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Rheumatology Advance Access originally published online on October 17, 2008
Rheumatology 2008 47(12):1832-1837; doi:10.1093/rheumatology/ken382
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Primary antiphospholipid syndrome: a low-grade auto-inflammatory disease?

P. R. J. Ames1,2, I. Antinolfi3, A. Ciampa4, J. Batuca5, G. Scenna3, L. R. Lopez6, J. Delgado Alves5, L. Iannaccone3 and E. Matsuura7

1Immunoclot Ltd, Leeds, 2Royal Preston Hospital, Preston, UK, 3Coagulation Unit, Cardarelli Hospital, Naples, 4Coagulation Unit, Moscati Hospital, Avellino, Italy, 5Pharmacology Department, New University of Lisbon, Lisbon, Portugal, 6Corgenix Inc., Broomfield, CO, USA and 7Biochemistry Department, University of Okayama, Okayama, Japan.

Correspondence to: P. R. J. Ames, 3 Malden Road, Leeds LS6 4QT, UK. E-mail: paxmes{at}aol.com


  Abstract

Objective. To test the inflammation and immune activation hypothesis in primary thrombotic APS (PAPS) and to identify clinical and laboratory factors related to inflammation and immune activation.

Methods. PAPS (n = 41) patients were compared with patients with inherited thrombophilia (IT, n = 44) and controls (CTR, n = 39). IgG aCL, IgG anti-β2-glycoprotein I (β2GPI), high-sensitivity CRP (hs-CRP), serum amyloid A (SAA), CRP bound to oxidized low-density lipoprotein–β2GPI complex (CRP–oxLDL–β2GPI) (as inflammatory markers) neopterin (NPT), soluble CD14 (sCD14) (as immune activation markers) were measured by ELISA.

Results. After correction for confounders, PAPS showed higher plasma levels of hs-CRP (P = 0.0004), SAA (P < 0.01), CRP–oxLDL–β2GPI (P = 0.0004), NPT (P < 0.0001) and sCD14 (P = 0.007) than IT and CTR. Two regression models were applied to the PAPS group: in the first, IgG aCL and IgG β2GPI were included amongst the independent variables and in the second they were excluded. In the first model, SAA (as the dependent variable) independently related to thrombosis number (P = 0.003); NPT (as the dependent variable) independently related to thrombosis type (arterial, P = 0.03) and number (P = 0.04); sCD14 (as the dependent variable) independently related to IgG β2GPI (P = 0.0001), age (0.001) and arterial thrombosis (P = 0.01); CRP–oxLDL–β2GPI (as the dependent variable) independently related to IgG β2GPI (P = 0.0001). In the second model, sCD14 and NPT independently related to each other (P = 0.002) (this was noted also in the IT group, P < 0.0001) and CRP–oxLDL–β2GPI independently predicted SAA (P = 0.002).

Conclusion. Low-grade inflammation and immune activation occur in thrombotic PAPS and relate to clinical features and aPL levels.

KEY WORDS: Anti-phospholipid syndrome, C-reactive protein, Serum amyloid A, Neopterin, Soluble CD14

Submitted 26 June 2008; revised version accepted 29 August 2008.
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