title: High-density lipoprotein inversely relates to its specific autoantibody favoring oxidation in thrombotic primary antiphospholipid syndrome.
abstract: Abnormalities of the lipid profile partly explain the atherogenic tendency of systemic lupus erythematosus but the picture is unclear in thrombotic primary antiphospholipid syndrome (PAPS). Herein we compare the lipid profile, high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol (CHO), apolipoprotein A (ApoA-I), apolipoprotein B (ApoB), triglycerides (TRY)), anti-lipoprotein antibodies, beta-2-glycoprotein I complexed to oxidized low-density lipoprotein (oxLDL-ss(2)GPI) and C-reactive protein (CRP) from thrombotic PAPS (n = 34), thrombotic patients with inherited thrombophilia (IT; n = 36), subjects persistently positive for antiphospholipid antibodies (aPL, n = 18) with no underlying autoimmune or non-autoimmune disorders and healthy controls (n = 28) and determined the reciprocal effects of anti-lipoprotein antibodies, the lipid profile, oxLDL-ss(2)GPI and CRP. Average concentrations of HDL (p < 0.0001), LDL (p < 0.0001), CHO (p = 0.0002), ApoA-I (p = 0.002) were lower in PAPS whereas average TRY was higher (p = 0.01) than other groups. Moreover, the aPL and PAPS group showed higher levels of IgG anti-HDL (p = 0.01) and IgG anti-ApoA-I (p < 0.0001) whereas the PAPS group showed greater average oxLDL-ss(2)GPI (p = 0.001) and CRP (p = 0.003). Within the PAPS group, IgG anti-HDL correlated negatively to HDL (p = 0.004) and was an independent predictor of oxLDL-ss2GPI (p = 0.009). HDL and ApoA-I correlated negatively with CRP (p = 0.001 and p = 0.007, respectively). IgG anti-HDL may hamper the antioxidant and anti-inflammatory effect of HDL favoring low-grade inflammation and enhanced oxidation in thrombotic PAPS.
authors.affiliation: Rheumatology and Haematology, Airedale District General Hospital, Steeton, UK. paxmes@aol.com
authors.forename: P R J
authors.initials: PR
authors.lastname: Ames
authors.forename: E
authors.initials: E
authors.lastname: Matsuura
authors.forename: J R
authors.initials: JR
authors.lastname: Batuca
authors.forename: A
authors.initials: A
authors.lastname: Ciampa
authors.forename: L L
authors.initials: LL
authors.lastname: Lopez
authors.forename: F
authors.initials: F
authors.lastname: Ferrara
authors.forename: L
authors.initials: L
authors.lastname: Iannaccone
authors.forename: J Delgado
authors.initials: JD
authors.lastname: Alves
mesh_terms: D000328:Adult; D016736:Antiphospholipid Syndrome / Q000097:blood* / Q000276:immunology*; D016632:Apolipoprotein A-I / Q000378:metabolism; D001323:Autoantibodies / Q000097:blood* / Q000276:immunology; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood* / Q000276:immunology; D008077:Lipoproteins, LDL / Q000097:blood / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D013927:Thrombosis / Q000378:metabolism*; D055815:Young Adult
chemical_list: D016632:Apolipoprotein A-I; D001323:Autoantibodies; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D002097:C-Reactive Protein