Rhematoid Arthritis_CME symposium program abstracts and introduction written by Crystal Kaczkowski

An Emerging Therapy for the Effective Treatmentof Rheumatoid Arthritis:

The Evidence for a Selective Co-Stimulation Modulator

FEBRUARY 20, 2006

THE FAIRMONT ACAPULCO PRINCESS

ACAPULCO, MEXICO

Mexican CanadianCongress ofRheumatology

Congreso Mexicano deRheumatologia

Annual Meeting of the CanadianRheumatologyAssociation

1st 34th 61st61st34th1st

A University of AlbertaCME accredited program

Mexican Canadian Congress of Rheumatology

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An Emerging Therapy for the Effective Treatment of Rheumatoid Arthritis:The Evidence for a Selective Co-Stimulation Modulator

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INTRODUCTIONRheumatoid Arthritis (RA) is a debilitating disease that results in significant morbidity,reduced quality of life, and a decreased life span. In recent years, major progress hasbeen made in understanding the immunopathology of RA, leading to the developmentof new therapeutic agents, biologics and non-biologics. Agents such as Disease-Modifying Anti-Rheumatic Drugs (DMARDs) and Tumour Necrosis Factor-α Inhibitorshave proven efficacious for many patients with RA. However, these agents are noteffective in all cases and some patients may experience side effects that can beproblematic. New options are needed for patients who do not benefit sufficiently from,or cannot tolerate, these therapeutics.

The immune system mediators have been targeted in the search for more effectivemanagement strategies, such as the actions of T and B lymphocytes, macrophages, andcytokines. The selective T cell co-stimulation modulator represents an emerging classof biologic agents that decrease the activation of T cells, which are critical to theinitiation and progression of RA. Results of current Phase III clinical trials investigatingthe first of these agents, abatacept, have shown that it is effective, safe, and offersconsiderable improvement in quality of life measures.

The complexity and rapid evolution of this field requires that physicians keep abreastof these new advances in preparation for providing optimal clinical treatment forpatients with RA. In this symposium, respected Canadian and Mexican rheumatologistswill discuss clinical and scientific developments in the evolving management of RA, andexamine the prevailing research related to the emerging role of selective T cellco-stimulation modulation.

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TARGET AUDIENCEThis symposium is intended primarily for rheumatologists from Canada and Mexico andother physicians with an interest in learning more about the pathophysiology,management, and emerging research in the care of patients with rheumatoid arthritis.

EDUCATIONAL OBJECTIVES• Identify the major immunological events underlying the initiation of RA

• Discuss the pivotal role of T cell co-stimulation in the development andperpetuation of RA

• Describe the mechanism of action of co-stimulation modulation

• Evaluate the latest Phase III safety, efficacy, and quality of life data onco-stimulation modulation in RA

ACCREDITATIONThis education event is approved as an AccreditedGroup Learning Activity under Section 1 of theFramework of Continuing Professional Developmentoptions for the Maintenance of Certification Program ofthe Royal College of Physicians and Surgeons of Canada.

FACULTYCarlos Abud-Mendoza, MD (Co-chair)Departmento de Immunologia, Facultad de Medicina Universidad Autónoma de San Luis Potosi (UASLP)Hospital Regional San Luis PotosiSan Luis Potosi, México

Anthony S. Russell, MB, ChB, FRCPC (Co-chair)Division of Rheumatology, Faculty of Medicine, University of AlbertaWalter C. Mackenzie Health Sciences CentreEdmonton, Alberta, Canada

Mario H. Cardiel, MD, MSc (Speaker)Unidad de Investigación, Hospital General “Dr. Miguel Silva”Morelia, Michoacan, México

J. Carter Thorne, MD, FRCPC, FACP (Speaker)Division of Rheumatology, Faculty of Medicine, University of TorontoToronto, Ontario, CanadaSouthlake Regional Health CareThe Arthritis Program Research GroupNewmarket, Ontario, Canada

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AGENDA

ChairmenCarlos Abud-Mendoza, MD

Anthony S. Russell, MD

14:00 – 14:10 Welcome and Introduction

Anthony S. Russell, MDCarlos Abud-Mendoza, MD

14:10 – 14:15 Establishing a Baseline for Current Knowledge andContemporary Practice (Touch Pad Response)


