Skip to main content

Non-criteria antiphospholipid antibodies and pediatric rheumatic disease: a case series



Non-criteria antiphospholipid antibodies (NC-aPL) are a relatively undefined subgroup of antiphospholipid antibodies (aPL). Knowledge about NC-aPL in adults is limited and even less is known in pediatric patients. Routine tests for antiphospholipid syndrome (APS)—a clinical state marked by the presence of aPL in association with vascular thrombosis—usually include lupus anticoagulant (LAC), anti-cardiolipin (aCL) and -beta-2 glycoprotein I (aβ2GPI). LAC is a functional screen for prothrombotic aPL, while the latter tests identify specific autoantibodies. Specific targets of NC-aPL include, but are not limited to, phosphatidylethanolamine, phosphatidylserine, and prothrombin.

Presentation of cases

We present single-center data from eight pediatric patients with NC-aPL identified during a three-year period. All patients had presenting features raising suspicion for APS. Most patients were female with a primary rheumatic disease. One patient had a stroke. Another patient had alveolar hemorrhage and pulmonary hypertension. Raynaud’s phenomenon, rashes involving distal extremities, and headaches were common. Most patients had a positive LAC, yet their routine aPL tests were negative, prompting testing for NC-aPL.


Our findings suggest NC-aPL are associated with typical signs and symptoms of APS in pediatric patients. Pediatricians and pediatric subspecialists should consider NC-aPL when clinical suspicion is high and routine aPL tests are negative, particularly when LAC is positive. While guidelines for NC-aPL do not yet exist for children or adults, these autoantibodies have pathogenic potential. Actionable items could include evaluation for the presence of other (primary) rheumatic diseases, and consultation with hematologists and/or obstetricians regarding anticoagulation/platelet inhibition and thrombosis education. Future guidelines regarding NC-aPL will only be generated by gathering more data, ideally prospectively.


Antiphospholipid antibodies (aPL) are autoantibodies that bind to phospholipid-binding proteins and can provoke tissue pathology [1,2,3,4,5]. The diagnosis of antiphospholipid syndrome (APS) is reserved for patients who develop vascular thrombosis in association with aPL or a lupus anticoagulant (LAC), which screens indirectly for the presence of aPL. APS can be a primary condition or can occur secondary to rheumatic diseases such as systemic lupus erythematosus (SLE). Both primary and secondary APS can also feature non-thrombotic manifestations, including Raynaud’s phenomenon, livedoid and/or vasculitic rashes, headaches and other neurologic manifestations, and cardiac valve inflammation [6,7,8,9,10,11,12,13].

The most common aPL tested in clinical laboratories are IgM and IgG anti-cardiolipin (aCL) and anti-beta 2 glycoprotein-I (aβ2GPI). Medium- or high-titers of these autoantibodies—when detected two or more times at least 12 weeks apart—can fulfill the laboratory criteria of the most highly utilized classification criteria for APS in adult patients [14]. Development of revised criteria are underway [15]. The presence of aPL can also be inferred indirectly by LAC testing. A positive LAC detects in vitro inhibition of the phospholipid-dependent steps of the coagulation cascade. This nomenclature is often confusing to clinicians since these autoantibodies are pro-coagulant in vivo but prolong this coagulation test in vitro. It is possible to have a positive LAC with negative aCL and aβ2GPI. In these cases, non-criteria aPL (NC-aPL) may be responsible for LAC positivity. NC-aPL bind to other unique phospholipid-associated targets such as phosphatidylethanolamine (PE), phosphatidylserine (PS), prothrombin (PT), and others [16,17,18,19,20,21]. NC-aPL are not well characterized even in adult patients. These antibodies are referred to as ‘non-criteria’ because there are insufficient prospective data available to justify including them in common classification criteria for APS [16]. Even less is known about NC-aPL in the pediatric population.

In the following single-center case series, NC-aPL testing was obtained in individual patients due to clinical suspicion for APS, particularly when aCL and aβ2GPI antibodies were negative in the setting of a positive LAC. Here we review the clinical presentation, laboratory and other diagnostic evaluation, and management of eight pediatric patients with NC-aPL.


