Biological modifier therapy for the treatment of rheumatoid arthritis.
The recent elucidation of pathogenic processes involving tumor necrosis factor alpha and interleukin-1beta in the pathogenesis and persistence of rheumatoid arthritis led to the development of biological modifier agents that have had significant impact on disease severity and progression. These agents--etanercept, infliximab, and anakinra--produce a dramatic reduction in RA disease activity with relatively low toxicity compared with currently available disease-modifying antirheumatic drugs. The main prohibition to their broader utilization is cost. The success of these agents underscores the investigative approaches to the pathogenesis of RA and the appropriate design of pharmaceutical agents to target specific proinflammatory molecules.
Jenkins
John K
JK
Department of Medicine, University of Mississippi Medical Center, Jackson 39216, USA.
Hardy
Kenneth J
KJ
D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000628:therapy*; D002448:Cell Adhesion; D002465:Cell Movement; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D007155:Immunologic Factors / Q000627:therapeutic use*; D000069285:Infliximab; D053590:Interleukin 1 Receptor Antagonist Protein; 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