The Gastroenterology

achieving Success in IBD management

LEARNING PATHWAY

This activity is supported by independenteducation grants from AbbVie, Shire, andTakeda Pharmaceuticals, U.S.A., Inc.

Accredited by Provided by

ACTIVITY PURPOSEThis educational program is designed for gastroenterologistsand gastroenterology clinicians who manage patientswith IBD.

ACTIVITY DETAILSSunday, September 11, 2016

Breakfast | 6:30 am

Presentation | 6:45 am – 7:45 am

Hyatt Regency Grand CypressOne Grand Cypress BoulevardOrlando, FL 32836

SPEAKERRaymond Cross, MD, MS, AGAFProfessor of MedicineDivision of Gastroenterology and HepatologyDirector of the Inflammatory Bowel Disease ProgramUniversity of maryland School of medicineCo-Director, Digestive Health CenterUniversity of maryland medical CenterBaltimore, mD

REGISTER ONLINEwww.RmeI.com/GImeetings

TENTATIVE MEETING AGENDAWelcome . . . . . . . . . . . . 5 minutesPresentations . . . . . . . 50 minutesClosing Remarks . . . . . . 5 minutes

FEE INFORMATIONThere is no fee for this educational activity.

Challenging Cases in IBD

©2016 RmeI medical education, LLC | all rights reserved | 139-16-201-mT1CHALLENGING CASES IN IBD | The Gastroenterology Learning Pathway: Achieving Success in IBD Management

TARGET AUDIENCEThis educational program is designed for gastroenterologists and gastroenterology clinicians who manage patientswith inflammatory bowel disease (IBD).

STATEMENT OF NEEDUlcerative colitis (UC) and Crohn’s disease (CD) are the most common forms of inflammatory bowel disease (IBD).1

IBD is associated with a large influx of immune cells into the gastrointestinal tract.2 Lymphocyte trafficking allowsthe capture and entry of activated lymphocytes into intestinal tissues, playing a key role in IBD, and providing anattractive therapeutic target.2,3

It is thought that an abnormal inflammatory response to enteric commensal bacteria can cause IBD in geneticallysusceptible individuals, and both genetic and environmental factors have been implicated in contributing to IBD.Genetic susceptibility factors associated with the development of UC are mHC locus HLa Class II alleles, theinterleukin-1 family of genes, and the multidrug resistance gene mDR1. In patients with CD, mutations in NOD2,aTG 16LI, or immunity-related GTPase m protein may render them genetically susceptible. The IL23R gene hasbeen associated with both UC and CD. However, the exact etiologies of UC and CD are not fully understood.1,4,5

In UC, inflammation typically begins in the rectum and extends proximally throughout the entire colon or may affectlocalized areas of the colon. UC is a clinically heterogeneous disease, but in adults the disease generally presentsas some combination of bloody diarrhea with mucus, abdominal pain and tenderness, loss of appetite and weight,fever, fatigue, and other symptoms.6

CD can affect any region of the gastrointestinal tract, but it often involves the ileum and colon. although thesymptoms of CD are dependent upon disease location, they include nocturnal or chronic diarrhea, abdominal painand tenderness, rectal bleeding, weight loss, fever, and fatigue. Upon clinical examination, patients with CD mayhave perianal fissures, fistulas, or abscesses.4,7

Diagnosis involves defining the extent and severity of inflammation. Both endoscopy and biopsy are required todetermine specific histologic characteristics and aid in differentiating UC and CD from each other and otherconditions such as infectious colitis. Both diseases are characterized by periods of acute, active disease of variableseverity with intermittent phases of asymptomatic remission. The onset of relapse is unpredictable and associatedwith a sharp reduction in quality of life.8-10

The treatment goals of IBD include, but should not be limited to, achieving and maintaining mucosal healing andremission. Several conventional therapeutic options are available for the management of IBD. There is also anever-growing list of newly approved and emerging therapies. While a wide range of medications to manage IBDare beneficial for patients, selecting and optimizing patient-specific treatment plans is a considerable challenge.11-16

Surgery is often required if remission cannot be achieved through therapeutic intervention.8,17 However, surgery forIBD has been associated with morbidity and mortality.18

approximately 40% of patients with refractory IBD19,20 do not respond to therapy and are termed primary non-responders. In addition, long-term therapy has been associated with significant loss of response (up to 40%),1 alsotermed secondary non-response. Therefore, new treatments with novel mechanisms of action are necessary toprovide patients with IBD with improved long-term outcomes.21

There has also been evidence that suggests that more aggressive therapy initiated earlier in the disease course forhigh-risk patients impacts prognosis and clinicians are encouraged to initiate biologic therapy earlier in the diseaseto achieve remission.8 a treat-to-target (T2T) approach is gaining mounting support among gastroenterologiststreating IBD. In contrast to what was previously thought, disease remission is achieved more effectively if objectivepatient characteristics (e.g., mucosal healing) are used to monitor disease progression versus subjective patientreports. moreover, the more severe disease warrants treatment with more advanced agents (thiopurines and anti-TNF agents), which are associated with potential toxicity and loss of response. To help overcome these obstacles,serum concentrations of these drugs can be measured through various therapeutic drug monitoring (TDm) approachesto guide treatment decisions and reduce risk of adverse events and unnecessary treatments in and their mechanismsof action patients with IBD.