All included patients were convenience samples. However, we also performed a database search of the electronic medical record at the University of Minnesota to ensure that all pediatric patients with positive NC-aPL tests were captured within the preceding 36 months. The University of Minnesota Institutional Review Board deemed this study exempt from full review. NC-aPL testing was not available at our institution, so samples were sent to ARUP laboratories (“Non-Criteria Antiphospholipid Syndrome Antibodies Panel” Ref# 2012729) and Mayo Clinic Laboratories (“Anti-Phosphatidylethanolamine Panel” Ref# FPHET). Tests for LAC, aCL, and aβ2GPI were performed in-house using commercially available, Clinical Laboratory Improvement Amendments (CLIA)-certified ELISA kits read on a BioRad BioPlex plate reader (Herculus, CA) in the University of Minnesota Specialty Protein Core Laboratory. LAC testing in the University of Minnesota Specialty Coagulation Laboratory is based on dilute Russel’s Viper Venom test (dRVVT). INR, PTT, and dRVVT tests are conducted and results are reported as a dRVVT normalized ratio. PTT testing and dRVVT reagents were manufactured by Stago (Parsippany, NJ). Normal human plasma was obtained from Precision Biologics (Dallas, TX). Internal QC ranges were re-established with each lot of normal human plasma. Samples with a dRVVT normalized ratio of ≥ 1.21 were considered positive. There are no pediatric-specific controls or age cut-offs in this assay.

Presentation of Cases

Key clinical features of the patients are summarized in Fig. 1A. Seven of the eight patients (88%) were female. The age at time of presentation ranged from 7–17 years (avg. 13.6) and most of the patients (75%) were post-pubertal at the time of presentation. Patients were of diverse racial and ethnic backgrounds and most had a family history of autoimmunity in either a first- or second-degree relative (Fig. 1A). Notable features at the time of NC-aPL testing included dermatologic, vascular, hematologic, and neurologic findings. Rashes were present in half of the patients, including livedoid rash in two patients and non-blanching purpura of the extremities in two others. Most patients had Raynaud’s phenomenon—a common APS-associated manifestation caused by vasospasm of digital arteries [22,23,24]. Neurologic findings included chronic headaches (n = 3), absence seizures (n = 1), and chorea and cerebellar stroke (n = 1; Fig. 1A). Only one patient had a documented thrombotic event (the cerebellar stroke). This patient also had mitral valve thickening and regurgitation, but the stroke was not suspected to be embolic based on MRI appearance. Evaluation for inherited thrombophilia in the patient who had a stroke was negative. One patient with concomitant systemic lupus erythematosus (SLE) developed alveolar hemorrhage and pulmonary hypertension believed to be secondary to pulmonary capillaritis; however, it was unclear if these were manifestations of SLE, NC-aPL, or both.

Fig. 1
figure 1

Clinical characteristics (A), hematologic (B) and rheumatologic (C) laboratory evaluation, and therapies and outcomes (D) observed in patients with NC-aPL. Interpretation key is shown to the right. Ranges of values for complement C3, C4, CH50, and total IgG for each individual patient are shown in cells in (C). Abbreviations: INR: international normalized ratio, PTT: partial thromboplastin time, ANA: antinuclear antibodies, ENA: antibodies to extractable nuclear antigens, dsDNA: anti-double stranded DNA

Laboratory and other diagnostic evaluations (Fig. 1B and C) showed that six of eight patients had anemia, leukopenia, and/or thrombocytopenia. Most patients had abnormal coagulation function (elevated and/or prolonged INR and/or PTT, respectively). Strikingly, while most patients had a positive LAC, 75% had negative aCL and aβ2GPI antibodies. Although the same NC-aPL panel was not sent on all patients, most had seropositivity to anti-PS and/or anti-PS/PT.

Pediatric-specific APS criteria have not yet been clearly established; however, none of the patients in this series met adult classification criteria for APS. Only one patient had a history of thrombosis, which is a requirement in the classification criteria for APS [14]. This patient was treated with the B cell-depleting monoclonal antibody, rituximab, prior to repeating NC-aPL testing; upon re-testing more than 12 weeks later, the originally detected NC-aPL were no longer present. We therefore suspect that treatment with rituximab likely ablated NC-aPL positivity. Even if NC-aPL were currently included in consensus laboratory classification criteria for APS, this patient would not have fulfilled laboratory criteria because the antibodies were not durably detectable (that is, present on at least two occasions, ≥ 12 weeks apart). Infections can commonly cause a transient positivity to aPL. No infectious causes were identified in the case of transient positivity to NC-aPL in this series.

