title: The APOM polymorphism as a novel risk factor for dyslipidaemia in rheumatoid arthritis: a possible shared link between disease susceptibility and dyslipidaemia.
abstract: OBJECTIVE
  A decrease in high-density lipoprotein (HDL) cholesterol during inflammation is common in many rheumatologic diseases, including rheumatoid arthritis (RA). Apolipoprotein M (apoM) is an apolipoprotein predominantly associated with HDL cholesterol. Recently, apoM polymorphisms have been related with RA susceptibility. We investigated the possible association between an APOM polymorphism and dyslipidaemia in Korean RA patients.
  
  
  METHODS
  Two hundred and fifteen RA patients and 215 controls that provided complete genotyping were included. Genetic distribution, RA-associated phenotype, lipid profiles, and lipoproteins were evaluated.
  
  
  RESULTS
  RA patients had increased frequencies of the APOM C-1065A A allele compared to the controls. RA patients with A/A genotypes had lower levels of HDL cholesterol than those with C/C genotypes. After adjustment for confounding factors, the A/A genotype was a risk factor for low HDL cholesterolaemia (OR=1.070, p=0.001). Subgroup analyses according to disease activity showed that the association between APOM genotype and HDL cholesterol levels was still significant in all subgroups, indicating that this APOM polymorphism may increase the dyslipidaemia risk, independently of RA disease activity.
  
  
  CONCLUSIONS
  These data support that the APOM C-1065A polymorphism is associated with increased risk for developing RA and dyslipidaemia in RA patients. Reduced HDL cholesterol levels are independent of disease activity but are significantly influenced by APOM genotype. These findings suggest that a specific genetic factor for RA could be linked to dyslipidaemia and this could increase the risk of atherosclerosis in RA patients.
authors.affiliation: Department of Internal Medicine, The Catholic University of Korea, Korea.
authors.forename: Yune-Jung
authors.initials: YJ
authors.lastname: Park
authors.forename: Seung-Ah
authors.initials: SA
authors.lastname: Yoo
authors.forename: Jeong-Hwa
authors.initials: JH
authors.lastname: Lee
authors.forename: Yeun-Jun
authors.initials: YJ
authors.lastname: Chung
authors.forename: Chul-Soo
authors.initials: CS
authors.lastname: Cho
authors.forename: Wan -Uk
authors.initials: W-
authors.lastname: Kim
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D001053:Apolipoproteins / Q000235:genetics*; D000075243:Apolipoproteins M; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000235:genetics*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D008076:Cholesterol, HDL / Q000097:blood; D003430:Cross-Sectional Studies; D050171:Dyslipidemias / Q000097:blood / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006801:Humans; D054834:Lipocalins / Q000235:genetics*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D010641:Phenotype; D011110:Polymorphism, Genetic; D056910:Republic of Korea; D018570:Risk Assessment; D012307:Risk Factors
chemical_list: C400523:APOM protein, human; D001053:Apolipoproteins; D000075243:Apolipoproteins M; D015415:Biomarkers; D008076:Cholesterol, HDL; D054834:Lipocalins