title: Infection, malignancy, switching, biosimilars, antibody formation, drug survival and withdrawal, and dose reduction: what have we learned over the last year about tumor necrosis factor inhibitors in rheumatoid arthritis?
abstract: OBJECTIVE
  This article reviews the most current studies investigating the use of tumor necrosis factor inhibitors (TNFis) in the treatment of rheumatoid arthritis.
  
  
  RESULTS
  Studies over the past year have clarified that suppressing TNF with monoclonal antibodies does increase infection risk, yet coupled with reduction in disease activity and less use of corticosteroids as a consequence, the overall risk to the population is balanced. With caution (provided by some recent studies) TNFi agents can be reduced (dosage intervals lengthened) and maintain benefit. Biosimilars, not surprisingly, are going to be therapeutically identical to the innovator, and not more of a risk for causing antibodies to interfere with benefit. Uncertainty remains about when and how to make the switch.
  
  
  CONCLUSIONS
  TNFi agents have made their powerful impact on management of patients with rheumatoid arthritis, but questions remain: what is their true infection and malignancy risk in the evolving populations using these drugs today; are we able to maintain their benefit with a reduced schedule (and presumed less cost) and yet recapture their benefit if we guess wrong; are biosimilars just as good, or even better with less cost; are there data to inform us about how to achieve successful switching among different mechanism of action TNFi agents? Finally, are we going to face the specter of cost containment causing change from innovator to biosimilars over which we have no control?
authors.affiliation: Division of Rheumatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
authors.forename: Irina
authors.initials: I
authors.lastname: Ianculescu
authors.forename: Michael H
authors.initials: MH
authors.lastname: Weisman
mesh_terms: D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000378:metabolism / Q000628:therapy; D015551:Autoimmunity; D059451:Biosimilar Pharmaceuticals / Q000494:pharmacology*; D019468:Disease Management; D006801:Humans; D007165:Immunosuppression Therapy / Q000379:methods; D007239:Infections / Q000276:immunology*; D009369:Neoplasms / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D059451:Biosimilar Pharmaceuticals; D014409:Tumor Necrosis Factor-alpha