Rhematoid Arthritis_CME symposium program abstracts and introduction written by Crystal Kaczkowski

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

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Mexican Canadian
th Congreso de Annual Meeting
61 st
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Mexicano of the Canadian
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Rheumatologia Rheumatology
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Rheumatology
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Association
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FEBRUARY 20, 2006
THE FAIRMONT ACAPULCO PRINCESS
ACAPULCO, MEXICO

Mexican Canadian Congress A University of Alberta
of Rheumatology CME accredited program

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

INTRODUCTION
Rheumatoid 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 has
been made in understanding the immunopathology of RA, leading to the development
of new therapeutic agents, biologics and non-biologics. Agents such as Disease-
Modifying Anti-Rheumatic Drugs (DMARDs) and Tumour Necrosis Factor-α Inhibitors
have proven efficacious for many patients with RA. However, these agents are not
effective in all cases and some patients may experience side effects that can be
problematic. 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 effective
management strategies, such as the actions of T and B lymphocytes, macrophages, and

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cytokines. The selective T cell co-stimulation modulator represents an emerging class
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of biologic agents that decrease the activation of T cells, which are critical to the
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initiation and progression of RA. Results of current Phase III clinical trials investigating
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the first of these agents, abatacept, have shown that it is effective, safe, and offers
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considerable improvement in quality of life measures.
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The complexity and rapid evolution of this field requires that physicians keep abreast
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of these new advances in preparation for providing optimal clinical treatment for
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patients with RA. In this symposium, respected Canadian and Mexican rheumatologists
will discuss clinical and scientific developments in the evolving management of RA, and
examine the prevailing research related to the emerging role of selective T cell
co-stimulation modulation.

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TARGET AUDIENCE
This symposium is intended primarily for rheumatologists from Canada and Mexico and
other 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 and
perpetuation of RA
• Describe the mechanism of action of co-stimulation modulation
• Evaluate the latest Phase III safety, efﬁcacy, and quality of life data on
co-stimulation modulation in RA

ACCREDITATION
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This education event is approved as an Accredited
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Group Learning Activity under Section 1 of the
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Framework of Continuing Professional Development
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options for the Maintenance of Certiﬁcation Program of
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the Royal College of Physicians and Surgeons of Canada.
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FACULTY
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Carlos Abud-Mendoza, MD (Co-chair)
Departmento de Immunologia, Facultad de Medicina
Universidad Autónoma de San Luis Potosi (UASLP)
Hospital Regional San Luis Potosi
San Luis Potosi, México
Anthony S. Russell, MB, ChB, FRCPC (Co-chair)
Division of Rheumatology, Faculty of Medicine, University of Alberta
Walter C. Mackenzie Health Sciences Centre
Edmonton, 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 Toronto
Toronto, Ontario, Canada
Southlake Regional Health Care
The Arthritis Program Research Group
Newmarket, Ontario, Canada

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AGENDA
Chairmen
Carlos Abud-Mendoza, MD
Anthony S. Russell, MD

14:00 – 14:10 Welcome and Introduction

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

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14:15 – 14:30 Immunopathology and Clinical Challenges
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in the Evolving Treatment of RA
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14:30 – 14:50 The Efficacy and Safety of Existing and
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Emerging RA Therapies: An Evidence Based Profile
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J. Carter Thorne, MD
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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 for
Clinical Application of New Scientific Information
(Touch Pad Response)

15:25 – 15:30 Conclusion

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ABSTRACTS
Immunopathology and Clinical Challenges
in the Evolving Treatment of RA

Anthony S. Russell, MB, ChB, FRCPC
Division of Rheumatology, Faculty of Medicine, University of Alberta
Walter C. Mackenzie Health Sciences Centre
Edmonton, Alberta, Canada

available in the management of rheumatoid arthritis (RA) have advanced considerably in the
T HERAPEUTIC OPTIONS
last 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 the
treatment of RA, some patients still suffer from inadequate response to treatment.2 A substantial proportion of RA
patients either do not respond to these agents or experience a reduction in their initial response.3,4 Furthermore, anti-