At the time NC-aPL were tested, a clear rheumatic disease was present in five of eight patients. After additional follow-up visits, one additional patient had evolved to demonstrate a clear primary rheumatic disease. The primary rheumatic diseases in these patients included SLE (n = 4), mixed connective tissue disease (n = 1), and Sjogren syndrome (n = 1) (Fig. 1A). Therefore, these six patients were suspected to have NC-aPL secondary to a known rheumatic disease. The other two patients had no discernable primary rheumatic disease associated with the presence of NC-aPL. Most patients had hypergammaglobulinemia and many had hypocomplementemia (Fig. 1C), which was not surprising given the primary rheumatic diseases present in this series of patients. In general, complements C3 and C4 began to increase and total IgG decreased after starting therapies in patients in which these levels were abnormal at the time of presentation and NC-aPL detection (data not shown).

Therapy was primarily directed at treating the underlying rheumatic diseases present in these patients, and a high degree of commonality in the treatments utilized was observed (Fig. 1D). Almost all patients were treated with hydroxychloroquine, a commonly prescribed antimalarial drug with immunomodulatory and antiplatelet effects [25,26,27,28,29,30]. Several patients also received glucocorticoids, mycophenolate, and rituximab. Five of eight patients were treated with conventional antiplatelet drugs, such as aspirin or clopidogrel. No patients were treated with long-term heparin or warfarin, although the former was utilized in select patients when hospitalized with other obvious risk factors for thrombosis (e.g., hemoconcentration, nephrotic range proteinuria, immobilization). Decisions regarding initiation of antiplatelet drugs and/or short-term anticoagulation were made in conjunction with pediatric hematologists. None of the patients in this series has suffered thrombotic or bleeding events after the initiation of therapy; however, the maximum period of observation of any individual patient is 36 months.

Discussion and conclusions

These data suggest that the clinical features associated with NC-aPL positivity in pediatric patients are similar to those seen in patients with positive conventional aPL tests or APS, including livedoid and/or vasculitic rashes, Raynaud’s phenomenon, CNS symptoms (headaches, seizures, strokes, and chorea), cardiac valve inflammation, and cytopenias [6,7,8,9,10,11,12]. While non-thrombotic manifestations that are commonly associated with aPL positivity and APS were seen in this series, thrombosis was notably rare.

NC-aPL positivity in these patients was most commonly observed in association with a well-defined primary rheumatic disease (i.e., NC-aPL positivity was most often presumed to be secondary to a known rheumatic disease). Amongst these diseases, SLE stood out as the most common. As such, many patients exhibited hypergammaglobulinemia, positive anti-nuclear antibodies (ANA), positive anti-double stranded DNA (dsDNA) and/or positivity to extractable nuclear antigens (ENA). However, it is important to point out that pediatric rheumatologists caring for patients either in outpatient clinics or during inpatient consultation identified all the patients in this series. Therefore, this series likely exhibits selection bias for patients with a primary rheumatic disease.

We hypothesize that in comparison to adult patients with NC-aPL or conventional aPL, thrombosis is less likely to be a frequent manifestation in pediatric patients [31]. Studies of developmental hemostasis have demonstrated that the levels of many procoagulant factors (FII, FV, FVII) increase throughout childhood and more so into adolescence after puberty [32,33,34]. Thrombosis risk is an age-dependent phenomenon [35,36,37,38]. We hypothesize that risk of thrombosis secondary to NC-aPL is also likely age-dependent. However, many pediatric/adolescent patients may not yet have had sufficient time to accumulate additional risk factors such as hyper-estrogenic states (e.g., pregnancy, obesity), atherosclerotic cardiovascular disease, peripheral arterial disease, kidney disease, and others. It is therefore important that pediatric rheumatologists recognize the non-thrombotic manifestations of NC-aPL and aPL in addition to assessing a patient’s broader risks for thrombosis.

