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Impact of JC Virus Antibody Testing in Patients with Crohn's Disease with Loss of Response to Infliximab: A Markov Model

Scott, Frank I. MD, MSCE*,†,‡; Osterman, Mark T. MD, MSCE*,‡; McConnell, Ryan A. MD; Lorusso, Monica MD§; Aberra, Faten MD, MSCE*,‡; Kerner, Caroline MD, MSCE*,‡; Lichtenstein, Gary R. MD*,‡; Lewis, James D. MD, MSCE*,†,‡

doi: 10.1097/01.MIB.0000437043.36338.21
Original Clinical Articles

Background: The optimal treatment strategy for patients with Crohn's disease who have loss of response to the anti–tumor necrosis factor α medication infliximab is uncertain. Natalizumab has an alternative mechanism of action, but its use has been limited by the risk of progressive multifocal leukoencephalopathy. In this study, we performed a decision analysis assessing the impact of JC virus (JCV) antibody testing and natalizumab utilization for loss of response to infliximab.

Methods: We constructed a Markov model to assess the difference between unscreened natalizumab use (option 1), JCV antibody testing with natalizumab when appropriate (option 2), and second anti–tumor necrosis factor α use (option 3). The base case was a 35-year-old man with severe Crohn's disease with loss of response to infliximab. The time horizon was 3 years. Results are reported in quality-adjusted life years (QALYs). Deterministic and probabilistic analyses were conducted. Markov analysis using a cohort of 5000 individuals was performed. The impact of JCV antibody status on outcomes in this model was assessed.

Results: Option 2 was the preferred strategy (2.0880 QALYs), followed by option 1 (2.0875 QALYs) and option 3 (2.0808 QALYs). Patients in option 2 required fewer surgeries compared with option 3. Previous JCV infection was associated with reduced QALYs with all options that allowed for natalizumab use.

Conclusions: JCV antibody testing and subsequent treatment selection yield improved outcomes over natalizumab without testing or using only a second anti–tumor necrosis factor α in all patients.

Article first published online 8 October 2013Supplemental Digital Content is Available in the Text.

*Division of Gastroenterology, University of Pennsylvania, Philadelphia, Pennsylvania;

Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania;

Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania; and

§Division of Gastroenterology and Nutrition, Department of Paediatrics, Anna Meyer Children's Hospital, University of Florence, Florence, Italy.

Reprints: Frank I. Scott MD, MSCE, Division of Gastroenterology, Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania, 1 Convention Avenue, Penn Tower, 9th Floor, Philadelphia, PA 19104 (e-mail: frankis@mail.med.upenn.edu).

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.ibdjournal.org).

Grant Support through NIH: T32-DK007066-36, K08-DK095951-01, and K24-DK078228.

The authors have no conflicts of interest to disclose.

Received July 19, 2013

Accepted August 26, 2013

© Crohn's & Colitis Foundation of America, Inc.
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