title: Treatment with anti–tumor necrosis factor biologic agents in human T lymphotropic virus type I–positive patients with rheumatoid arthritis.
abstract: OBJECTIVE
  To investigate the response to and safety of anti–tumor necrosis factor (anti-TNF) therapy in human T lymphotropic virus type I (HTLV-I)–positive patients with rheumatoid arthritis (RA).
  
  
  METHODS
  Therapeutic response was evaluated in 10 HTLV-I–positive and 20 HTLV-I–negative patients with RA (sex and age matched) at 3 months after the beginning of anti-TNF therapy using the European League Against Rheumatism improvement criteria. As secondary end points, the discontinuation rate of anti-TNF therapy and its safety, especially the development of adult T cell leukemia (ATL), were evaluated over a 2-year period.
  
  
  RESULTS
  Significantly higher baseline levels of C-reactive protein (CRP) were observed in HTLV-I–positive patients than in HTLV-I–negative patients (P = 0.0003). The response rate to anti-TNF therapy was lower in HTLV-I–positive patients than in HTLV-I–negative patients. The median CRP level, erythrocyte sedimentation rate, and Disease Activity Score in 28 joints at 3 months after anti-TNF treatment in HTLV-I–positive patients were significantly higher than in HTLV-I– negative patients (P = 0.003, P = 0.03, and P = 0.003, respectively). The discontinuation rate due to insufficient response was significantly higher in HTLV-I–positive patients than in HTLV-I–negative patients (P = 0.013). During the 2-year observation period, no patients developed ATL.
  
  
  CONCLUSIONS
  These data suggest that HTLV-I–positive patients with RA had higher inflammation and greater resistance to anti-TNF treatment than HTLV-I–negative patients. Further study is necessary to determine whether HTLV-I infection should be measured when anti-TNF agents are administered to patients with RA, especially in areas were HTLV-I is endemic.
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Umekita
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Hidaka
authors.forename: Shunichi
authors.initials: S
authors.lastname: Miyauchi
authors.forename: Shiro
authors.initials: S
authors.lastname: Ueno
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Kubo
authors.forename: Ichiro
authors.initials: I
authors.lastname: Takajo
authors.forename: Yayoi
authors.initials: Y
authors.lastname: Hashiba
authors.forename: Yasufumi
authors.initials: Y
authors.lastname: Kai
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Nagatomo
authors.forename: Akihiko
authors.initials: A
authors.lastname: Okayama
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D001685:Biological Factors / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D015490:HTLV-I Infections / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D015368:Human T-lymphotropic virus 1 / Q000378:metabolism; D006801:Humans; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D001685:Biological Factors; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab