title: Effectiveness of etanercept vs cyclophosphamide as treatment for patients with amyloid A amyloidosis secondary to rheumatoid arthritis.
abstract: OBJECTIVE
  To compare the effectiveness of an alkylating agent with that of a biologic agent in the treatment of patients with amyloid A (AA) amyloidosis secondary to RA and to assess the association of the serum AA (SAA) 1.3 allele with treatment.
  
  
  METHODS
  CYC and etanercept (ETN) were administered to 62 and 24 RA patients, respectively, who were confirmed with biopsy as having AA amyloidosis. We evaluated whether the SAA1.3 allele, a factor indicating genetic risk and poor prognosis of Japanese RA patients with AA amyloidosis, influenced treatments and retrospectively analysed the effectiveness of both agents via statistical methods.
  
  
  RESULTS
  Two treatment groups were similar, except for the SAA1.3 genotype (P = 0.015) and duration of AA amyloidosis since diagnosis (P < 0.001). Also, patients given ETN had somewhat worse renal function, i.e. 24-h proteinuria (P = 0.02), at the initiation of treatment. ETN demonstrated greater effectiveness than CYC, as shown by significantly improved levels of serum CRP and serum albumin (both P < 0.01) and estimated glomerular filtration rate (eGFR; P = 0.032). ETN improved survival (P = 0.025), and the hazard ratios for the risk of death endpoint with eGFR and 24-h proteinuria were significant by P = 0.024 and P = 0.025, respectively. The SAA1.3 allele did not affect the response to medications in AA amyloidosis secondary to RA.
  
  
  CONCLUSIONS
  ETN treatment was more effective than CYC treatment, and CRP, albumin and eGFR may be valuable biomarkers for analysis. The SAA1.3 allele was not a factor affecting treatment in Japanese patients with AA amyloidosis secondary to RA.
authors.affiliation: Section of Internal Medicine and Rheumatology, Kumamoto Center for Arthritis and Rheumatology, 1-15-7 Kuhonji, Chuo-ku, Kumamoto 862-0976, Japan. nakamura@souki-kai.or.jp
authors.forename: Tadashi
authors.initials: T
authors.lastname: Nakamura
authors.forename: Syu-Ichi
authors.initials: S
authors.lastname: Higashi
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Tomoda
authors.forename: Michishi
authors.initials: M
authors.lastname: Tsukano
authors.forename: Masahiro
authors.initials: M
authors.lastname: Shono
mesh_terms: D000368:Aged; D000686:Amyloidosis / Q000188:drug therapy* / Q000209:etiology / Q000235:genetics; D001172:Arthritis, Rheumatoid / Q000150:complications*; D002423:Cause of Death; D003520:Cyclophosphamide / Q000627:therapeutic use*; D000068800:Etanercept; D005260:Female; D005838:Genotype; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use*; D007674:Kidney Diseases / Q000188:drug therapy* / Q000209:etiology / Q000235:genetics; D008297:Male; D011110:Polymorphism, Genetic / Q000235:genetics; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D012189:Retrospective Studies; D000685:Serum Amyloid A Protein / Q000235:genetics*; D016896:Treatment Outcome
chemical_list: D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D000685:Serum Amyloid A Protein; D003520:Cyclophosphamide; D000068800:Etanercept