14:15 – 14:30 Immunopathology and Clinical Challenges in the Evolving Treatment of RA


14:30 – 14:50 The Efficacy and Safety of Existing and Emerging RA Therapies: An Evidence Based Profile

J. Carter Thorne, MD

14:50 – 15:05 Maximizing Quality of Life for RA Patients with Emerging Therapies: Key Findings from Clinical Trials

Mario H. Cardiel, MD

15:05 – 15:20 Questions and Answers

Carlos Abud-Mendoza MD

15:20 – 15:25 Measuring Post-Meeting Knowledge and Propensity forClinical Application of New Scientific Information (Touch Pad Response)

Carlos Abud-Mendoza, MD

15:25 – 15:30 Conclusion

Anthony S. Russell, MDCarlos Abud-Mendoza, MD

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ABSTRACTSImmunopathology and Clinical Challenges in the Evolving Treatment of RA

Anthony S. Russell, MB, ChB, FRCPCDivision of Rheumatology, Faculty of Medicine, University of Alberta

Walter C. Mackenzie Health Sciences Centre

Edmonton, Alberta, Canada

THERAPEUTIC OPTIONS available in the management of rheumatoid arthritis (RA) have advanced considerably in thelast two decades. Biological therapies hold the promise of targeted intervention. Recent progress in the develop-

ment of these therapies shows that rational targeting can provide clinical benefit to RA patients.1 Although the devel-opment of biologic agents (eg, tumour necrosis factor-α inhibitors, interleukin inhibitors) have revolutionized thetreatment of RA, some patients still suffer from inadequate response to treatment.2 A substantial proportion of RApatients either do not respond to these agents or experience a reduction in their initial response.3,4 Furthermore, anti-TNF agents are associated with increased rates of infection, lymphoma, and tuberculosis. These issues of long-termefficacy and safety have created a compelling need to develop new therapeutic strategies.

Ongoing research efforts have resulted in a clearer understanding of the role of inflammatory mediators and haveled to the development of additional biologic agents. These agents fall into three major groups: those that target T cells,those that target B cells, and those that target the cytokine pathways involved in RA. Novel therapeutic options on thehorizon include: abatacept, a selective T cell co-stimulation modulator; rituximab (RTX), a B cell depleting agent; andtocilizumab (MRA), an interleukin-6 (IL-6) inhibitor. Clinical trials are underway to investigate the efficacy and safetyof these emerging therapeutic agents.

Abatacept has demonstrated considerable efficacy and safety in treating the signs and symptoms of RA.5-9 Thisagent has recently gained regulatory approval in the United States. Two recent Phase III trials and two long-term exten-sion trials evaluated the efficacy of abatacept, one in patients who were not responding adequately to methotrexate(MTX)6 and the other in patients who were not responding adequately to anti-TNF-α therapy.7 A third Phase III clin-ical study compared the safety of abatacept use with other RA therapies.9 Rituximab is a genetically engineered chimericmonoclonal antibody against CD20, and has been approved for the treatment of relapsed or refractory B cell non-Hodgkin’s lymphoma in Canada and the United States. This agent is undergoing clinical trials for treatment of RA, withearly studies showing promising results in patients who were not responding adequately to methotrexate10,11 and inpatients who were not responding adequately to management with anti-TNF-α therapy.12 IL-6 is a pleiotropic cytokinethat plays an important role in immune response.13,14 It is involved in both initiation and maintenance of inflammatoryand immunologic responses in certain autoimmune diseases and plays a key role in acute phase protein induction aswell as B and T cell growth and differentiation. Tocilizumab is the first humanized anti-IL-6 receptor antibody to reachPhase III clinical trials. It is now being studied in RA patients, with early studies showing promising results.15-18

Like other biologic disease-modifying anti-rheumatic drugs (DMARDs), these agents are associated with slightlyincreased rates of infection and serious infection. Phase III trials and long-term extension studies are being carried outto provide further evidence of the relative efficacy and safety of these drugs for the treatment of RA.

References:

1. Carter RH. B cell signaling as therapeutic target. Ann Rheum Dis. 2004;63(Suppl II):ii65-ii66.

2. Weinblatt ME. Will our current success in treating rheumatoid arthritis hinder new drug development? That is the question!! Ann Rheum Dis2005;64:1529–1531.

