title: Treatment with biologic agents improves the prognosis of patients with rheumatoid arthritis and amyloidosis.
abstract: OBJECTIVE
  Reactive amyloid A (AA) amyloidosis is a serious and life-threatening systemic complication of rheumatoid arthritis (RA). We evaluated the safety of therapy with anti-tumor necrosis factor and anti-interleukin 6 biologic agents in RA patients with reactive AA amyloidosis, together with prognosis and hemodialysis (HD)-free survival, in comparison with patients with AA amyloidosis without such therapy.
  
  
  METHODS
  One hundred thirty-three patients with an established diagnosis of reactive AA amyloidosis participated in the study. Clinical data were assessed from patient records at the time of amyloid detection and administration of biologics. Survival was calculated from the date when amyloid was first demonstrated histologically or the date when biologic therapy was started until the time of death or to the end of 2010 for surviving patients. Patients who had started HD were selected for inclusion only after the presence of amyloid was demonstrated.
  
  
  RESULTS
  Fifty-three patients were treated with biologic agents (biologic group) and 80 were not (nonbiologic group). Survival rate was significantly higher in the biologic group than in the nonbiologic group. Nine patients in the biologics group and 33 in the nonbiologic group started HD. Biologic therapy had a tendency for reduced risk of initiation of HD without any statistical significance.
  
  
  CONCLUSIONS
  Patients with amyloidosis have a higher mortality rate, but the use of biologic agents can reduce risk of death. The use of biologics may not significantly influence the HD-free survival rate.
authors.affiliation: Niigata University Health Administration Center; Department of Health and Nutrition, Faculty of Human Life Studies, University of Niigata Prefecture, Japan. kurodat@med.niigata-u.ac.jp
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kuroda
authors.forename: Naohito
authors.initials: N
authors.lastname: Tanabe
authors.forename: Daisuke
authors.initials: D
authors.lastname: Kobayashi
authors.forename: Hiroe
authors.initials: H
authors.lastname: Sato
authors.forename: Yoko
authors.initials: Y
authors.lastname: Wada
authors.forename: Shuichi
authors.initials: S
authors.lastname: Murakami
authors.forename: Takako
authors.initials: T
authors.lastname: Saeki
authors.forename: Masaaki
authors.initials: M
authors.lastname: Nakano
authors.forename: Ichiei
authors.initials: I
authors.lastname: Narita
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000686:Amyloidosis / Q000188:drug therapy* / Q000401:mortality; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000401:mortality; D001688:Biological Products / Q000627:therapeutic use*; D002648:Child; D005260:Female; D006801:Humans; D008727:Methotrexate / Q000627:therapeutic use; D008875:Middle Aged; D011379:Prognosis; D000685:Serum Amyloid A Protein / Q000032:analysis; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D055815:Young Adult; D000093242:Interleukin-6 Inhibitors; D015850:Interleukin-6
chemical_list: D018501:Antirheumatic Agents; D001688:Biological Products; D008727:Methotrexate; D000685:Serum Amyloid A Protein; D014409:Tumor Necrosis Factor-alpha; D000093242:Interleukin-6 Inhibitors; C508600:IL6 protein, human; D015850:Interleukin-6