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TNF agents are associated with increased rates of infection, lymphoma, and tuberculosis. These issues of long-term
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efficacy and safety have created a compelling need to develop new therapeutic strategies.
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Ongoing research efforts have resulted in a clearer understanding of the role of inflammatory mediators and have
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led to the development of additional biologic agents. These agents fall into three major groups: those that target T cells,
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those that target B cells, and those that target the cytokine pathways involved in RA. Novel therapeutic options on the
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horizon include: abatacept, a selective T cell co-stimulation modulator; rituximab (RTX), a B cell depleting agent; and
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tocilizumab (MRA), an interleukin-6 (IL-6) inhibitor. Clinical trials are underway to investigate the efficacy and safety
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of these emerging therapeutic agents.
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Abatacept has demonstrated considerable efficacy and safety in treating the signs and symptoms of RA.5-9 This
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agent 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 chimeric
monoclonal 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, with
early studies showing promising results in patients who were not responding adequately to methotrexate10,11 and in
patients who were not responding adequately to management with anti-TNF-α therapy.12 IL-6 is a pleiotropic cytokine
that plays an important role in immune response.13,14 It is involved in both initiation and maintenance of inflammatory
and immunologic responses in certain autoimmune diseases and plays a key role in acute phase protein induction as
well as B and T cell growth and differentiation. Tocilizumab is the first humanized anti-IL-6 receptor antibody to reach
Phase 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 slightly
increased rates of infection and serious infection. Phase III trials and long-term extension studies are being carried out
to 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 Dis
2005;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 protein
CTLA4Ig. 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 Med
2005;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 and
biologic 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 Engl
J 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 response
to 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 of
arthritis. 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 with

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rheumatoid arthritis. Paper presented at: Program and Abstracts of the American College of Rheumatology 67th Annual Scientific Meeting;

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October 23-28, 2003; Orlando, Florida. Abstract S216.
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16. Nishimoto N, Yoshizaki K, Maeda K, et al. Toxicity, pharmacokinetics, and dose-finding study of repetitive treatment with the humanized anti-
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interleukin 6 receptor antibody MRA in rheumatoid arthritis. Phase I/II clinical study. J Rheumatol 2003;30:1426-1435.
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17. Nishimoto N, Yoshizaki K, Miyasaka N, et al. Treatment of rheumatoid arthritis with humanized anti-interleukin-6 receptor antibody: a mul-
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ticenter, double-blind, placebo-controlled trial. Arthritis Rheum 2004;50:1761-1769.
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18. Maini RN, Taylor PC, Pavelka K, et al. Efficacy of IL-6 receptor antagonist MRA in rheumatoid arthritis patients with an incomplete response
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to methotrexate (CHARISMA). Paper presented at: Program and Abstracts of the American College of Rheumatology 67th Annual Scientific
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Meeting; 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, FACP
Division of Rheumatology, Faculty of Medicine, University of Toronto
Toronto, Ontario, Canada
Southlake Regional Health Care
The Arthritis Program Research Group
Newmarket, Ontario, Canada

EW PARADIGMS in the management of Rheumatoid Arthritis have permitted the concept of ‘Treatment to Remission’
N 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 strategies
and agents, a ‘State of Remission’ is achieved and sustained in only approximately 40% of patients. Other options are
required, 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 the
signs and symptoms of RA. The first agent in this class, abatacept, has been investigated in Phase III trials.1-4 The

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Phase III AIM (Abatacept in Inadequate Responders to Methotrexate [MTX]) trial,2 assessed efficacy, safety, and qual-
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ity of life (QoL) parameters in patients with inadequate responses to MTX. Patients were randomized to receive a fixed
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dose of abatacept (~10 mg/kg) or placebo intravenously on Days 1, 15, and 29, and every 28 days thereafter. Treatment
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with abatacept produced statistically significant improvements in American College of Rheumatology (ACR) 20, 50,
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and 70 responses at 6 months and 1 year compared with placebo (p<0.001). Disease Activity Score 28 (DAS28) <2.6
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remission rates were also significantly higher at 6 months (14.8% vs 2.8%) and 1 year (23.8% vs 1.9%) in abatacept-
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and placebo-treated patients respectively (p<0.001). A Phase II, open-label, long-term extension of this trial up to 3
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years provided further evidence of the efficacy of abatacept in this patient population with significantly improved ACR
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scores and pain reduction.5
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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 months
of double-blind treatment and a 1-year, open-label, long-term extension. Clinical improvements in ACR and health
assessment questionnaire scores were noted soon after treatment commenced (at Day 15). Sustained improvements
continued throughout the 18-month study. DAS28 remission was achieved in 22.5% of the patients who completed
18 months of abatacept treatment. Treatment with abatacept/MTX demonstrated significantly better ACR 50 and 70
scores (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 the
results 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), and
discontinuations were comparable between abatacept and placebo treatment groups. The most commonly reported
AEs with abatacept/DMARD treatment (occurring at a rate > 2% higher than placebo/DMARD treatment) were
headache (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 have
been reported.7 Thus, abatacept is not recommended in combination with biologic DMARDs. Like other biologic
DMARDs, 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-term
extension studies should give further supportive evidence of relative safety. Registry databases that have been set up to
monitor 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 protein
CTLA4Ig. 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 Med
2005;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 3
years 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 an
inadequate 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 at
http://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, MSc
Unidad de Investigación, Hospital General “Dr. Miguel Silva”
Morelia, Michoacan, México

(QoL) is considerably reduced in rheumatoid arthritis (RA) patients despite advanced treat-
Q UALITY OF LIFE
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 targeted
intervention.
Rituximab is a genetically engineered, chimeric, monoclonal antibody against CD20, currently approved for the
treatment of relapsed or refractory B-cell non-Hodgkin’s lymphoma. RTX is now being investigated for the treatment
of 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-

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nificant and clinically meaningful improvements in QoL (ie, physical function, fatigue reduction, and pain reduction)
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as measured by Health Assessment Questionnaire Disability Index, Short Form-36, visual analog scale, and Functional
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Assessment of Chronic Illness Therapy – Fatigue. These findings support the possibility of RTX as an important ther-
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apeutic option for RA patients in the coming years.
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A second emerging therapy, abatacept, was recently approved by the FDA in the United States. Abatacept is a
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chimeric fusion protein of CTLA4, a surface receptor on T cells and the Fc portion of Immunoglobulin (Ig)G1. Two
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key Phase III clinical trials, AIM (Abatacept in Inadequate Responders to MTX) and ATTAIN (Abatacept Trial in
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Treatment of Anti-TNF INadequate Responders), assessed efficacy, safety, and QoL parameters in patients with inad-
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equate responses to MTX and anti-TNF-α therapies, respectively. Patients were randomized to receive a fixed dose of
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abatacept (~10 mg/kg) or placebo intravenously on Days 1, 15, and 29, and every 28 days thereafter.
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In the AIM study, significant improvements were demonstrated for pain and all eight subscales of the physical and
mental component summaries with abatacept/MTX therapy.9 Sleep quality and fatigue were also significantly
improved 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, up
to 3 years in a Phase II open-label, long-term extension, lending credence of a real-life setting.10 These QoL benefits
were also consistent with the ATTAIN trial. Clinically meaningful benefits were seen after the first dose in physical
function, pain, fatigue, and sleep quality.11 Sustained improvements continued throughout the 18-month study in the
ATTAIN long-term extension.12
Together, these trials provide evidence of clinically meaningful QoL benefits with RTX and abatacept in patients
previously 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 Rheumatol
2004;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 5
years 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 Engl
J 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 in
rheumatoid 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 in
rheumatoid 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 3
years 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 to
anti-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 an
inadequate response to anti-TNF therapy. Arthritis Rheum 2005;52(9 Suppl):S659(Abstract L16)..

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EVALUATION FORM
Academic/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 minutes
of your time to complete this evaluation. Your comments and suggestions will help us to plan future activi-
ties that meet your educational needs.

OVERALL PROGRAM
Please 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?

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Yes No m
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Please rate the degree of objectivity you observed in the educational material of this CME activity:
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None – 1 2 3 4 5 – Completely
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Did this activity comply with the Code of Ethics for parties involved in CME?
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Yes No
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Potential conflicts of interest of speakers were disclosed:
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Yes No
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Comments:
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PROGRAM CONTENT
Please 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?
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 of
life 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 EVALUATIONS
Please rate the degree to which the following objectives were met, using the scale provided:
Immunopathology and Clinical Challenges in the Evolving Treatment of RA
Poor Fair Neutral Good Excellent Not Applicable
Stated objectives were met 1 2 3 4 5 NA
Ideas expressed clearly 1 2 3 4 5 NA
Material well organized 1 2 3 4 5 NA
Useful examples presented 1 2 3 4 5 NA
Content thorough 1 2 3 4 5 NA
Tables and figures clear and effective 1 2 3 4 5 NA
Content 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 Profile
J. Carter Thorne, MD

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Comments:
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Maximizing Quality-of-Life for RA Patients with Emerging Therapies:
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Key Findings from Clinical Trials
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Mario H. Cardiel, MD
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Comments:

Establishing Current Knowledge and Practice, Questions and Answers
Anthony S. Russell, MD, and Carlos Abud-Mendoza, MD
Access instructions clear and easy to understand 1 2 3 4 5 NA
Technology operated well 1 2 3 4 5 NA
Discussion was well moderated 1 2 3 4 5 NA
Information 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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16

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This symposium has been made possible
A continuing medical education program of
by the independent sponsorship
SNELL Medical Communication Inc.
of Bristol-Myers Squibb.

SNELL

Rhematoid Arthritis_CME symposium program abstracts and introduction written by Crystal Kaczkowski

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Rhematoid Arthritis_CME symposium program abstracts and introduction written by Crystal Kaczkowski