Mihir D Wechalekar1, Ophir Vinik1, John H Y Moi1, Francisca Sivera1, Irene A A M van Echteld1, Caroline van Durme1, Louise Falzon1, Claire Bombardier1, Loreto Carmona1, Daniel Aletaha1, Robert B Landewé1, Désirée M F M van der Heijde1, Rachelle Buchbinder1. 1. From the Rheumatology Research Unit, Repatriation General Hospital, Daw Park, South Australia; and Flinders University, Bedford Park, South Australia, Australia; Division of Rheumatology, University of Toronto, Toronto, Ontario, Canada; Department of Rheumatology, The Royal Melbourne Hospital, Melbourne, Australia; Department of Rheumatology, Hospital General Universitario Elda, Alicante, Spain; Rheumatology Department, St. Elisabeth Hospital, Tilburg, The Netherlands; Rheumatology Department, Maastricht University Medical Centre, Maastricht, The Netherlands; and Rheumatology Department, Centre Hospitalier Universitaire, Liège, Belgium; Center for Behavioral Cardiovascular Health, Columbia University Medical Center, New York, NY, USA; Division of Rheumatology and Institute of Health Policy, Management, and Evaluation, University of Toronto; and Toronto General Research Institute, University Health Network; Institute for Work and Health, Mount Sinai Hospital, Toronto, Ontario, Canada; Facultad de Ciencias de la Salud, Universidad Camilo Jose Cela, Madrid, Spain; Internal Medicine, Rheumatology Department, Medical University of Vienna, Vienna, Austria; Department of Clinical Immunology and Rheumatology, Academic Medical Center, Amsterdam, The Netherlands; and Atrium Medical Center; Rheumatology Department, Leiden University Medical Center, Leiden, The Netherlands; Monash Department of Clinical Epidemiology, Cabrini Hospital, Malvern, Victoria, Australia; and Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Malvern, Victoria, Australia.M.D. Wechalekar, MD, FRACP, Rheumatology Unit, Repatriation General Hospital, Daw Park, South Australia, Australia; and Flinders University; O. Vinik, MD, FRCPC, Division of Rheumatology, University of Toronto; J.H.Y. Moi, BPhysio (Hons), MBBS (Hons), FRACP, Rheumatologist, Department of Rheumatology, The Royal Melbourne Hospital, Melbourne, Australia; F. Sivera, MD,
Abstract
OBJECTIVE: To determine the efficacy and safety of glucocorticoids (GC), colchicine, nonsteroidal antiinflammatory drugs (NSAID), interleukin-1 (IL-1) inhibitors, and paracetamol to treat acute gout. METHODS: We searched MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials to September 2011. Randomized controlled trials (RCT) or quasi-RCT in adults with acute gout that compared GC, colchicine, NSAID, IL-1 inhibitors, and paracetamol to no treatment, placebo, another intervention, or combination therapy were included. Two authors independently extracted data and assessed risk of bias. Primary endpoints were pain and adverse events. Data were pooled where appropriate. RESULTS: Twenty-six trials evaluating GC (N = 5), NSAID (N = 21), colchicine (N = 2), and canakinumab (N = 1) were included. No RCT assessed paracetamol or intraarticular (IA) GC. No RCT compared systemic GC with placebo. Moderate quality evidence (3 trials) concluded that systemic GC were as effective as NSAID but safer. Low quality evidence (1 trial) showed that both high- and low-dose colchicine were more effective than placebo, and low-dose colchicine was no different to placebo with respect to safety but safer than high-dose colchicine. Low quality evidence (1 trial) showed no difference between NSAID and placebo with regard to pain or inflammation. No NSAID was superior to another. Moderate quality evidence (1 trial) found that 150 mg canakinumab was more effective than a single dose of intramuscular GC (40 mg triamcinolone) and equally safe. CONCLUSION: GC, NSAID, low-dose colchicine, and canakinumab all effectively treat acute gout. There was insufficient evidence to rank them. Systemic GC appeared safer than NSAID and lower-dose colchicine was safer than higher-dose colchicine.
OBJECTIVE: To determine the efficacy and safety of glucocorticoids (GC), colchicine, nonsteroidal antiinflammatory drugs (NSAID), interleukin-1 (IL-1) inhibitors, and paracetamol to treat acute gout. METHODS: We searched MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials to September 2011. Randomized controlled trials (RCT) or quasi-RCT in adults with acute gout that compared GC, colchicine, NSAID, IL-1 inhibitors, and paracetamol to no treatment, placebo, another intervention, or combination therapy were included. Two authors independently extracted data and assessed risk of bias. Primary endpoints were pain and adverse events. Data were pooled where appropriate. RESULTS: Twenty-six trials evaluating GC (N = 5), NSAID (N = 21), colchicine (N = 2), and canakinumab (N = 1) were included. No RCT assessed paracetamol or intraarticular (IA) GC. No RCT compared systemic GC with placebo. Moderate quality evidence (3 trials) concluded that systemic GC were as effective as NSAID but safer. Low quality evidence (1 trial) showed that both high- and low-dose colchicine were more effective than placebo, and low-dose colchicine was no different to placebo with respect to safety but safer than high-dose colchicine. Low quality evidence (1 trial) showed no difference between NSAID and placebo with regard to pain or inflammation. No NSAID was superior to another. Moderate quality evidence (1 trial) found that 150 mg canakinumab was more effective than a single dose of intramuscular GC (40 mg triamcinolone) and equally safe. CONCLUSION: GC, NSAID, low-dose colchicine, and canakinumab all effectively treat acute gout. There was insufficient evidence to rank them. Systemic GC appeared safer than NSAID and lower-dose colchicine was safer than higher-dose colchicine.
Authors: Viola Klück; Tim L Th A Jansen; Matthijs Janssen; Antoaneta Comarniceanu; Monique Efdé; Isak W Tengesdal; Kiki Schraa; Maartje C P Cleophas; Curtis L Scribner; Damaris B Skouras; Carlo Marchetti; Charles A Dinarello; Leo A B Joosten Journal: Lancet Rheumatol Date: 2020-04-08