Challenges in Designing a National Surveillance Program for Inflammatory Bowel Disease in the United States

Long, Millie D.; Hutfless, Susan; Kappelman, Michael D.; Khalili, Hamed; Kaplan, Gilaad G.; Bernstein, Çharles N.; Colombel, Jean Fréd́eric; Gower‐Rousseau, Corinne; Herrinton, Lisa J.; Velayos, Fernando; Loftus, Edward V.; Nguyen, Geoffrey C.; Ananthakrishnan, Ashwin N.; Sonnenberg, Amnon; Chan, Andrew T.; Sandler, Robert S.; Atreja, Ashish; Shah, Samir A.; Rothman, Kenneth J.; LeLeiko, Neal S.; Bright, Renee; Boffetta, Paolo; Myers, Kelly D.; Sands, Bruce E.

doi:10.1097/01.mib.0000435441.30107.8b

Cited by 34 publications

(28 citation statements)

References 108 publications

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“…States (1)(2)(3). In 2008, the direct costs associated with the disease exceeded 6.8 billion dollars (4), and furthermore, the worldwide prevalence of IBD appears to be increasing (5).…”

Section: In the Unitedmentioning

confidence: 99%

Peroxisome Proliferator-activated Receptor-γ Coactivator 1-α (PGC1α) Protects against Experimental Murine Colitis

Cunningham

Vincent

Sodhi

et al. 2016

Journal of Biological Chemistry

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Peroxisome proliferator-activated receptor-␥ coactivator 1-␣ (PGC1␣) is the primary regulator of mitochondrial biogenesis and was recently found to be highly expressed within the intestinal epithelium. PGC1␣ is decreased in the intestinal epithelium of patients with inflammatory bowel disease, but its role in pathogenesis is uncertain. We now hypothesize that PGC1␣ protects against the development of colitis and helps to maintain the integrity of the intestinal barrier. We selectively deleted PGC1␣ from the intestinal epithelium of mice by breeding a PGC1␣ loxP/loxP mouse with a villin-cre mouse. Their progeny (PGC1␣ ⌬IEC mice) were subjected to 2% dextran sodium sulfate (DSS) colitis for 7 days. The SIRT1 agonist SRT1720 was used to enhance PGC1␣ activation in wild-type mice during DSS exposure. Mice lacking PGC1␣ within the intestinal epithelium were more susceptible to DSS colitis than their wild-type littermates. Pharmacologic activation of PGC1␣ successfully ameliorated disease and restored mitochondrial integrity. These findings suggest that a depletion of PGC1␣ in the intestinal epithelium contributes to inflammatory changes through a failure of mitochondrial structure and function as well as a breakdown of the intestinal barrier, which leads to increased bacterial translocation. PGC1␣ induction helps to maintain mitochondrial integrity, enhance intestinal barrier function, and decrease inflammation.

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“…States (1)(2)(3). In 2008, the direct costs associated with the disease exceeded 6.8 billion dollars (4), and furthermore, the worldwide prevalence of IBD appears to be increasing (5).…”

Section: In the Unitedmentioning

confidence: 99%

Peroxisome Proliferator-activated Receptor-γ Coactivator 1-α (PGC1α) Protects against Experimental Murine Colitis

Cunningham

Vincent

Sodhi

et al. 2016

Journal of Biological Chemistry

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“…IBD is an umbrella term that regroups a number of inflammatory diseases affecting the gastrointestinal tract, the two main forms of which are Crohn's disease and ulcerative colitis [10]. The increasing incidence of IBD in countries with a more westernized lifestyle [10] suggests the influence of environmental factors, which may alter the microbiota in favor of disease onset and/or progression [11].…”

Section: Inflammatory Bowel Diseasesmentioning

confidence: 99%

“…The increasing incidence of IBD in countries with a more westernized lifestyle [10] suggests the influence of environmental factors, which may alter the microbiota in favor of disease onset and/or progression [11]. A large body of evidence also points to genetic factors in the cause of IBD, with at least 163 loci now known to influence predisposition to Crohn's disease and ulcerative colitis [12].…”

Section: Inflammatory Bowel Diseasesmentioning

confidence: 99%

Role of programmed necrosis and cell death in intestinal inflammation

Dagenais

Douglas²,

Saleh³

2014

Current Opinion in Gastroenterology

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“…Common symptoms for these diseases include diarrhea, abdominal tenderness or pain, rectal bleeding, and possible weight loss [Lichenstein et al 2008;Kornbluth et al 2010;Cosnes et al 2011;Danese et al 2014]. In the United States, the incidence and prevalence rates for UC and CD have been increasing and are reported as 7.9 and 8.8 cases per 100,000 person years and 263 and 241 per 100,000 adults diagnosed with UC and CD, respectively [Kappelman et al 2013;Long et al 2014].…”

Section: Introductionmentioning

confidence: 99%

Vedolizumab: an α4β7 integrin antagonist for ulcerative colitis and Crohn’s disease

Cherry

Yunker

Lambert

et al. 2015

Therapeutic Advances in Chronic Disease

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Ulcerative colitis (UC) and Crohn's disease (CD) are chronic, relapsing inflammatory bowel diseases associated with significant morbidity. Conventional therapies for these diseases include corticosteroids, aminosalicylates, immunomodulators, and monoclonal antibodies. Over the years tumor necrosis factor (TNF)-α antagonists alone or in combination with other therapies have emerged as the cornerstone of treatment for induction and maintenance of remission of moderate to severe UC and CD. Unfortunately, some patients with moderate to severe UC and CD are unable to attain or maintain remission with TNF-α antagonist treatment. Vedolizumab, a humanized monoclonal antibody, is the first integrin receptor antagonist approved that selectively antagonizes α4β7 gastrointestinal integrin receptors. US Food and Drug Administration approval is for treatment of patients with moderate to severe active UC and CD who have inadequate response with, lost response to, or are intolerant to a TNF-α antagonist or an immunomodulator; or have inadequate response with, are intolerant to, or demonstrate dependence on corticosteroids. When administered according to approved dosing in patients with moderate to severe CD and UC, vedolizumab induces clinical response rates up to 31.4% and 47.1% at week 6, and clinical remission rates up to 39% and 41.8% at week 52, respectively. Serious adverse events reported with vedolizumab include serious infections, malignancies, and anaphylaxis. Since vedolizumab is gastrointestinal selective, to date, it has not shown evidence of causing progressive multifocal leukoencephalopathy; however, postmarketing studies monitoring for this adverse effect are ongoing. Further assessment of vedolizumab earlier in the course of these diseases and in combination with other therapies is warranted.

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Challenges in Designing a National Surveillance Program for Inflammatory Bowel Disease in the United States

Cited by 34 publications

References 108 publications

Peroxisome Proliferator-activated Receptor-γ Coactivator 1-α (PGC1α) Protects against Experimental Murine Colitis

Peroxisome Proliferator-activated Receptor-γ Coactivator 1-α (PGC1α) Protects against Experimental Murine Colitis

Role of programmed necrosis and cell death in intestinal inflammation

Vedolizumab: an α4β7 integrin antagonist for ulcerative colitis and Crohn’s disease

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