title: Detection of Anti-Type II Collagen Antibodies in Patients With Chronic Gouty Arthritis: Findings From a Pilot Study.
abstract: OBJECTIVE
  We hypothesized that chronic gouty arthritis patients would develop an immune response to type II collagen that would be revealed by the presence of anti-type II collagen (CII) antibodies in serum, which may in turn be involved in progression to non-remitting arthritis.
  
  
  METHODS
  Chronic gouty arthritis was defined as crystal-confirmed gout in patients with no pain-free intercritical period, with or without the presence of tophi, who did not have clinical features of other forms of chronic arthritis. Age-matched gout patients suffering acute gouty attacks who had definite intercritical periods were selected as a control group. Four RA patients who had active disease were enrolled as a positive control group. Anti-CII antibodies were quantified in patient sera via ELISA using a human IgG anti-CII antibody assay kit. Correlations between anti-CII levels and clinical parameters were sought.
  
  
  RESULTS
  Fifteen chronic gouty arthritis patients were identified. The anti-CII level was significantly higher among subjects with chronic gout compared to controls, but did not significantly differ in control gout patients during acute attacks and in the intercritical periods. Five patients with chronic gouty arthritis had anti-CII antibody levels higher than 200 AU/mL, whereas only one control gout patient exhibited this feature. Two of four patients with active RA had anti-CII antibody levels higher than 200 U/mL.Patients with tophi had significantly higher anti-CII levels than those without, whereas patients showing radiographic erosion tended to have higher anti-CII levels than those without.
  
  
  CONCLUSIONS
  Patients with chronic gouty arthritis had significantly higher levels of anti-CII antibodies than control gout patients. Such antibody production would be triggered by initiation of cartilage damage but may also play a role in perpetuation of inflammation.
authors.affiliation: From the *Division of Rheumatology, Department of Internal Medicine, Hallym University Sacred Heart Hospital, Anyang; †Division of Rheumatology, Department of Internal Medicine, Ewha Womans University Mokdong Hospital, Seoul; and ‡Division of Rheumatology, Department of Internal Medicine, Gangnam Sacred Heart Hospital, Seoul, Korea.
authors.forename: Hyun Ah
authors.initials: HA
authors.lastname: Kim
authors.forename: Young-Il
authors.initials: YI
authors.lastname: Seo
authors.forename: Jisoo
authors.initials: J
authors.lastname: Lee
authors.forename: Young Ok
authors.initials: YO
authors.lastname: Jung
mesh_terms: D000917:Antibody Formation / Q000276:immunology; D015210:Arthritis, Gouty / Q000276:immunology*; D001323:Autoantibodies / Q000276:immunology*; D002908:Chronic Disease; D024043:Collagen Type II / Q000276:immunology*; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects
chemical_list: D001323:Autoantibodies; D024043:Collagen Type II; D007074:Immunoglobulin G