title: Considerations with the use of biological therapy in the treatment of rheumatoid arthritis.
abstract: The treatment of rheumatoid arthritis (RA) has changed dramatically over the past 15 years with the realisation that earlier, aggressive therapy limits progression. There is evidence that biological response modifiers (BRMs), which target specific cytokines such as TNF-alpha and IL-1, are more effective than traditional disease-modifying antirheumatic drugs (DMARDs), especially in combination with methotrexate. Four therapies are approved for use in RA; three target TNF-alpha (etanercept [Enbrel, Amgen Inc.], infliximab [Remicade, Centocor Inc.], and adalimumab [Humira, Abbott]), and one targets IL-1 (anakinra [Kineret, Amgen Inc.]). It is clear from both the clinical trials and postmarketing reports that all four agents have a different safety profile compared with traditional DMARDs. There are several areas of concern with the use of the BRMs, which include serious and opportunistic infections, malignancy/lymphoma, congestive heart failure, demyelination, injection/infusion reactions, development of autoantibodies and lupus-like disease. It is important to be fully aware of the safety profile and differences between BRMs in order to use them appropriately.
authors.affiliation: University of Texas Southwestern Medical Center, 5939 Harry Hines Boulevard, Suite 400, Dallas, Texas 75235-5360, USA.
authors.forename: Roy M
authors.initials: RM
authors.lastname: Fleischmann
authors.forename: Imran
authors.initials: I
authors.lastname: Iqbal
authors.forename: Richard L
authors.initials: RL
authors.lastname: Stern
mesh_terms: D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000628:therapy*; D001323:Autoantibodies / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology / Q000628:therapy*; D002986:Clinical Trials as Topic; D003131:Combined Modality Therapy; D016207:Cytokines / Q000037:antagonists & inhibitors; D003711:Demyelinating Diseases / Q000139:chemically induced; D018450:Disease Progression; D004359:Drug Therapy, Combination; D004890:Erythema / Q000139:chemically induced; D006333:Heart Failure / Q000150:complications; D006801:Humans; D016867:Immunocompromised Host; D007155:Immunologic Factors / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D007375:Interleukin-1 / Q000037:antagonists & inhibitors; D008727:Methotrexate / Q000008:administration & dosage / Q000627:therapeutic use; D009369:Neoplasms / Q000209:etiology; D009894:Opportunistic Infections / Q000209:etiology; D014376:Tuberculosis / Q000209:etiology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D001323:Autoantibodies; D016207:Cytokines; D007155:Immunologic Factors; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D008727:Methotrexate