3. Keystone EC. Tumor necrosis factor-a blockade in the treatment of rheumatoid arthritis. Rheum Dis Clin North Am 2001;27:427-443.

4. Olsen NJ, Stein CM. New drugs for rheumatoid arthritis. N Engl J Med 2004;350:2167-2179.

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5. Moreland LW, Alten R, Van den Bosch F, et al. Costimulatory blockade in patients with rheumatoid arthritis: a pilot, dose-finding, double-blind, placebo-controlled clinical trial evaluating CTLA-4Ig and LEA29Y eighty-five days after the first infusion. Arthritis Rheum 2002;46:1470-1479.

6. Kremer JM, Westhovens R, Leon M. et al. Treatment of rheumatoid arthritis by selective inhibition of T-cell activation with fusion proteinCTLA4Ig. N Engl J Med 2003;349:1907-1915.

7. Genovese MC, Becker JC, Schiff M, et al. Abatacept for rheumatoid arthritis refractory to Tumor Necrosis Factor α inhibition. N Engl J Med2005;353:1114-1123.

8. Kremer JM, Dougados M, Emery P, et al. Treatment of rheumatoid arthritis with the selective costimulation modulator abatacept: twelve-month results of a phase IIb, double-blind, randomized, placebo-controlled trial. Arthritis Rheum 2005;52:2263-2271.

9. Weinblatt M, Combe B, White A, et al. Safety of Abatacept in patients with active rheumatoid arthritis receiving background non-biologic andbiologic DMARDS: 1-year results of the ASSURE trial. Ann Rheum Dis 2005;64(Suppl. 3):60(Abstract OP0012).

10. Edwards JC, Szczepanski L, Szechinski J, et al. Efficacy of B-cell-targeted therapy with rituximab in patients with rheumatoid arthritis. N EnglJ Med 2004;350:2572-2581.

11. Edwards JC, Leandro MJ, Cambridge G. B lymphocyte depletion in rheumatoid arthritis: targeting of CD20. Curr Dir Autoimmun 2005;8:175-192.

12. Cohen SB, Greenwald M, Dougados MR, et al. Efficacy and safety of rituximab in active RA patients who experienced an inadequate responseto one or more anti-TNF-α therapies (REFLEX study). Arthritis Rheum 2005;52(9 Suppl):S677(Abstract 1830).

13. KishimotoT. Interleukin-6 and its receptor in autoimmunity. J Autoimmune 1992;5:I123-132.

14. Guerne PA, Zuraw BL, Vaughan JH, et al. Synovium as a source of interleukin 6 in vitro. Contribution to local and systemic manifestations ofarthritis. J Clin Invest 1989;83:585-592.

15. Nishimoto N, Yoshizaki K, Miyasaka N, et al. Long-term safety and efficacy of anti-interleukin 6 receptor antibody (MRA) in patients withrheumatoid arthritis. Paper presented at: Program and Abstracts of the American College of Rheumatology 67th Annual Scientific Meeting;October 23-28, 2003; Orlando, Florida. Abstract S216.

16. Nishimoto N, Yoshizaki K, Maeda K, et al. Toxicity, pharmacokinetics, and dose-finding study of repetitive treatment with the humanized anti-interleukin 6 receptor antibody MRA in rheumatoid arthritis. Phase I/II clinical study. J Rheumatol 2003;30:1426-1435.

17. Nishimoto N, Yoshizaki K, Miyasaka N, et al. Treatment of rheumatoid arthritis with humanized anti-interleukin-6 receptor antibody: a mul-ticenter, double-blind, placebo-controlled trial. Arthritis Rheum 2004;50:1761-1769.

18. Maini RN, Taylor PC, Pavelka K, et al. Efficacy of IL-6 receptor antagonist MRA in rheumatoid arthritis patients with an incomplete responseto methotrexate (CHARISMA). Paper presented at: Program and Abstracts of the American College of Rheumatology 67th Annual ScientificMeeting; October 23-28, 2003; Orlando, Florida. Abstract S1704.

