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

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Rheumatology Advance Access published online on October 17, 2008

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

P. R. J. Ames1,2, I. Antinolfi3, A. Ciampa4, J. Batuca5, G. Scenna3,

L. R. 6, 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.

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-¦Â2-glycoprotein I (¦Â2GPI), high-sensitivity CRP

(hs-CRP), serum amyloid A (SAA), CRP bound to oxidized low-density

lipoprotein¨C¦Â2GPI complex (CRP¨LDL¨C¦Â2GPI) (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¨LDL¨C¦Â2GPI (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 ¦Â2GPI 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 ¦Â2GPI (P =

0.0001), age (0.001) and arterial thrombosis (P = 0.01);

CRP¨LDL¨C¦Â2GPI (as the dependent variable) independently related to

IgG ¦Â2GPI (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¨LDL¨C¦Â2GPI 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.

http://rheumatology.oxfordjournals.org/cgi/content/abstract/ken382v1?papetoc

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