EditorialTNFα antagonists in rheumatoid arthritis patients seen in everyday practice
Section snippets
Effectiveness of TNFα antagonist therapy
TNFα antagonist therapy was effective in numerous clinical trials in patients with recent-onset or established RA. Although no comparative studies have been published to date, the three currently available TNFα antagonists seem similar in terms of efficacy, with response rates of 55%–80% for ACR20, 45%–65% for ACR50, and 35%–40% for ACR70 [2], [3], [4]. The results are best when the TNFα antagonist is combined with another drug, chiefly methotrexate. Although 40% of patients can expect to
Reasons for TNFα antagonist therapy discontinuation
Lack of efficacy and side effects explain similar proportions of treatment discontinuation [17], about 10%–30% for each. The remaining third is ascribable to financial reasons and to personal preferences of patients and physicians. Among RA patients who were switched to a second TNFα antagonist for lack of efficacy or toxicity, the hazards ratio of discontinuing the second drug for the same reason as the first was about 2 [18]. On the other hand, etanercept continuation rates were higher in
Side effects
The risk of infection is increased about twofold in RA patients overall and increases further with TNFα antagonist therapy [20]. In clinical therapeutic trials, the risk of infection was slightly higher with anti-TNFα antibodies given in combination with methotrexate, with about 5–6.5 serious infections/patient-year. The main reason for combining methotrexate with TNFα antagonist therapy is that efficacy is greater with combination therapy. In observational cohorts, the risk increase was
Dosage adjustment and treatment continuation
An important question is whether TNFα antagonist therapy reduces glucocorticoid requirements and/or the overall cost of RA management. Study reports have supplied little information on a possible glucocorticoid-sparing effect. The methotrexate–etanercept combination may decrease glucocorticoid requirements, perhaps at the expense of greater NSAID use [28]. Decreasing the etanercept dosage may diminish the cost of treatment and reduce side effects. Overall, the cost of TNFα antagonist treatment
Future limitations
The high prevalence of infection with the hepatitis B and C viruses requires routine screening, as chronic carriers may be at risk for reactivation after the introduction of TNFα antagonist therapy [30]. Administration of an antiviral drug such as lamivudine may reduce the risk of reactivation. Other viral infections (e.g., herpes) may be increased and require specific surveillance.
In patients who want to become pregnant, TNFα antagonist therapy should be stopped, as proof of safety for the
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Cited by (22)
Associations of vitamin D receptor gene polymorphisms FokI and BsmI with susceptibility to rheumatoid arthritis and Behçet's disease in Tunisians
2012, Joint Bone SpineCitation Excerpt :The Th1 phenotype is associated with inflammation, whereas the Th2 phenotype tends to have antiinflammatory effects. The pathogenesis of RA rests on a dual hierarchy of proinflammatory factors and autoimmunity involving both Th1 cells and the proinflammatory cytokine TNFα [6,7]. An excess of proinflammatory cytokines with a relative deficiency in antiinflammatory cytokines creates a Th1-Th2 imbalance, which is a characteristic of many autoimmune diseases (known as Th1 diseases) including RA, diabetes mellitus, and Behçet's disease (BD).
Study of the association of FokI and BsmI vitamin D receptor gene polymorphisms with the susceptibility to rheumatoid arthritis and Behcet disease in the Tunisian population
2012, Revue du Rhumatisme (Edition Francaise)Outcome and safety of TNFα antagonist therapy in 475 consecutive outpatients (with rheumatoid arthritis or spondyloarthropathies) treated by a single physician according to their eligibility for clinical trials
2010, Joint Bone SpineCitation Excerpt :Therefore, the effectiveness analysis included 435 patients. Effectiveness [1] was assessed semi-quantitatively [23], given the retrospective study design and fluctuations in RA and SpA activity in individual patients [24,25]. The data in correspondence to the patients’ usual physicians were used to classify patients into four subgroups, as follows: very good response (DAS28-ESR usually less than 3.2 and BASDAI usually improved by more than 60% or less than 2.0); satisfactory response (DAS28-ESR usually between 3.2 and 4.0 and BASDAI usually improved by more than 30% or lower than 4.0); fair response (DAS28-ESR between 4.0 and 5.1 and BASDAI usually improved by less than 30% or between 4.0 and 5.0); and failure (DAS28-ESR usually unchanged or greater than 5.1 and BASDAI usually unchanged or worsened).
Regulatory T cells (Treg) in rheumatoid arthritis
2009, Joint Bone SpineCitation Excerpt :Under this hypothesis, targeted treatments act predominantly or secondarily via indirect effects on Treg cells. Variations in the efficacy of targeted treatments may be related in part to the Treg status of the patients, which remains to be determined [30]. Activation or reactivation of Treg cells in patients with RA may restore the balance of the immune response and halt the inflammatory process, thereby preventing further disease.
Regulatory T-cells (Treg) in rheumatoid arthritis
2009, Revue du Rhumatisme (Edition Francaise)