title: HLA-DRB1 status affects endothelial function in treated patients with rheumatoid arthritis.
abstract: OBJECTIVE
  To examine endothelial function in rheumatoid arthritis patients and to assess whether clinical or genetic factors affect the development of endothelial dysfunction.
  
  
  METHODS
  Fifty-five patients fulfilling the 1987 American College of Rheumatology classification criteria for rheumatoid arthritis were recruited from Hospital Xeral-Calde, Lugo, Spain. Patients were required to have been treated for at least 5 years, including current treatment with one or more disease-modifying antirheumatic drugs. Patients with diabetes mellitus, renal insufficiency, or cardiovascular disease were excluded. Thirty-one age-, sex-, and ethnically matched controls were also studied. Endothelium-dependent (postischemia) and -independent (postnitroglycerin) vasodilatation were measured by brachial ultrasonography. Patients were genotyped for human leukocyte antigen (HLA)-DRB1.
  
  
  RESULTS
  Patients had decreased endothelium-dependent vasodilatation (mean [+/- SD], 3.8% +/- 4.9%) compared with controls (8.0% +/- 4.5%; P <0.001). There were no differences in endothelium-independent vasodilatation. Clinical features were not associated with endothelial dysfunction. Endothelium-dependent vasodilatation was lower in the 30 rheumatoid arthritis patients with the HLA-DRB1*04 shared epitope alleles (2.4% +/- 4.1%) than in the remaining patients (5.5% +/- 5.3%; P = 0.01). Similar results were seen for patients with the HLA-DRB1*0404 shared epitope allele (-0.4% +/- 2.5%) compared with other patients (4.4% +/- 4.9%; P = 0.01).
  
  
  CONCLUSIONS
  Patients with chronically treated rheumatoid arthritis had evidence of endothelial dysfunction, especially those with certain HLA-DRB1 genotypes. If confirmed, our results suggest that HLA-DRB1 status may be a predictor of cardiovascular risk in these patients.
authors.affiliation: Division of Cardiology, Hospital Xeral-Calde, Dr. Ochoa s/n, 27004 Lugo, Spain.
authors.forename: Carlos
authors.initials: C
authors.lastname: Gonzalez-Juanatey
authors.forename: Ana
authors.initials: A
authors.lastname: Testa
authors.forename: Alberto
authors.initials: A
authors.lastname: Garcia-Castelo
authors.forename: Carlos
authors.initials: C
authors.lastname: Garcia-Porrua
authors.forename: Javier
authors.initials: J
authors.lastname: Llorca
authors.forename: Juan
authors.initials: J
authors.lastname: Vidan
authors.forename: Ali H
authors.initials: AH
authors.lastname: Hajeer
authors.forename: William E
authors.initials: WE
authors.lastname: Ollier
authors.forename: Derek L
authors.initials: DL
authors.lastname: Mattey
authors.forename: Miguel A
authors.initials: MA
authors.lastname: Gonzalez-Gay
mesh_terms: D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000235:genetics / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D020022:Genetic Predisposition to Disease; D006684:HLA-DR Antigens; D059811:HLA-DRB1 Chains; D006650:Histocompatibility Testing; D006801:Humans; D008297:Male; D008875:Middle Aged; D014664:Vasodilation
chemical_list: D006684:HLA-DR Antigens; D059811:HLA-DRB1 Chains