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The Efficacy and Safety of Existing and Emerging RA Therapies: An Evidence Based Profile

J. Carter Thorne, MD, FRCPC, FACPDivision of Rheumatology, Faculty of Medicine, University of Toronto

Toronto, Ontario, Canada

Southlake Regional Health Care

The Arthritis Program Research Group

Newmarket, Ontario, Canada

NEW PARADIGMS in the management of Rheumatoid Arthritis have permitted the concept of ‘Treatment to Remission’rather than just ‘Improvement’. These treatment initiatives have included: Early Diagnosis and Treatment; Early

Combination Treatment; Treatment based on Outcomes; Introduction of Biologic Agents. Yet, using current strategiesand agents, a ‘State of Remission’ is achieved and sustained in only approximately 40% of patients. Other options arerequired, and these may be best attained by recognition of ‘Mechanism of Action’ as a determinant of Outcome.

Selective co-stimulation modulation of T cell activation has been shown to be efficacious and safe in treating thesigns and symptoms of RA. The first agent in this class, abatacept, has been investigated in Phase III trials.1-4 ThePhase III AIM (Abatacept in Inadequate Responders to Methotrexate [MTX]) trial,2 assessed efficacy, safety, and qual-ity of life (QoL) parameters in patients with inadequate responses to MTX. Patients were randomized to receive a fixeddose of abatacept (~10 mg/kg) or placebo intravenously on Days 1, 15, and 29, and every 28 days thereafter. Treatmentwith abatacept produced statistically significant improvements in American College of Rheumatology (ACR) 20, 50,and 70 responses at 6 months and 1 year compared with placebo (p<0.001). Disease Activity Score 28 (DAS28) <2.6remission rates were also significantly higher at 6 months (14.8% vs 2.8%) and 1 year (23.8% vs 1.9%) in abatacept-and placebo-treated patients respectively (p<0.001). A Phase II, open-label, long-term extension of this trial up to 3years provided further evidence of the efficacy of abatacept in this patient population with significantly improved ACRscores and pain reduction.5

The ATTAIN (Abatacept Trial in Treatment of Anti-TNF INadequate responders) trial3 assessed efficacy, safety,and QoL parameters in patients who had failed one or more TNF-α inhibitors over 18 months, comprising 6 monthsof double-blind treatment and a 1-year, open-label, long-term extension. Clinical improvements in ACR and healthassessment questionnaire scores were noted soon after treatment commenced (at Day 15). Sustained improvementscontinued throughout the 18-month study. DAS28 remission was achieved in 22.5% of the patients who completed18 months of abatacept treatment. Treatment with abatacept/MTX demonstrated significantly better ACR 50 and 70scores (35.0% and 18.0%, respectively) at 18 months compared with MTX/placebo treatment.

The safety of the co-stimulation modulator, abatacept, has also been demonstrated. Moreland et al evaluated theresults of five clinical trials, including 1955 patients treated with abatacept and DMARDs, representing 1527.4 person-years of exposure.7 Results demonstrated that overall deaths, adverse events (AEs), serious adverse events (SAEs), anddiscontinuations were comparable between abatacept and placebo treatment groups. The most commonly reportedAEs with abatacept/DMARD treatment (occurring at a rate > 2% higher than placebo/DMARD treatment) wereheadache (18.2%), nasopharyngitis (11.5%), dizziness (9.4%), hypertension (6.6%), and dyspepsia (6.4%).

Abatacept is generally safe and well-tolerated, especially when given in combination with non-biologic DMARDs.However, when abatacept is coadministered with biologic DMARDs, higher rates of AEs, SAEs, and infections havebeen reported.7 Thus, abatacept is not recommended in combination with biologic DMARDs. Like other biologicDMARDs, abatacept is associated with slightly increased rates of infection and serious infection. These adverse reac-tions may be related to blockade of TNF-α and thus represent class effects of these agents.8 Results from long-termextension studies should give further supportive evidence of relative safety. Registry databases that have been set up tomonitor biologic therapies in a number of countries will be required to provide evidence of the safety of these prod-ucts when administered outside the constraints of a clinical trial.

