrenia Patients: Evidence of a Potential Autoimmune Link.Antibodies (Basel, Switzerland) · 2024Article
- Antiphospholipid Syndrome in Pregnancy: New and Old Pathogenetic Mechanisms.International journal of molecular sciences · 2023Review
- Anticardiolipin and anti-beta 2-glycoprotein I antibodies in patients with unexplained articular manifestations.Journal of clinical laboratory analysis · 2023Article
- Research trends and frontiers on antiphospholipid syndrome: A 10-year bibliometric analysis (2012-2021).Frontiers in pharmacology · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Objective: To define the role of IgA antibodies to cardiolipin (aCL) and IgA antibodies to beta-2 glycoprotein 1 (anti-β2-GP1) in the development of vascular complications in patients with antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE). Material and methods: A total of 187 patients with one of the following diagnoses: primary APS (PAPS), probable APS, SLE with APS, and SLE without APS. The comparison group consisted of 49 patients with other rheumatic diseases (RD), the control group included 100 relatively healthy individuals (without RD, oncological pathology, and infectious diseases). All patients underwent standard clinical, laboratory, and instrumental examinations before being included in the study and during follow-up. The aPL study included the determination of IgG/IgM aCL, IgG/IgM anti-β2-GP1 by enzyme-linked immunosorbent assay (ELISA), IgG/IgM/IgA aCL, IgG/IgM/IgA anti-β2-GP1 by chemiluminescence analysis (CLA), and lupus anticoagulant (LA). Results: IgA aCL were detected in 75 (40%) of the 187 patients with APS and SLE, in none of the comparison group, and in 2 (2%) of the control one. IgA anti-β2-GP1 were detected in 63 (34%) of the 187 patients with APS and SLE, in none of the patients in the comparison group, and in one (1%) of the control group. The prevalence of IgA aCL and IgA anti-β2-GP1 and their levels were statistically significantly higher in patients with APS (PAPS and SLE + APS) than the levels in patients with SLE and those of the comparison and control groups (p < 0.05). IgA aCL and IgA anti-β2-GP1 were significantly associated with thrombosis in APS (χ2 = 4.96; p = 0.02 and χ2 = 4.37; p = 0.04, respectively). The risk of thrombosis was 2.04 times higher in patients with positive IgA aCL than in patients without these antibodies, as well as in patients with positive IgA anti-β2-GP1; it was twice as high as in patients without antibodies. There was a high specificity of IgA aCL and IgA anti-β2-GP1 for both the diagnosis of APS and its clinical manifestations, despite a low sensitivity. Conclusions: The study revealed a relationship of thrombosis and APS with IgA aCL and IgA anti-β2-GP1. There was a high specificity of IgA aCL and IgA anti-β2-GP1 (95% and 93%, respectively) for the diagnosis of APS with a low sensitivity (54% and 44%, respectively). There were no patients with isolated positivity of IgA aCL and IgA anti-β2-GP1.
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