EDUCATIONAL OBJECTIVESAfter engaging in this educational initiative, learners will be able to:• Compare and contrast the clinical effects of IBD therapies• Select individualized treatments for patients with IBD that maximize the opportunity to achieve remission and avoid relapse while minimizing toxicity• Utilize available disease progression and drug monitoring strategies for patients with IBD• Implement aGa practice measures in managing patients with IBD

STATEMENT OF SUPPORTThis activity is supported by independent education grants from abbVie, Shire, and Takeda Pharmaceuticals,U.S.a., Inc.

PROVIDER INFORMATIONThis activity is accredited by The american Gastroenterological association (aGa) Institute, and provided byRmeI medical education, LLC.

CONTINUING MEDICAL EDUCATION INFORMATIONThe aGa Institute is accredited by the accreditation Council for Continuing medical education to provide continuingmedical education for physicians.

The aGa Institute designates this live activity for a maximum of 1.0 AMA PRA Category 1 Credit(s) Tm. Physiciansshould claim only the credit commensurate with the extent of their participation in the activity.

In accordance with the aCCme’s Standards for Commercial Support of Continuing medical education, all facultyand planning partners must disclose any financial relationship(s) or other relationship(s) held within the past 12months. The aGa Institute implements a mechanism to identify and resolve all conflicts of interest prior todelivering the educational activity to learners.

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2. Villablanca eJ, Cassani B, von andrian UH, mora JR. Blocking lymphocyte localization to the gastrointestinal mucosa as a therapeutic strategy for inflammatory bowel diseases. Gastroenterology. 2011;140(6):1776-1784.

3. von andrian UH, mackay CR. T-cell function and migration. Two sides of the same coin. N Engl J Med. 2000;343:1020-1034.

4. abraham C, Cho JH. Inflammatory Bowel Disease. N Engl J Med. 2009;361:2066-2078.

5. Ordás I, eckmann L, Talamini m, Baumgart D, Sandborn WJ. Ulcerative Colitis. Lancet. 2012;380.

6. Danese S, Fiocchi C. Ulcerative colitis. N Engl J Med. 2011;365:1713-1725.

7. Dretzke J, edlin R, Round J, et al. a systematic review and economic evaluation of the use of tumour necrosis factor-alpha (TNF-a) inhibitors, adalimumab and infliximab, for Crohn’s disease. Health Technol Assess. 2011;15(6):1-244.

8. Lichtenstein GR, Hanauer SB, Sandborn WJ; Practice Parameters Committee of american College of Gastroenterology. management of Crohn’s disease in adults. Am J Gastroenterol. 2009;104(2):465-483.

9. Lichtenstein GR, Ramsey D, Rubin DT. Randomised clinical trial: delayed- release oral mesalazine 4.8 g/day vs. 2.4 g/day in endoscopic mucosal healing--aSCeND I and II combined analysis. Aliment Pharmacol Ther. 2011;33(6):672-678.

10. Oliveira L, Cohen RD. maintaining remission in ulcerative colitis—role ofonce daily extended-release mesalamine. Drug Des Devel Ther. 2011;5:111-116.

11. Reinisch W, et al. Long-term infliximab maintenance therapy for ulcerative colitis: The aCT-1 and -2 extension studies. Inflamm Bowel Dis. 2012;18:201-211.

12. Levesque BG, Sandborn WJ. Infliximab versus ciclosporin in severe ulcerative colitis. Lancet. 2012a;S0140-6736(12):61259-8.

13. Sandborn WJ, et al. adalimumab induces and maintains clinical remission in patients with moderate-to- severe ulcerative colitis. Gastroenterology. 2012;142:257-265.

14. Sandborn WJ, Danese S, Ballard eD, et al. efficacy of Budesonide-mmX®; 6 mg QD for the maintenance of remission in patients with ulcerative colitis: results from a phase III, 12 month safety and extended use study. Presented at: Digestive Disease Week 2012; may 19-22, 2012; San Diego, Ca. abstract Su2080.

15. Sandborn WJ, Gasink C, Gao LL, et al; CeRTIFI Study Group. Ustekinumab induction and maintenance therapy in refractory Crohn’s disease. N Engl J Med. 2012;367(16):1519-1528.

16. Sandborn WJ, Ghosh S, Panes J, Vranic I, Su C, Rousell S, Niezychowski W; Study a3921063 Investigators. Tofacitinib, an oral Janus kinase inhibitor, in active ulcerative colitis. N Engl J Med. 2012;367(7):616-624.

17. Kornbluth a, Sachar DB. Ulcerative Colitis Practice Guidelines in adults: american College of Gastroenterology, Practice Parameters Committee. Am J Gastroenterol. 2010;105:501-523.

18. Reddy Sl, Friedman S, Telford JJ, et al. are patients with inflammatory bowel disease receiving optimal care? Am J Gastroenterol. 2005;100: 1357-1361.

19. Rutgeerts P, Sandborn WJ, Feagan BG, et al. Infliximab for induction and maintenance therapy for ulcerative colitis. N Engl J Med. 2005;353:2462-2476.

20. Colombel JF, Sandborn WJ, Rutgeerts P, et al. adalimumab for maintenance of clinical response and remission in patients with Crohn’s disease: the CHaRm trial. Gastroenterology. 2007;132(1):52-65.

21. mcLean LP, Shea-Donohue T, Cross RK. Vedolizumab for the treatment of ulcerative colitis and Crohn’s disease. Immunotherapy. 2012;4(9):883-898.