Tanaz A Kermani1, Kenneth J Warrington1, David Cuthbertson1, Simon Carette1, Gary S Hoffman1, Nader A Khalidi1, Curry L Koening1, Carol A Langford1, Kathleen Maksimowicz-McKinnon1, Carol A McAlear1, Paul A Monach1, Philip Seo1, Peter A Merkel1, Steven R Ytterberg. 1. From the Division of Rheumatology, Mayo Clinic College of Medicine, Rochester, Minnesota; 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 and Clinical Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania; The Vasculitis Center, Section of Rheumatology, Boston University School of Medicine, Boston, Massachusetts; Division of Rheumatology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania; Division of Rheumatology, Johns Hopkins University, Baltimore, Maryland; University of California at Los Angeles (UCLA), Los Angeles, California, USA.T.A. Kermani, MD, MS, UCLA; K.J. Warrington, MD, Division of Rheumatology, Mayo Clinic College of Medicine; 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. Maksimowicz-McKinnon, DO, Division of Rheumatology and Clinical Immunology, University of Pittsburgh; C.A. McAlear, MA, The Vasculitis Center, Section of Rheumatology, Boston University School of Medicine, and Division of Rheumatology, University of Pennsylvania School of Medicine; P.A. Monach, MD, PhD, The Vasculitis Center, Section of Rheumatology, Boston University School of Medicine; P. Seo, MD, MHS, Division of Rheumatology, Johns Hopkins University
Abstract
OBJECTIVE: To evaluate the frequency, timing, and clinical features of relapses in giant cell arteritis (GCA). METHODS: Patients with GCA enrolled in a prospective, multicenter, longitudinal study were included in the analysis. Relapse was defined as either new disease activity after a period of remission or worsening disease activity. RESULTS: The study included 128 subjects: 102 women (80%) and 26 men (20%). Mean ± SD age at diagnosis of GCA was 69.9 ± 8.6 years. Mean followup for the cohort was 21.4 ± 13.9 months. Median (interquartile range) duration of disease at study enrollment was 4.6 months (1.2, 16.8). During followup, 59 relapses were observed in 44 patients (34%). Ten patients (8%) experienced 2 or more relapses. The most common symptoms at relapse were headache (42%) and polymyalgia rheumatica (51%), but ischemic (some transient) manifestations (visual symptoms, tongue or jaw claudication, and/or limb claudication) occurred in 29% of relapses (12% cohort). Forty-three relapses (73%) occurred while patients were taking glucocorticoid therapy at a median (range) prednisone dose of 7.5 (0-35) mg. In 21% of relapses, both erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were normal. Among 69 patients enrolled in the cohort with newly diagnosed disease, 24% experienced a first relapse within 12 months after diagnosis. CONCLUSION: Among patients with GCA, relapses are common, often occurring during treatment. ESR and CRP are frequently normal at times of clinical relapse, highlighting the need for better biomarkers to assess disease activity in GCA. There remains a need for effective therapeutic alternatives to glucocorticoids in GCA.
OBJECTIVE: To evaluate the frequency, timing, and clinical features of relapses in giant cell arteritis (GCA). METHODS:Patients with GCA enrolled in a prospective, multicenter, longitudinal study were included in the analysis. Relapse was defined as either new disease activity after a period of remission or worsening disease activity. RESULTS: The study included 128 subjects: 102 women (80%) and 26 men (20%). Mean ± SD age at diagnosis of GCA was 69.9 ± 8.6 years. Mean followup for the cohort was 21.4 ± 13.9 months. Median (interquartile range) duration of disease at study enrollment was 4.6 months (1.2, 16.8). During followup, 59 relapses were observed in 44 patients (34%). Ten patients (8%) experienced 2 or more relapses. The most common symptoms at relapse were headache (42%) and polymyalgia rheumatica (51%), but ischemic (some transient) manifestations (visual symptoms, tongue or jaw claudication, and/or limb claudication) occurred in 29% of relapses (12% cohort). Forty-three relapses (73%) occurred while patients were taking glucocorticoid therapy at a median (range) prednisone dose of 7.5 (0-35) mg. In 21% of relapses, both erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were normal. Among 69 patients enrolled in the cohort with newly diagnosed disease, 24% experienced a first relapse within 12 months after diagnosis. CONCLUSION: Among patients with GCA, relapses are common, often occurring during treatment. ESR and CRP are frequently normal at times of clinical relapse, highlighting the need for better biomarkers to assess disease activity in GCA. There remains a need for effective therapeutic alternatives to glucocorticoids in GCA.
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