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References:

1. Moreland LW, Alten R, Van den Bosch F, et al. Costimulatory blockade in patients with rheumatoid arthritis: a pilot, dose-finding, double-blind, placebo-controlled clinical trial evaluating CTLA-4Ig and LEA29Y eighty-five days after the first infusion. Arthritis Rheum 2002;46:1470-1479.

2. Kremer JM, Westhovens R, Leon M. et al. Treatment of rheumatoid arthritis by selective inhibition of T-cell activation with fusion proteinCTLA4Ig. N Engl J Med 2003;349:1907-1915.

3. Genovese MC, Becker JC, Schiff M, et al. Abatacept for rheumatoid arthritis refractory to Tumor Necrosis Factor α inhibition. N Engl J Med2005;353:1114-1123.

4. Kremer JM, Dougados M, Emery P, et al. Treatment of rheumatoid arthritis with the selective costimulation modulator abatacept: twelve-month results of a phase IIb, double-blind, randomized, placebo-controlled trial. Arthritis Rheum 2005;52:2263-2271.

5. Russell A, Kremer J, Zhou Y, Mokliatchouk O, Moreland L. Abatacept induces sustained improvements in physical function and pain over 3years in rheumatoid arthritis patients with inadequate responses to methotrexate. Arthritis Rheum 2005;52(9 Suppl):S659(Abstract 1778).

6. Genovese M, Luggen M, Schiff M, et al. Sustained improvements through 18 months with abatacept in rheumatoid arthritis patients with aninadequate response to anti-TNF therapy. Presented at: The 69th Annual Scientific Meeting of The American College of Rheumatology (ACR)2005; November 12–17, 2005; San Diego, California. Late-breaking Abstract L16.

7. Moreland L, Kaine J, Espinoza L, et al. Safety of abatacept in rheumatoid arthritis patients in five double-blind, placebo-controlled trials.Arthritis Rheum. 2005;52(9 Suppl):S350(Abstract 886).

8. US Food and Drug Administration: Arthritis Advisory Committee March 4, 2003. Update on the TNF-α Blocking Agents. Available athttp://www.fda.gov/ohrms/dockets/ac/03/briefing/3930B1_01_B-TNF.Briefing.htm. Accessed November 23, 2005.

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Maximizing Quality of Life for RA Patients with Emerging Therapies: Key Findings from Clinical Trials

Mario H. Cardiel, MD, MScUnidad de Investigación, Hospital General “Dr. Miguel Silva”

Morelia, Michoacan, México

QUALITY OF LIFE (QoL) is considerably reduced in rheumatoid arthritis (RA) patients despite advanced treat-ments.1-3 Even with current therapeutic options, most patients report that their disease limits normal daily

living.3,4 Treatment with emerging therapies such as rituximab (RTX) and abatacept holds the promise of targetedintervention.

Rituximab is a genetically engineered, chimeric, monoclonal antibody against CD20, currently approved for thetreatment of relapsed or refractory B-cell non-Hodgkin’s lymphoma. RTX is now being investigated for the treatmentof RA, with early studies showing promising results.5,6 Two recent reports assessed QoL measures in randomized,double-blind studies with RTX.7,8 Patients had active disease despite treatment with DMARDs, other than MTX,and/or biological response modifiers. Patients received a single course of placebo or RTX (500 mg or 1000 mg) admin-istered on Days 1 and 15 by IV infusion along with concurrent MTX. Results from these trials with RTX showed sig-nificant and clinically meaningful improvements in QoL (ie, physical function, fatigue reduction, and pain reduction)as measured by Health Assessment Questionnaire Disability Index, Short Form-36, visual analog scale, and FunctionalAssessment of Chronic Illness Therapy – Fatigue. These findings support the possibility of RTX as an important ther-apeutic option for RA patients in the coming years.

A second emerging therapy, abatacept, was recently approved by the FDA in the United States. Abatacept is achimeric fusion protein of CTLA4, a surface receptor on T cells and the Fc portion of Immunoglobulin (Ig)G1. Twokey Phase III clinical trials, AIM (Abatacept in Inadequate Responders to MTX) and ATTAIN (Abatacept Trial inTreatment of Anti-TNF INadequate Responders), assessed efficacy, safety, and QoL parameters in patients with inad-equate responses to MTX and anti-TNF-α therapies, respectively. Patients were randomized to receive a fixed dose ofabatacept (~10 mg/kg) or placebo intravenously on Days 1, 15, and 29, and every 28 days thereafter.