Our case series further suggests that NC-aPL may be pathogenic and associated with signs and symptoms of APS. Prospective data regarding these autoantibodies and the risk of thrombosis, association with non-thrombotic manifestations of APS, and response to therapy are needed. Pediatric rheumatologists should consider ordering NC-aPL testing when there is strong clinical suspicion for APS and when routine tests for aCL and aβ2GPI are negative, particularly when LAC is positive. A positive LAC is not highly specific. It may suggest the presence of aPL or NC-aPL. However, it may be positive in genetic or acquired deficiencies of factors in the coagulation cascade (FI, FII, FV, FVIII or FX). Similarly, patients with highly elevated levels of FVIII, as can be seen in active SLE or acute infection may have a false negative LAC [39]. Identification of positive NC-aPL should lead to further evaluation to determine if an underlying primary rheumatic disease is also present. Moreover, hematology consultation may be warranted in patients with NC-aPL to consider antiplatelet drugs and/or anticoagulation. Patients with NC-aPL should be educated about thrombosis and its risk factors, and about potential implications associated with the presence of these autoantibodies later in life, especially during pregnancy or if starting estrogen-containing contraceptive agents.

Evidence-based recommendations for the diagnosis and management of pediatric APS with patients with conventional aPL are evolving [40]. However, guidelines for diagnosing APS in pediatric patients based on NC-aPL positivity do not currently exist, nor are there guidelines for how to manage patients with NC-aPL without a history of thrombosis. However, through future prospective studies, guidelines may be developed that are applicable to pediatric patients.

Availability of data and materials

The datasets analyzed during the current study are available from the corresponding author upon reasonable request.



Non-criteria antiphospholipid antibodies


Antiphospholipid antibodies


Antiphospholipid syndrome


Lupus anticoagulant




Anti-β2 glycoprotein I


Systemic lupus erythematosus








Anti-nuclear antibodies


Double stranded DNA


Extractable nuclear antigens


  1. Vreede AP, Bockenstedt PL, Knight JS. Antiphospholipid syndrome: an update for clinicians and scientists. Curr Opin Rheumatol. 2017;29:458–66.

    Article  Google Scholar 

  2. Knight JS, Kanthi Y. Mechanisms of immunothrombosis and vasculopathy in antiphospholipid syndrome. Semin Immunopathol. 2022.

    Article  PubMed  PubMed Central  Google Scholar 

  3. Giannakopoulos B, Krilis SA. The pathogenesis of the antiphospholipid syndrome. N Engl J Med. 2013;368:1033–44.

    Article  CAS  Google Scholar 

  4. Noureldine MHA, Nour-Eldine W, Khamashta MA, Uthman I. Insights into the diagnosis and pathogenesis of the antiphospholipid syndrome. Semin Arthritis Rheum. 2019;48:860–6.

    Article  CAS  Google Scholar 

  5. Lackner KJ, Müller-Calleja N. Pathogenesis of antiphospholipid syndrome: recent insights and emerging concepts. Expert Rev Clin Immunol. 2019;15:199–209.

    Article  CAS  Google Scholar 

  6. Sloan E, Wright T, Zuo Y. Identifying additional risk factors for arterial and venous thrombosis among pediatric antiphospholipid antibodies carriers. Lupus. 2021;30:828–32.

    Article  CAS  Google Scholar 

  7. Francès C, et al. Dermatologic manifestations of the antiphospholipid syndrome: two hundred consecutive cases. Arthritis Rheum. 2005;52:1785–93.

    Article  Google Scholar 

  8. Avcin T, et al. Pediatric antiphospholipid syndrome: clinical and immunologic features of 121 patients in an international registry. Pediatrics. 2008;122:e1100–7.

    Article  Google Scholar 

  9. Leal Rato M, Bandeira M, Romão VC, Aguiar de Sousa D. Neurologic Manifestations of the Antiphospholipid Syndrome - an Update. Curr Neurol Neurosci Rep. 2021;21:41.

    Article  Google Scholar 

  10. Kolitz T, Shiber S, Sharabi I, Winder A, Zandman-Goddard G. Cardiac Manifestations of Antiphospholipid Syndrome With Focus on Its Primary Form. Front Immunol. 2019;10:941.

