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

P. R J Ames, I. Antinolfi, A. Ciampa, J. Batuca, G. Scenna, L. R. Lopez, J. Delgado Alves, L. Iannaccone, Eiji Matsuura

Research output: Contribution to journalArticle

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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-β2 GPI) (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 β2 GPI (P = 0.0001), age (0.001) and arterial thrombosis (P = 0.01); CRP-oxLDL-β2 GPI (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.

Original languageEnglish
Pages (from-to)1832-1837
Number of pages6
JournalRheumatology
Volume47
Issue number12
DOIs
Publication statusPublished - 2008

Fingerprint

Antiphospholipid Syndrome
Neopterin
Serum Amyloid A Protein
Immunoglobulin G
Glycoproteins
Thrombosis
Inflammation
Thrombophilia
LDL Lipoproteins
Biomarkers
Enzyme-Linked Immunosorbent Assay
oxidized low density lipoprotein

Keywords

  • Anti-phospholipid syndrome
  • C-reactive protein
  • Neopterin
  • Serum amyloid A
  • Soluble CD14

ASJC Scopus subject areas

  • Rheumatology
  • Pharmacology (medical)

Cite this

Ames, P. R. J., Antinolfi, I., Ciampa, A., Batuca, J., Scenna, G., Lopez, L. R., ... Matsuura, E. (2008). Primary antiphospholipid syndrome: A low-grade auto-inflammatory disease? Rheumatology, 47(12), 1832-1837. https://doi.org/10.1093/rheumatology/ken382

Primary antiphospholipid syndrome : A low-grade auto-inflammatory disease? / Ames, P. R J; Antinolfi, I.; Ciampa, A.; Batuca, J.; Scenna, G.; Lopez, L. R.; Delgado Alves, J.; Iannaccone, L.; Matsuura, Eiji.

In: Rheumatology, Vol. 47, No. 12, 2008, p. 1832-1837.

Research output: Contribution to journalArticle

Ames, PRJ, Antinolfi, I, Ciampa, A, Batuca, J, Scenna, G, Lopez, LR, Delgado Alves, J, Iannaccone, L & Matsuura, E 2008, 'Primary antiphospholipid syndrome: A low-grade auto-inflammatory disease?', Rheumatology, vol. 47, no. 12, pp. 1832-1837. https://doi.org/10.1093/rheumatology/ken382
Ames PRJ, Antinolfi I, Ciampa A, Batuca J, Scenna G, Lopez LR et al. Primary antiphospholipid syndrome: A low-grade auto-inflammatory disease? Rheumatology. 2008;47(12):1832-1837. https://doi.org/10.1093/rheumatology/ken382
Ames, P. R J ; Antinolfi, I. ; Ciampa, A. ; Batuca, J. ; Scenna, G. ; Lopez, L. R. ; Delgado Alves, J. ; Iannaccone, L. ; Matsuura, Eiji. / Primary antiphospholipid syndrome : A low-grade auto-inflammatory disease?. In: Rheumatology. 2008 ; Vol. 47, No. 12. pp. 1832-1837.
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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-β2 GPI) (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 β2 GPI (P = 0.0001), age (0.001) and arterial thrombosis (P = 0.01); CRP-oxLDL-β2 GPI (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.",
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T1 - Primary antiphospholipid syndrome

T2 - A low-grade auto-inflammatory disease?

AU - Ames, P. R J

AU - Antinolfi, I.

AU - Ciampa, A.

AU - Batuca, J.

AU - Scenna, G.

AU - Lopez, L. R.

AU - Delgado Alves, J.

AU - Iannaccone, L.

AU - Matsuura, Eiji

PY - 2008

Y1 - 2008

N2 - 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-β2 GPI) (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 β2 GPI (P = 0.0001), age (0.001) and arterial thrombosis (P = 0.01); CRP-oxLDL-β2 GPI (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.

AB - 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-β2 GPI) (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 β2 GPI (P = 0.0001), age (0.001) and arterial thrombosis (P = 0.01); CRP-oxLDL-β2 GPI (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.

KW - Anti-phospholipid syndrome

KW - C-reactive protein

KW - Neopterin

KW - Serum amyloid A

KW - Soluble CD14

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