title: Serum paraoxonase activity decreases in rheumatoid arthritis.
abstract: OBJECTIVE
  To estimate the alterations of paraoxonase 1 (PON1) and high-density lipoprotein (HDL) in rheumatoid arthritis (RA).
  
  
  METHODS
  We investigated the serum enzyme activity and concentration of PON1 and their relationship with serum lipids, high-density lipoprotein (HDL) parameters, and acute phase reactants of serum amyloid A (SAA) and C-reactive protein (CRP) in patients with RA.
  
  
  RESULTS
  Serum paraoxonase (PON) activity was significantly decreased in RA patients (n = 64, 131 +/- 53 micro mol/min/L) compared with healthy subjects (n = 155, 164 +/- 59) despite the absence of any difference in serum lipid levels between the two groups. This decrease of serum PON activity in RA patients was found in every genotype (Q/Q, Q/R, R/R) of PON1 at 192 Q/R. There was a different distribution in PON1 Q/R genotypes between RA patients and healthy subjects, and RA patients exhibited less (44%) positive PON1-Q than did the healthy subjects (66%). In a further investigation of age- and gender-matched subgroups of RA (n = 25) and healthy subjects (n = 25), not only serum PON activity, but also lecithin-cholesterol acyltransferase (LCAT) was found to be significantly decreased in RA patients (125 +/- 61 micro mol/min/L, 63.2 +/- 17.2 nmol/ml/hr/37 degrees C) than in healthy subjects (169 +/- 67, 74.7 +/- 19.5), respectively. PON1 and LCAT as well as HDL constituent apolipoprotein (apo) AI and apo AII, were altered significantly in RA patients.
  
  
  CONCLUSIONS
  Acute-phase HDL, which is remodeled structurally and functionally in RA, might be less anti-atherogenic due to the impairment of original HDL function. These alterations of HDL in RA patients may explain in part the reported increase in cardiovascular mortality in patients with RA.
authors.affiliation: Second Department of Internal Medicine, Kochi Medical School, Kohasu Okoh-Cho, Nankoku, Kochi, 783-8505, Japan.
authors.forename: Noriyasu
authors.initials: N
authors.lastname: Tanimoto
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Kumon
authors.forename: Tadashi
authors.initials: T
authors.lastname: Suehiro
authors.forename: Susumu
authors.initials: S
authors.lastname: Ohkubo
authors.forename: Yukio
authors.initials: Y
authors.lastname: Ikeda
authors.forename: Koji
authors.initials: K
authors.lastname: Nishiya
authors.forename: Kozo
authors.initials: K
authors.lastname: Hashimoto
mesh_terms: D000368:Aged; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000235:genetics; D043303:Aryldialkylphosphatase; D002097:C-Reactive Protein / Q000378:metabolism; D004950:Esterases / Q000097:blood*; D005260:Female; D005838:Genotype; D006801:Humans; D008075:Lipoproteins, HDL / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000097:blood; D000685:Serum Amyloid A Protein / Q000378:metabolism
chemical_list: D008075:Lipoproteins, HDL; D000685:Serum Amyloid A Protein; D002097:C-Reactive Protein; D007862:Phosphatidylcholine-Sterol O-Acyltransferase; D004950:Esterases; D043303:Aryldialkylphosphatase; C468406:PON1 protein, human