    Article  CAS  Google Scholar 

  11. Amigo M-C. What do we know about the cardiac valve lesion in the antiphospholipid syndrome (APS)? Lupus. 2014;23:1259–61.

    Article  Google Scholar 

  12. Miyamae T, Kawabe T. Non-criteria manifestations of juvenile antiphospholipid syndrome. J Clin Med. 2021;10(6):1240.

    Article  CAS  Google Scholar 

  13. Abreu MM, et al. The relevance of ‘non-criteria’ clinical manifestations of antiphospholipid syndrome: 14th international congress on antiphospholipid antibodies technical task force report on antiphospholipid syndrome clinical features. Autoimmun Rev. 2015;14:401–14.

    Article  Google Scholar 

  14. Miyakis S, et al. International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS). J Thromb Haemost. 2006;4:295–306.

    Article  CAS  Google Scholar 

  15. Barbhaiya M, et al. Development of a new international antiphospholipid syndrome classification criteria phase i/ii report: generation and reduction of candidate criteria. Arthritis Care Res (Hoboken). 2021;73:1490–501.

    Article  Google Scholar 

  16. Zohoury N, et al. Closing the serological gap in the antiphospholipid syndrome: the value of ‘non-criteria’ antiphospholipid antibodies. J Rheumatol. 2017;44:1597–602.

    Article  CAS  Google Scholar 

  17. Mekinian A, et al. Non-conventional antiphospholipid antibodies in patients with clinical obstetrical APS: Prevalence and treatment efficacy in pregnancies. Semin Arthritis Rheum. 2016;46:232–7.

    Article  Google Scholar 

  18. Truglia S, et al. A monocentric cohort of obstetric seronegative anti-phospholipid syndrome. Front Immunol. 2018;9:1678.

    Article  Google Scholar 

  19. Staub HL, Bertolaccini ML, Khamashta MA. Anti-phosphatidylethanolamine antibody, thromboembolic events and the antiphospholipid syndrome. Autoimmun Rev. 2012;12:230–4.

    Article  CAS  Google Scholar 

  20. Korematsu S, Yamada H, Miyahara H, Ihara K. Increased levels of anti-phosphatidylcholine and anti-phosphatidylethanolamine antibodies in pediatric patients with cerebral infarction. Brain Dev. 2017;39:542–6.

    Article  Google Scholar 

  21. Rodríguez-García V, Ioannou Y, Fernández-Nebro A, Isenberg DA, Giles IP. Examining the prevalence of non-criteria anti-phospholipid antibodies in patients with anti-phospholipid syndrome: a systematic review. Rheumatology (Oxford). 2015;54:2042–50.

    Article  Google Scholar 

  22. Wigley FM, Flavahan NA. Raynaud’s Phenomenon. N Engl J Med. 2016;375:556–65.

    Article  CAS  Google Scholar 

  23. Flavahan NA. A vascular mechanistic approach to understanding Raynaud phenomenon. Nat Rev Rheumatol. 2015;11:146–58.

    Article  Google Scholar 

  24. Herrick AL. The pathogenesis, diagnosis and treatment of Raynaud phenomenon. Nat Rev Rheumatol. 2012;8:469–79.

    Article  CAS  Google Scholar 

  25. Schrezenmeier E, Dörner T. Mechanisms of action of hydroxychloroquine and chloroquine: implications for rheumatology. Nat Rev Rheumatol. 2020;16:155–66.

    Article  CAS  Google Scholar 

  26. Ben-Zvi I, Kivity S, Langevitz P, Shoenfeld Y. Hydroxychloroquine: from malaria to autoimmunity. Clin Rev Allergy Immunol. 2012;42:145–53.

    Article  CAS  Google Scholar 

  27. Babary H, et al. Favorable effects of hydroxychloroquine on serum low density lipid in patients with systemic lupus erythematosus: A systematic review and meta-analysis. Int J Rheum Dis. 2018;21:84–92.