In the AIM study, significant improvements were demonstrated for pain and all eight subscales of the physical andmental component summaries with abatacept/MTX therapy.9 Sleep quality and fatigue were also significantlyimproved in patients treated with abatacept in the AIM trial.9 Treatment with abatacept/MTX demonstrated signifi-cant and clinically meaningful improvements in physical function and reductions in pain.10 Reductions in pain (aver-aging over 50%) were seen even after the first dose. Furthermore, sustained improvements continued throughout, upto 3 years in a Phase II open-label, long-term extension, lending credence of a real-life setting.10 These QoL benefitswere also consistent with the ATTAIN trial. Clinically meaningful benefits were seen after the first dose in physicalfunction, pain, fatigue, and sleep quality.11 Sustained improvements continued throughout the 18-month study in theATTAIN long-term extension.12

Together, these trials provide evidence of clinically meaningful QoL benefits with RTX and abatacept in patientspreviously non-responsive to treatment.

References:

1. Fraenkel L, Bogardus ST, Concato J, et al. Patient preference for treatment of rheumatoid arthritis. Ann Rheum Dis 2004;63:1372-1378.

2. Wolfe F, Michaud K. Fatigue, rheumatoid arthritis, and anti-tumor necrosis factor therapy: an investigation in 24,831 patients. J Rheumatol2004;31:2115-2120.

3. Arthritis Foundation. Living with Rheumatoid Arthritis: Unmet Needs. Available at: http://www.arthritis.org/conditions/diseasecenter/RA/RASurveyWhitePaperFinal.pdf . Accessed November 23, 2005.

4. Young A, Dixey J, Cox N, et al. How does functional disability in early rheumatoid arthritis (RA) affect patients and their lives? Results of 5years of follow-up in 732 patients from the Early RA Study (ERAS). Rheumatology (Oxford) 2000;39:603-611.

5. Edwards JC, Szczepanski L, Szechinski J, et al. Efficacy of B-cell-targeted therapy with rituximab in patients with rheumatoid arthritis. N EnglJ Med 2004;350:2572-2581.

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6. Edwards JC, Leandro MJ, Cambridge G. B lymphocyte depletion in rheumatoid arthritis: targeting of CD20. Curr Dir Autoimmun 2005;8:175-192.

7. Keystone EC, Burmester GR, Furie R, et al. Improved quality of life with rituximab plus methotrexate in patients with active rheumatoid arthri-tis who experienced inadequate response to one or more anti-TNF-α therapies. Arthritis Rheum 2005;52(9 Suppl):S659(Abstract 287).

8. Mease P, Szechinski J, Greenwald M, et al. Improvements in patient reported outcomes over 24 weeks for rituximab with methotrexate inrheumatoid arthritis patients in phase IIb trial (DANCER). Arthritis Rheum 2005;52(9 Suppl):S258(Abstract 280).

9. Emery P, Russell A, Markenson J, et al. Abatacept induces sustained improvements in quality of life, sleep quality and fatigue over 3 years inrheumatoid arthritis patients with inadequate responses to methotrexate. Arthritis Rheum 2005;52(9 Suppl):S258(Abstract 626).

10. Russell A, Kremer J, Zhou Y, Mokliatchouk O, Moreland L. Abatacept induces sustained improvements in physical function and pain over 3years in rheumatoid arthritis patients with inadequate responses to methotrexate. Arthritis Rheum 2005;52(9 Suppl):S659(Abstract 1778).

11. Westhovens R, Schiff M, Russell A, et al. Abatacept significantly improves health-related quality of life in patients with inadequate responses toanti-TNF therapy: the Attain trial. Arthritis Rheum 2005;52(9 Suppl):S659(Abstract 1781).

12. Genovese M, Luggen M, Schiff M, et al. Sustained improvements through 18 months with abatacept in rheumatoid arthritis patients with aninadequate response to anti-TNF therapy. Arthritis Rheum 2005;52(9 Suppl):S659(Abstract L16)..

