Abstract
Gastrointestinal (GI) strictures are difficult to treat in a variety of disease processes. Currently, there are no Food and Drug Administration (FDA) approved drugs for fibrosis in the GI tract. One of the limitations to developing anti-fibrotic drugs has been the lack of a reproducible, relatively inexpensive, large animal model of fibrosis-driven luminal stricture. This study aimed to evaluate the feasibility of creating a model of luminal GI tract strictures. Argon plasma coagulation (APC) was applied circumferentially in porcine esophagi in vivo. Follow-up endoscopy (EGD) was performed at day 14 after the APC procedure. We noted high grade, benign esophageal strictures (n = 8). All 8 strictures resembled luminal GI fibrotic strictures in humans. These strictures were characterized, and then successfully dilated. A repeat EGD was performed at day 28 after the APC procedure and found evidence of recurrent, high grade, fibrotic, strictures at all 8 locations in all pigs. Pigs were sacrificed and gross and histologic analyses performed. Histologic examination showed extensive fibrosis, with significant collagen deposition in the lamina propria and submucosa, as well as extensive inflammatory infiltrates within the strictures. In conclusion, we report a porcine model of luminal GI fibrotic stricture that has the potential to assist with developing novel anti-fibrotic therapies as well as endoscopic techniques to address recurring fibrotic strictures in humans.
Highlights
Gastrointestinal (GI) strictures are difficult to treat in a variety of disease processes
A fibrotic stricture can occur at several locations in the GI tract, such as the esophagus[1], small bowel (Crohn’s disease, CD), colon ( CD2, ulcerative colitis (UC)[3], ischemic, post-diverticulitis), biliary tree and other locations
One of the limitations to advancing anti-fibrotics to date has been the lack of a large animal model of fibrosis-driven luminal stricture
Summary
Gastrointestinal (GI) strictures are difficult to treat in a variety of disease processes. One of the limitations to developing anti-fibrotic drugs has been the lack of a reproducible, relatively inexpensive, large animal model of fibrosis-driven luminal stricture. One of the limitations to advancing anti-fibrotics to date has been the lack of a large animal model of fibrosis-driven luminal stricture. The two approaches, are technically complex, time consuming, and are often marred by a high rate of complications[14,15,16] Other methods such as endoscopic radiofrequency ablation (RFA), it is technically quite simple, the stricture created are short and not durable[17]. The aim of this study was to create a large animal model of luminal GI strictures that can demonstrate a strong fibrotic component, as well as tendency to recur after endoscopic treatment
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