Tanaz A Kermani1, David Cuthbertson1, Simon Carette1, Gary S Hoffman1, Nader A Khalidi1, Curry L Koening1, Carol A Langford1, Kathleen McKinnon-Maksimowicz1, Carol A McAlear1, Paul A Monach1, Philip Seo1, Kenneth J Warrington1, Steven R Ytterberg1, Peter A Merkel1, Eric L Matteson1. 1. From the Division of Rheumatology, University of California, Los Angeles, Los Angeles, California; Department of Biostatistics, University of South Florida, Tampa, Florida, USA; Division of Rheumatology, Mount Sinai Hospital, Toronto, Ontario, Canada; Center for Vasculitis Care and Research, Cleveland Clinic, Cleveland, Ohio, USA; Division of Rheumatology, St. Joseph's Healthcare, McMaster University, Hamilton, Ontario, Canada; Division of Rheumatology, University of Utah, Salt Lake City, Utah; Division of Rheumatology, University of Pittsburgh, Pittsburgh, Pennsylvania; Division of Rheumatology and Clinical Immunology, University of Pennsylvania, Philadelphia, Pennsylvania; The Vasculitis Center, Section of Rheumatology, and the Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts; Division of Rheumatology, Johns Hopkins University, Baltimore, Maryland; Division of Rheumatology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.T.A. Kermani, MD, MS, Division of Rheumatology, University of California, Los Angeles; D. Cuthbertson, MS, Department of Biostatistics, University of South Florida; S. Carette, MD, FRCPC, Division of Rheumatology, Mount Sinai Hospital; G.S. Hoffman, MD, MS, Center for Vasculitis Care and Research, Cleveland Clinic; N.A. Khalidi, MD, FRCPC, Division of Rheumatology, St. Joseph's Healthcare, McMaster University; C.L. Koening, MD, MS, Division of Rheumatology, University of Utah; C.A. Langford, MD, MHS, Center for Vasculitis Care and Research, Cleveland Clinic; K. McKinnon-Maksimowicz, DO, Division of Rheumatology, University of Pittsburgh; C.A. McAlear, MA, Division of Rheumatology and Clinical Immunology, University of Pennsylvania; P.A. Monach, MD, PhD, The Vasculitis Center, Section of Rheumatology, and the Clinical Epidemiology Unit, Boston University School of Medicine; P. Seo, MD, MHS, Division of Rheumatology, Johns Hopkins University; K.J. Warrington, MD, Division of Rheumatology, Mayo Clinic
Abstract
OBJECTIVE: To evaluate the performance of the Birmingham Vasculitis Activity Score (BVAS) in the assessment of disease activity in giant cell arteritis (GCA). METHODS: Patients with GCA enrolled in a prospective, multicenter, longitudinal study with symptoms of active vasculitis during any visit were included. Spearman's rank correlation was used to explore the association of the BVAS with other measures of disease activity. RESULTS: During a mean (SD) followup of 2.3 (1.6) years, symptoms of active GCA were present in 236 visits in 136 subjects (100 female, 74%). Median (range) BVAS1 (new/worse symptoms) was 1 (0-10) and median (range) BVAS2 (persistent symptoms) was 0 (0-5). Median (range) physician's global assessment (PGA) was 4 (0-9) for disease activity in the past 28 days and 2 (0-9) for activity on the day of the visit. Important ischemic manifestations of active vasculitis not recorded by the BVAS included tongue/jaw claudication (27%), upper extremity claudication (15%), lower extremity claudication (5%), carotidynia (7%), and ischemic retinopathy (5%). During 25 visits (11%) with active disease, all symptoms of active vasculitis were placed in the "Other" category yet still resulted in a BVAS1 and BVAS2 of 0. BVAS1 moderately correlated with PGA for the past 28 days (Spearman's correlation 0.50) and physician-rated disease activity for the past 28 days (Spearman's correlation 0.46). CONCLUSION: The BVAS has limited utility in GCA. Patients with active GCA can have a BVAS of 0. Many important ischemic symptoms attributable to active vasculitis are not included in the composite score.
OBJECTIVE: To evaluate the performance of the Birmingham Vasculitis Activity Score (BVAS) in the assessment of disease activity in giant cell arteritis (GCA). METHODS:Patients with GCA enrolled in a prospective, multicenter, longitudinal study with symptoms of active vasculitis during any visit were included. Spearman's rank correlation was used to explore the association of the BVAS with other measures of disease activity. RESULTS: During a mean (SD) followup of 2.3 (1.6) years, symptoms of active GCA were present in 236 visits in 136 subjects (100 female, 74%). Median (range) BVAS1 (new/worse symptoms) was 1 (0-10) and median (range) BVAS2 (persistent symptoms) was 0 (0-5). Median (range) physician's global assessment (PGA) was 4 (0-9) for disease activity in the past 28 days and 2 (0-9) for activity on the day of the visit. Important ischemic manifestations of active vasculitis not recorded by the BVAS included tongue/jaw claudication (27%), upper extremity claudication (15%), lower extremity claudication (5%), carotidynia (7%), and ischemic retinopathy (5%). During 25 visits (11%) with active disease, all symptoms of active vasculitis were placed in the "Other" category yet still resulted in a BVAS1 and BVAS2 of 0. BVAS1 moderately correlated with PGA for the past 28 days (Spearman's correlation 0.50) and physician-rated disease activity for the past 28 days (Spearman's correlation 0.46). CONCLUSION: The BVAS has limited utility in GCA. Patients with active GCA can have a BVAS of 0. Many important ischemic symptoms attributable to active vasculitis are not included in the composite score.
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