title: Reduction of oxidative stress marker levels by anti-TNF-alpha antibody, infliximab, in patients with rheumatoid arthritis.
abstract: OBJECTIVE
  The aim of this study was to evaluate the effects of anti-TNF-alpha antibody, infliximab, on oxidative stress markers representing DNA damage, lipid peroxidation, and glycoxidation.
  
  
  METHODS
  Twenty-three RA patients underwent infliximab treatment and were analyzed for 30 weeks. Six patients who experienced side effects and one patient who had a reduced efficacy of infliximab were discontinued the infliximab treatment at 30-54 weeks. Sixteen patients were analyzed for 54 weeks. The levels of serum total, urinary total, and free pentosidine, which is an advanced glycation end-product (AGE), and of urinary 15-Isoprostane F2t and 8-hydroxy-deoxy guanosine (8-OHdG) were determined at baseline and at 14, 30, and 54 weeks after initial treatment with infliximab.
  
  
  RESULTS
  Serum total, urinary total, and free pentosidine levels were reduced at 54 weeks after initial infliximab treatment. Urinary 15-Isoprostane F2t and 8-OHdG levels were also reduced at 14, 30, and 54 weeks. Urinary 8-OHdG levels in RA patients correlated with CRP and the Disease Activity Score of 28 joints.
  
  
  CONCLUSIONS
  In RA patients, infliximab plays an essential role as an anti-oxidative agent against AGE formation, oxidative DNA damage and lipid peroxydation.
authors.affiliation: Department of Orthopaedic Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan. Tsukatonpipi@nifty.com
authors.forename: Y
authors.initials: Y
authors.lastname: Kageyama
authors.forename: M
authors.initials: M
authors.lastname: Takahashi
authors.forename: T
authors.initials: T
authors.lastname: Ichikawa
authors.forename: E
authors.initials: E
authors.lastname: Torikai
authors.forename: A
authors.initials: A
authors.lastname: Nagano
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000911:Antibodies, Monoclonal / Q000494:pharmacology* / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001120:Arginine / Q000031:analogs & derivatives* / Q000032:analysis / Q000097:blood / Q000652:urine; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects; D003849:Deoxyguanosine / Q000031:analogs & derivatives* / Q000652:urine; D005260:Female; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D000069285:Infliximab; D028421:Isoprostanes / Q000652:urine*; D015227:Lipid Peroxidation; D008239:Lysine / Q000031:analogs & derivatives* / Q000032:analysis / Q000097:blood / Q000652:urine; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D017382:Reactive Oxygen Species
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D017127:Glycation End Products, Advanced; D028421:Isoprostanes; D017382:Reactive Oxygen Species; D000080242:8-Hydroxy-2'-Deoxyguanosine; D001120:Arginine; D000069285:Infliximab; C062187:pentosidine; D003849:Deoxyguanosine; D008239:Lysine