Efficacy of anakinra in bone: comparison to other biologics.
Three biologic therapies significantly slow radiographic progression in active rheumatoid arthritis. This paper compares the effects of anakinra, a recombinant human interleukin-1 receptor antagonist, with those of etanercept and infliximab, two drugs that target tumor necrosis factor-alpha. A Medline search identified controlled clinical trials that included radiographic progression as an endpoint. Anakinra 30 to 150 mg subcutaneously each day for 24 weeks was significantly more effective than placebo in slowing progression of erosion, joint-space narrowing, and total composite scores, as assessed by the Genant method, and erosive joint count, as assessed by the Larsen method. Erosion scores were slowed even further during a 24-week extension. Etanercept 25 mg subcutaneously twice weekly and infliximab 3 to 10 mg/kg intravenously every 4 or 8 weeks also slowed progressive joint damage, but these agents were studied under different study designs, patient populations, and radiographic assessments than those used in the anakinra study. Despite these differences, however, each biologic therapy appeared to slow progressive joint damage. In some studies, control of clinical symptoms did not correlate with slowing of radiographic progression. Agents that block interleukin-1 or tumor necrosis factor-alpha appear similarly effective in slowing radiographic progression in patients with active rheumatoid arthritis. Treatment strategies for this disease may need to consider clinical symptoms, progressive joint damage, and long-term safety effects separately.
Paget
Stephen A
SA
Hospital for Special Surgery, Department of Rheumatic Disease, New York, New York 10021, USA.
D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000473:pathology; D001842:Bone and Bones / Q000187:drug effects* / Q000473:pathology; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D007155:Immunologic Factors / Q000627:therapeutic use*; D000069285:Infliximab; D053590:Interleukin 1 Receptor Antagonist Protein; D007596:Joints / Q000187:drug effects* / Q000473:pathology; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012795:Sialoglycoproteins / Q000627:therapeutic use*
D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; C507763:IL1RN protein, human; D007074:Immunoglobulin G; D007155:Immunologic Factors; D053590:Interleukin 1 Receptor Antagonist Protein; D018124:Receptors, Tumor Necrosis Factor; D012795:Sialoglycoproteins; D000069285:Infliximab; D000068800:Etanercept