QOL Assessment in Rheumatoid Arthritis 839 etes with the natural IL-I ligand for eriod of months but since binding sites.it does not itself induce signal trans. duction after binding.s51 Anakinra is indicated for fits.with the reduction in signs and symptoms and slowing preliminary evidence suggesting the clinical bene. the progression of structural damage in adults with fits of such re-treatment in some patients.0 Ritux imab is indicated for use in exate in adult pati erately to review anak a on severely active RA who ed to one agents squate cluded was a t effects of rituximab plus methotrexate comp re Health Profile as well as changes in productivi- with placebo plus methotrexate in a randomized ty. 51 This review reported that,among the studies clinical trial.HR-QOL outcomes included the HAQ that incorporated the HAQ as an outcome,use of DI,the SF-36 and the Functional Assessment of F).m -Fatigue Scale (FACIT proven lated HR-QOl After weeks o rapy ce These reported clinic ant improv AO-D than those obtained with placebo.The study that change in the placebo g In addition.patients in incorporated the Nottingham Health Profile as an p rep oved sc res on the outcome showed that the improvements in the pain. SF-36 and sig ificant reduction in fatigue as mea energy.physical mobility and emotional reactions sured by FACIT-F.with a mean change from base subs ales obtained at 24 weeks of treatment with line that exceeded the MCID.Patients in the placebo antly greater than with place group had only slight improvements in fatigue and re lated ments SE36 statis cally nong patie 5.5 Rituximab 5.6 Abatacept Despite der strated improvements in clinical Abatacept,another biological DMARD with a L in patients treated with anti many pa are ory no trea ae no t uncom or that b h othe definition of failur to he safe ell t ed and able it has been reported that 25-30%of patients fail to a significant dose-den ndent reduction in disease respond to these agents.o activity in patients with RA.Abatacept is indicat. Rituximab is a genetically engineered,chimeric ed for reducing signs and symptoms of RA.inducing (murine/human)monoclonal antibody with a target major clinical response,inhibiting the progression f structu al damage and improving physical fu s.It is directed inst the CD20 anti rately to severely active R gen fo on the su a sing acept may anti-TNFo denlet lation n a phase mib clinical trial evaluating the efficacy dependent cell-mediated cvtotoxicity and con of abatacept 2 mg/kg and abatacept 10 mg/kg in ment-dependent cytotoxicity.B-cell depletion is combination with methotrexate compared with e 2008 Ads Data loform ation BV.All rights reserved conomics 2008:26 (10) QOL Assessment in Rheumatoid Arthritis 839 competes with the natural IL-1 ligand for receptor sustained over a period of months, but since repopu￾binding sites, it does not itself induce signal trans- lation occurs,[69] multiple courses of therapy may be duction after binding.[55] Anakinra is indicated for required for maintenance of long-term benefits, with the reduction in signs and symptoms and slowing preliminary evidence suggesting the clinical bene￾the progression of structural damage in adults with fits of such re-treatment in some patients.[70] Ritux￾moderately to severely active RA for whom therapy imab is indicated for use in combination with with one or more DMARDs has failed.[55] methotrexate in adult patients with moderately to The effects of anakinra on HR-QOL were recent- severely active RA who have had an inadequate response to one or more anti-TNFα agents.[54] ly reviewed,[64] primarily based on functional out￾comes assessed using the HAQ, although also in- To investigate HR-QOL in patients refractory to cluded was a placebo controlled monotherapy study anti-TNFα therapy, Cohen et al.[71] evaluated the which evaluated HR-QOL using the Nottingham effects of rituximab plus methotrexate compared Health Profile as well as changes in productivi- with placebo plus methotrexate in a randomized ty.[64,65] This review reported that, among the studies clinical trial. HR-QOL outcomes included the HAQ￾that incorporated the HAQ as an outcome, use of DI, the SF-36 and the Functional Assessment of anakinra (compared with placebo) resulted in im- Chronic Illness Therapy-Fatigue Scale (FACIT￾provements in functionally related HR-QOL, as sug- F).[71] After 24 weeks of therapy, patients who re￾gested by both the total HAQ score and individual ceived rituximab reported clinically meaningful and components. These improvements were clinically statistically significant improvements in HAQ-DI relevant and, in general, were significantly greater scores from baseline compared with little or no than those obtained with placebo. The study that change in the placebo group. In addition, patients in incorporated the Nottingham Health Profile as an the rituximab group reported improved scores on the outcome showed that the improvements in the pain, SF-36 and significant reduction in fatigue as mea￾energy, physical mobility and emotional reactions sured by FACIT-F, with a mean change from base￾subscales obtained at 24 weeks of treatment with line that exceeded the MCID. Patients in the placebo anakinra were significantly greater than with place- group had only slight improvements in fatigue and bo.[64,65] A dose-related increase in productivity was lesser, but still statistically significant, improve￾also observed among patients receiving anakinra. ments in SF-36 scores from baseline.[71] 5.5 Rituximab 5.6 Abatacept Despite demonstrated improvements in clinical Abatacept, another biological DMARD with a efficacy and HR-QOL in patients treated with anti- mechanism of action different from the anti-TNFα TNFα therapies, many patients are refractory to agents, is a novel selective T-cell co-stimulation these agents, and treatment failures are not uncom- modulator that blocks the co-stimulatory signal re￾mon. Although the proportion of patients for whom quired for activation of T cells. Abatacept has been therapy fails may depend on the definition of failure, shown to be safe, well tolerated and able to produce it has been reported that 25–30% of patients fail to a significant dose-dependent reduction in disease respond to these agents.[66,67] activity in patients with RA.[72] Abatacept is indicat￾Rituximab is a genetically engineered, chimeric ed for reducing signs and symptoms of RA, inducing (murine/human) monoclonal antibody with a target major clinical response, inhibiting the progression and mechanism of action different from the anti- of structural damage and improving physical func￾TNFα agents. It is directed against the CD20 anti- tion in adults with moderately to severely active RA. gen found on the surface of B cells, and a single Abatacept may be used as monotherapy or concomi￾course of treatment with rituximab results in a rapid, tantly with DMARDs other than anti-TNFα agents.[53] selective and transient depletion of the B-cell popu￾lation via several mechanisms, including antigen- In a phase IIb clinical trial evaluating the efficacy dependent cell-mediated cytotoxicity and comple- of abatacept 2 mg/kg and abatacept 10 mg/kg in ment-dependent cytotoxicity.[68] B-cell depletion is combination with methotrexate compared with © 2008 Adis Data Information BV. All rights reserved. Pharmacoeconomics 2008; 26 (10)