title: The impact of new biologicals in the treatment of rheumatoid arthritis.
abstract: The past decade has seen a shift in the paradigm for RA management. DMARDs have been introduced at earlier stages of disease in an effort to slow or stop radiographic disease progression before irreversible joint damage, work disability, functional decline and other adverse outcomes are seen. Although often effective, DMARDs have been limited in treatment durability over the long term due to side-effects and declining efficacy. Combination regimens, often involving weekly methotrexate as the anchor drug, have been used increasingly to overcome the limitations of DMARD monotherapy. The advent of biological therapies that specifically target key proinflammatory cytokines, believed to be important in disease pathogenesis, provides several new treatment options. In controlled clinical trials, the IL-1 blocker anakinra (r-metHuIL-1ra) significantly reduced the clinical signs and symptoms of RA when used alone or in combination with weekly methotrexate. The TNF inhibitors etanercept, infliximab and adalimumab have shown similar efficacy; indeed, higher response rates for clinical and radiological parameters have been seen with the TNF blockers. Importantly, each of these biological response modifiers significantly reduced radiographic disease progression in 6- to 12-month studies, and some radiographic data extend to 24 months. Despite these promising findings, it remains to be determined whether slowing radiographic progression will translate into significant improvements in long-term outcomes.
authors.affiliation: University of Nebraska Medical Center, Omaha, NE, USA. weaver2a@tds.net
authors.forename: A L
authors.initials: AL
authors.lastname: Weaver
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000000981:diagnostic imaging / Q000188:drug therapy*; D001175:Arthrography; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D007155:Immunologic Factors / Q000627:therapeutic use*; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D000069285:Infliximab; D053590:Interleukin 1 Receptor Antagonist Protein; D008727:Methotrexate / Q000627:therapeutic use; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012795:Sialoglycoproteins / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; C507763:IL1RN protein, human; D007074:Immunoglobulin G; D007155:Immunologic Factors; D007166:Immunosuppressive Agents; D053590:Interleukin 1 Receptor Antagonist Protein; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068800:Etanercept; D008727:Methotrexate