title: Humanized anti-interleukin-6-receptor antibody (tocilizumab) monotherapy is more effective in slowing radiographic progression in patients with rheumatoid arthritis at high baseline risk for structural damage evaluated with levels of biomarkers, radiography, and BMI: data from the SAMURAI study.
abstract: Our aim was to assess the ability of tocilizumab monotherapy to reduce progressive structural joint damage in rheumatoid arthritis patients at high risk of progression. This study was a subanalysis from a prospective 1-year, multicenter, X-ray-reader-blinded, randomized controlled trial of tocilizumab [Study of Active Controlled Monotherapy Used for Rheumatoid Arthritis, an IL-6 Inhibitor (SAMURAI) trial]. All patients were categorized into two or three groups according to four independent predictive markers for progressive joint damage [urinary C-terminal crosslinking telopeptide (uCTX-II), urinary pyridinoline/deoxypyridinoline (uPYD/DPD) ratio, body mass index (BMI), and joint-space narrowing (JSN) score at baseline]. One-year progression of joint destruction was assessed in high-risk versus low-risk groups receiving tocilizumab monotherapy and compared with patients receiving conventional disease-modifying antirheumatic drugs (DMARDs) (n = 157 and 145, respectively). In patients at high risk of progression of erosion as estimated by high uCTX-II, uPYD/DPD, or low BMI, and at high risk of progression of JSN as estimated by low BMI or high JSN score, the 52-week changes in radiological erosion and JSN, respectively, were significantly less in patients treated with tocilizumab monotherapy compared with those receiving DMARDs for each type of risk factor. In patients at low risk, those receiving tocilizumab also progressed less than those on DMARDs, although the difference did not reach statistical significance. Tocilizumab monotherapy is more effective in reducing radiological progression in patients presenting with risk factors for rapid progression than in low-risk patients. Patients at high risk for progression may benefit more from tocilizumab treatment.
authors.affiliation: Osaka University Graduate School of Medicine, Osaka, Japan.
authors.forename: Jun
authors.initials: J
authors.lastname: Hashimoto
authors.forename: Patrick
authors.initials: P
authors.lastname: Garnero
authors.forename: Désirée
authors.initials: D
authors.lastname: van der Heijde
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Miyasaka
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Yamamoto
authors.forename: Shinichi
authors.initials: S
authors.lastname: Kawai
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Takeuchi
authors.forename: Hideki
authors.initials: H
authors.lastname: Yoshikawa
authors.forename: Norihiro
authors.initials: N
authors.lastname: Nishimoto
mesh_terms: D000596:Amino Acids / Q000652:urine; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000473:pathology / Q000652:urine; D015415:Biomarkers / Q000652:urine; D015992:Body Mass Index; D024042:Collagen Type I / Q000652:urine; D018450:Disease Progression; D006801:Humans; D007596:Joints / Q000473:pathology; D010455:Peptides / Q000652:urine; D011446:Prospective Studies; D016896:Treatment Outcome
chemical_list: D000596:Amino Acids; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D015415:Biomarkers; D024042:Collagen Type I; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide; C015484:pyridinoline; C036020:deoxypyridinoline; C502936:tocilizumab