    Article  CAS  Google Scholar 

  28. Espinola RG, Pierangeli SS, Gharavi AE, Harris EN, Ghara AE. Hydroxychloroquine reverses platelet activation induced by human IgG antiphospholipid antibodies. Thromb Haemost. 2002;87:518–22.

    Article  CAS  Google Scholar 

  29. Achuthan S, et al. Hydroxychloroquine’s efficacy as an antiplatelet agent study in healthy volunteers: a proof of concept study. J Cardiovasc Pharmacol Ther. 2015;20:174–80.

    Article  CAS  Google Scholar 

  30. Rand JH, et al. Hydroxychloroquine directly reduces the binding of antiphospholipid antibody-beta2-glycoprotein I complexes to phospholipid bilayers. Blood. 2008;112:1687–95.

    Article  CAS  Google Scholar 

  31. Torres-Jimenez A-R, et al. Primary antiphospholipid syndrome in pediatrics: beyond thrombosis report of 32 cases and review of the evidence. Pediatr Rheumatol Online J. 2022;20:13.

    Article  Google Scholar 

  32. Jaffray J, Young G. Developmental hemostasis: clinical implications from the fetus to the adolescent. Pediatr Clin North Am. 2013;60:1407–17.

    Article  Google Scholar 

  33. Kuhle S, Male C, Mitchell L. Developmental hemostasis: pro- and anticoagulant systems during childhood. Semin Thromb Hemost. 2003;29:329–38.

    Article  CAS  Google Scholar 

  34. Rumsey DG, Myones B, Massicotte P. Diagnosis and treatment of antiphospholipid syndrome in childhood: a review. Blood Cells Mol Dis. 2017;67:34–40.

    Article  CAS  Google Scholar 

  35. Deitelzweig SB, Johnson BH, Lin J, Schulman KL. Prevalence of clinical venous thromboembolism in the USA: current trends and future projections. Am J Hematol. 2011;86:217–20.

    Article  CAS  Google Scholar 

  36. Montagnana M, Favaloro EJ, Franchini M, Guidi GC, Lippi G. The role of ethnicity, age and gender in venous thromboembolism. J Thromb Thrombolysis. 2010;29:489–96.

    Article  Google Scholar 

  37. White RH. The epidemiology of venous thromboembolism. Circulation. 2003;107:I4-8.

    Article  Google Scholar 

  38. Previtali E, Bucciarelli P, Passamonti SM, Martinelli I. Risk factors for venous and arterial thrombosis. Blood Transfus. 2011;9:120–38.

    PubMed  PubMed Central  Google Scholar 

  39. Nakashima MO, Rogers HJ. Hypercoagulable states: an algorithmic approach to laboratory testing and update on monitoring of direct oral anticoagulants. Blood Res. 2014;49:85–94.

    Article  CAS  Google Scholar 

  40. Groot N, et al. European evidence-based recommendations for diagnosis and treatment of paediatric antiphospholipid syndrome: the SHARE initiative. Ann Rheum Dis. 2017;76:1637–41.

    Article  CAS  Google Scholar 

Download references


The authors wish to thank Sara Kramer, MPH, Clinical Research Coordinator in the Department of Pediatrics at the University of Minnesota, for her assistance with submitting the study for IRB review.


No honorarium, grant, or other form of payment was given to anyone to produce this manuscript.

Author information

Authors and Affiliations



Dr. Mahmud conceptualized and designed the study, drafted the initial manuscript, and reviewed and revised the manuscript. Drs. Bullock, Correll, Hobday, Riskalla, and Vehe collected data and reviewed and revised the manuscript. Dr. Binstadt coordinated and supervised data collection and critically reviewed the manuscript. All authors approved the final manuscript as submitted and agree to be accountable for all aspects of the work.

Corresponding author

Correspondence to Bryce A. Binstadt.

Ethics declarations

Ethics approval and consent to participate

Institutional Review Board oversight was provided by the University of Minnesota (STUDY00011855). The current study was deemed exempt from official review.

Consent for publication

Not applicable.

Competing interests

There are no conflicts of interest.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Mahmud, S.A., Bullock, D.R., Correll, C.K. et al. Non-criteria antiphospholipid antibodies and pediatric rheumatic disease: a case series. Pediatr Rheumatol 20, 70 (2022).

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: