Advances in Understanding the Pathophysiology of Rheumatoid Arthritis
In accordance with Discovery Institute of Medical Education (DIME) policies regarding financial and off-label disclosure, the audience is advised that the newsletter in this continuing medical education (CME) activity may contain references to off-label or unapproved uses of drugs or devices. Participants should note that the use of these agents outside currently approved labeling is considered experimental and are advised to consult prescribing information for these products. This CME activity was planned and produced in accordance with ACCME Essential Areas and Policies.
This activity is funded through an educational grant from Genentech, Inc., and Biogen Idec. The activity content was developed independently by the contributing faculty. The materials included in this activity have undergone peer review by the chairperson. All materials are included with the permission of the authors. The opinions expressed are those of the faculty and are not to be construed as those of the publisher or grantor.
Release date: February 13, 2008
Expiration date: February 13, 2009
Term of Offering
This activity has a release date of February 13, 2008, and is valid for 1 year. Requests for credit must be received no later than February 13, 2009. This CME activity was planned and produced in accordance with ACCME Essential Areas and Policies. Please refer to the posttest at the end of this activity for further instruction regarding credit.
A review committee has agreed that this material can be completed in 1 hour. This estimated study time in turn has determined the credit hours being offered.
All inquiries should be directed to:
DIME
35 West Wacker Drive Suite 1200
Chicago, IL 60601-1636
dimeinfo@dimeded.org
Accreditation Statement
DIME is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.
Designation Statement
DIME designates this educational activity for a maximum of 1.0 AMA PRA Category 1 Credit™. Physicians should only claim credit commensurate with the extent of their participation in the activity.
Statement of Need
The pathogenesis of autoimmune disorders such as rheumatoid arthritis (RA) is complex, involving all elements of the immune system, including B cells, T cells, innate recognition systems, pathogenic antibodies, and complement and effector cells. The role of T cells in the pathogenesis of RA has been well characterized, leading to the development and approval of biologic therapy, such as the tumor necrosis factor (TNFα) and IL-1 receptor antagonists. Despite the success of these agents in treating RA, about one-third of patients remain unresponsive to biologic therapy.
The role of B cells in the pathogenesis of RA is not as well defined as that of T cells; however, early studies showed that targeting B cells resulted in sustained ACR50 and ACR70 responses. This triggered a major shift in thinking about this disease. Multiple B-cell targets are now a focus of further study.
An unprecedented number of randomized controlled trials in rheumatology have been conducted in the past decade, bringing much clinical data to practical application in the community. To bridge the gap between leading-edge research and the clinic, recent consensus statements have provided guidelines for the use of T- and B-cell–targeted agents. An understanding of the pathophysiology of RA, recent clinical trial data, and the clinical application of T- and B-cell therapies in RA is essential to improving patient care.
Activity Purpose
The purpose of this series of four newsletters is to enhance the knowledge and competence of members of the target audience in the treatment of RA.
Each newsletter is intended to provide an expert review of the most current research related to the management of RA, emphasizing the clinical implications of B- and T-cell–targeted therapies.
Learning Objectives
On completion of this activity, participants should be able to:
- Describe the T-cell–mediated pathways in RA
- Describe the role of B cells in the pathophysiology of RA
- Enumerate strategies to control pathoimmunologic events in disease progression
Target Audience
This activity is targeted to rheumatologists with an interest in B- and T-cell–targeted therapies in RA.
Funding Statement
This activity is funded through an educational grant from Genentech/Biogen Idec.
Faculty
Chairperson
Clifton O. Bingham III, MD
Assistant Professor of Medicine
Divisions of Rheumatology and Allergy
Department of Medicine
The Johns Hopkins University
Baltimore, Maryland
Arthur Kavanaugh, MD
Professor of Clinical Medicine
Director, Center of Innovative Therapy
Division of Rheumatology, Allergy, and Immunology
University of California at San Diego
La Jolla, CA
Disclosures
DIME requires that those involved in the content development and/or presentation of this CME activity disclose to the participants any relevant financial interest or other relationship with (1) the manufacturers of any commercial products or providers of commercial services discussed in an educational presentation and (2) any commercial supporters of the activity.
This CME/CE activity may include discussions regarding the use of medications that may be outside the approved labeling for these products. Physicians should consult the current prescribing information for these products. DIME requires the author to disclose that the product is not labeled for the use under discussion. The provider’s documentation of common practices that make the disclosure requirement known to faculty demonstrates compliance with ACCME guidelines.
Clifton O. Bingham III, MD
Sources of Funding for Research: Abbott Laboratories; Amgen, Inc.; Biogen Idec; Bristol-Myers Squibb Company; Centocor, Inc.; Genentech, Inc.; Wyeth Pharmaceuticals
Consulting Agreements: Abbott Laboratories; Amgen, Inc.; Genentech, Inc.; Merck & Co., Inc.; Novartis Pharmaceuticals Corp; Targeted Genetics Corporation
Financial Interests/Stock Ownership: None
Speakers’ Bureau/Honorarium Agreements: None
Discussion of Off-Label, Investigational, or Experimental Drug Use: Atacicept, certolizumab pegol, golimumab, ocrelizumab, ofatumumab, tocilizumab, TRU-015
Arthur Kavanaugh, MD
Sources of Funding for Research: Biogen Idec; Bristol-Myers Squibb Company; Genentech, Inc.
Consulting Agreements: None
Financial Interests/Stock Ownership: None
Speakers’ Bureau/Honorarium Agreements: None
Discussion of Off-Label, Investigational, or Experimental Drug Use: Atacicept, certolizumab pegol, golimumab, ocrelizumab, ofatumumab, tocilizumab, TRU-015
It is the policy of DIME to ensure that its CME/CE activities are independent, free of commercial bias, and beyond the control of persons or organizations with an economic interest in influencing the content of CME/CE. Everyone who is in a position to control the content of this educational activity has disclosed all relevant financial relationships with any commercial interest (including but not limited to pharmaceutical companies, biomedical device manufacturers, or other corporations whose products or services are related to the subject matter of the presentation topic) within the preceding 12 months. Any relationships that created a conflict of interest were resolved by the DIME Scientific Director before the participation of the individual in the development or presentation of course content.
No DIME staff member who was in a position to control or influence the content of this educational activity had a conflict of interest.
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