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EVALUATION FORMAcademic/Professional Degree(s):

Hospital/Professional Affiliation:

City/Province-State/Country:

In order to improve the quality of educational programming, we would appreciate you taking a few minutesof your time to complete this evaluation. Your comments and suggestions will help us to plan future activi-ties that meet your educational needs.

OVERALL PROGRAMPlease circle the appropriate response.

What is your overall rating of this program? Poor – 1 2 3 4 5 – Excellent

Please rate the overall educational quality of this CME activity.Poor – 1 2 3 4 5 – Excellent

To what extent will the information provided in this program contribute to your clinical practice?Not at all – 1 2 3 4 5 – Completely NA – Not Applicable

Did this CME activity receive support from a commercial source?Yes No

Please rate the degree of objectivity you observed in the educational material of this CME activity:None – 1 2 3 4 5 – Completely

Did this activity comply with the Code of Ethics for parties involved in CME?Yes No

Potential conflicts of interest of speakers were disclosed:Yes No

Comments:

PROGRAM CONTENTPlease rate the degree to which the following objectives were met using the following scale:(1 = Not at all; 2 = Minimally; 3 = Moderately; 4 = Largely; 5 = Completely)

After taking part in this program, how well do you understand the immunopathology of RA and of emerg-ing therapies, such as T cell co-stimulators, as related to the treatment of patients with rheumatoid arthri-tis (RA)?

Not at all – 1 2 3 4 5 – Completely

Are you now better able to assess the role of targeted therapies and their efficacy in the management of RA?Not at all – 1 2 3 4 5 – Completely

Have you become more familiar with the safety issues associated with the management of RA T cell co-stimulators?


Do you have a clearer understanding of the role of T cell co-stimulation in the management of quality oflife in patients with RA?


Comments:

In future CME activities, what topics and/or teaching formats would you like to include?

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SECTION EVALUATIONSPlease rate the degree to which the following objectives were met, using the scale provided:

Immunopathology and Clinical Challenges in the Evolving Treatment of RA Anthony S. Russell, MD

Poor Fair Neutral Good Excellent Not ApplicableStated objectives were met 1 2 3 4 5 NAIdeas expressed clearly 1 2 3 4 5 NAMaterial well organized 1 2 3 4 5 NAUseful examples presented 1 2 3 4 5 NAContent thorough 1 2 3 4 5 NATables and figures clear and effective 1 2 3 4 5 NAContent at an appropriate level of complexity 1 2 3 4 5 NA

Comments:

Examining the Efficacy and Safety of Existing and Emerging RA Therapies: An Evidence Based ProfileJ. Carter Thorne, MDStated objectives were met 1 2 3 4 5 NAIdeas expressed clearly 1 2 3 4 5 NAMaterial well organized 1 2 3 4 5 NAUseful examples presented 1 2 3 4 5 NATables and figures clear and effective 1 2 3 4 5 NAContent thorough 1 2 3 4 5 NAContent at an appropriate level of complexity 1 2 3 4 5 NA

Comments:

Maximizing Quality-of-Life for RA Patients with Emerging Therapies: Key Findings from Clinical TrialsMario H. Cardiel, MDStated objectives were met 1 2 3 4 5 NAIdeas expressed clearly 1 2 3 4 5 NAMaterial well organized 1 2 3 4 5 NAUseful examples presented 1 2 3 4 5 NATables and figures clear and effective 1 2 3 4 5 NAContent thorough 1 2 3 4 5 NAContent at an appropriate level of complexity 1 2 3 4 5 NA

Comments:

Establishing Current Knowledge and Practice, Questions and AnswersAnthony S. Russell, MD, and Carlos Abud-Mendoza, MDStated objectives were met 1 2 3 4 5 NAAccess instructions clear and easy to understand 1 2 3 4 5 NATechnology operated well 1 2 3 4 5 NADiscussion was well moderated 1 2 3 4 5 NAInformation was useful 1 2 3 4 5 NA

Comments:

Please provide us with any additional comments you may have regarding this educational program.We welcome your feedback.

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NOTES

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This symposium has been made possible by the independent sponsorship

of Bristol-Myers Squibb.

A continuing medical education program of SNELL Medical Communication Inc.

S N E L L

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Health & Medicine

Rhematoid Arthritis_CME symposium program abstracts and introduction written by Crystal Kaczkowski