Désirée van der Heijde1,2, Dafna D Gladman3,4, Oliver FitzGerald3,4, Arthur Kavanaugh3,4, Daniela Graham3,4, Cunshan Wang3,4, Lara Fallon3,4. 1. From the Department of Rheumatology, Leiden University Medical Center, Leiden, the Netherlands; Department of Rheumatology, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada; Department of Rheumatology, St. Vincent's University Hospital, Dublin, Ireland; Division of Rheumatology, Allergy, and Immunology, University of California, San Diego School of Medicine, La Jolla, San Diego, California, USA; Pfizer Inc., Groton, Connecticut, USA; Pfizer Inc., Montreal, Quebec, Canada. mail@dvanderheijde.nl. 2. D. van der Heijde, MD, Department of Rheumatology, Leiden University Medical Center; D.D. Gladman, MD, Department of Rheumatology, University of Toronto, Toronto Western Hospital; O. FitzGerald, MD, Department of Rheumatology, St. Vincent's University Hospital; A. Kavanaugh, MD, Division of Rheumatology, Allergy, and Immunology, University of California, San Diego School of Medicine; D. Graham, MD, Pfizer Inc., Groton, Connecticut; C. Wang, PhD, Pfizer Inc., Groton; L. Fallon, PhD, Pfizer Inc., Montreal. mail@dvanderheijde.nl. 3. From the Department of Rheumatology, Leiden University Medical Center, Leiden, the Netherlands; Department of Rheumatology, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada; Department of Rheumatology, St. Vincent's University Hospital, Dublin, Ireland; Division of Rheumatology, Allergy, and Immunology, University of California, San Diego School of Medicine, La Jolla, San Diego, California, USA; Pfizer Inc., Groton, Connecticut, USA; Pfizer Inc., Montreal, Quebec, Canada. 4. D. van der Heijde, MD, Department of Rheumatology, Leiden University Medical Center; D.D. Gladman, MD, Department of Rheumatology, University of Toronto, Toronto Western Hospital; O. FitzGerald, MD, Department of Rheumatology, St. Vincent's University Hospital; A. Kavanaugh, MD, Division of Rheumatology, Allergy, and Immunology, University of California, San Diego School of Medicine; D. Graham, MD, Pfizer Inc., Groton, Connecticut; C. Wang, PhD, Pfizer Inc., Groton; L. Fallon, PhD, Pfizer Inc., Montreal.
Abstract
OBJECTIVE: To evaluate the effect of baseline risk factors on radiographic progression in patients with active psoriatic arthritis (PsA) who had an inadequate response to conventional synthetic disease-modifying antirheumatic drugs (csDMARD) and were treated withtofacitinib or adalimumab (ADA). METHODS:Tofacitinib is an oral Janus kinase inhibitor for the treatment of PsA. OPAL Broaden was a 12-month, double-blind phase III trial. Patients received tofacitinib 5 mg twice daily (BID; n = 107), tofacitinib 10 mg BID (n = 104), or ADA 40 mg once every 2 weeks (n = 106), all with 1 background csDMARD. Radiographs (baseline and Month 12) were scored using the van der Heijde-modified total Sharp score (mTSS) for PsA. Radiographic nonprogression was defined as an increase from baseline in mTSS ≤ 0.5, ≤ 0, or ≤ 0.66. Changes from baseline in mTSS and nonprogression (≤ 0.5 increase from baseline in mTSS) were analyzed by baseline C-reactive protein (CRP) > 2.87 or ≤ 2.87 mg/l. Baseline predictors of radiographic progression were analyzed. RESULTS: At Month 12, > 90% of patients receiving tofacitinib or ADA met all radiographic nonprogression criteria. Mean changes from baseline through Month 12 in mTSS, erosion, and joint space narrowing scores were close to 0. Changes in radiographic outcomes were minimal, irrespective of baseline CRP levels > 2.87 or ≤ 2.87 mg/l, with a small numerical difference observed for tofacitinib 5 mg BID. A significant relationship was observed between baseline CRP level and increases from baseline in mTSS > 0.5 at Month 12. CONCLUSION:Elevated CRP levels at baseline were associated with greater structural progression. Changes in radiographic outcomes were minimal regardless of CRP levels. [Clinical trial registration number (www.ClinicalTrials.gov): NCT01877668].
RCT Entities:
OBJECTIVE: To evaluate the effect of baseline risk factors on radiographic progression in patients with active psoriatic arthritis (PsA) who had an inadequate response to conventional synthetic disease-modifying antirheumatic drugs (csDMARD) and were treated with tofacitinib or adalimumab (ADA). METHODS:Tofacitinib is an oral Janus kinase inhibitor for the treatment of PsA. OPAL Broaden was a 12-month, double-blind phase III trial. Patients received tofacitinib 5 mg twice daily (BID; n = 107), tofacitinib 10 mg BID (n = 104), or ADA 40 mg once every 2 weeks (n = 106), all with 1 background csDMARD. Radiographs (baseline and Month 12) were scored using the van der Heijde-modified total Sharp score (mTSS) for PsA. Radiographic nonprogression was defined as an increase from baseline in mTSS ≤ 0.5, ≤ 0, or ≤ 0.66. Changes from baseline in mTSS and nonprogression (≤ 0.5 increase from baseline in mTSS) were analyzed by baseline C-reactive protein (CRP) > 2.87 or ≤ 2.87 mg/l. Baseline predictors of radiographic progression were analyzed. RESULTS: At Month 12, > 90% of patients receiving tofacitinib or ADA met all radiographic nonprogression criteria. Mean changes from baseline through Month 12 in mTSS, erosion, and joint space narrowing scores were close to 0. Changes in radiographic outcomes were minimal, irrespective of baseline CRP levels > 2.87 or ≤ 2.87 mg/l, with a small numerical difference observed for tofacitinib 5 mg BID. A significant relationship was observed between baseline CRP level and increases from baseline in mTSS > 0.5 at Month 12. CONCLUSION: Elevated CRP levels at baseline were associated with greater structural progression. Changes in radiographic outcomes were minimal regardless of CRP levels. [Clinical trial registration number (www.ClinicalTrials.gov): NCT01877668].
Authors: Sayam Dubash; Oras A Alabas; Xabier Michelena; Leticia Garcia-Montoya; Richard J Wakefield; Philip S Helliwell; Paul Emery; Dennis G McGonagle; Ai Lyn Tan; Helena Marzo-Ortega Journal: Ann Rheum Dis Date: 2021-12-10 Impact factor: 19.103