Inflammatory bowel disease–associated digestive disorders

Abbreviations

Introduction

Inflammatory bowel disease (IBD), that is, Crohn’s disease (CD) and ulcerative colitis (UC), can affect any organ of the digestive disease system. The involvement of gastrointestinal (GI) tract, liver, gall bladder, or pancreas in IBD may manifest as a part of the disease process [such as primary sclerosing cholangitis (PSC)], associated autoimmune disorders [such as autoimmune hepatitis (AIH) and autoimmune pancreatitis (AIP)], or adverse consequences of IBD-associated bowel obstruction, IBD medications, or IBD surgery. Complications of these associated digestive system disorders may in return affect the GI tract, such as esophageal or gastric varices from portal hypertension in patients with concurrent IBD and PSC. Finally, functional bowel diseases may overlap with the disease course of IBD.

Esophagus and stomach

While gastroesophageal reflux disorder (GERD) is common in general population, reflux esophagitis with erosions is common in patients with partial bowel obstruction from CD, small intestinal bacterial overgrowth, and IBD-associated surgery (such as strictureplasty) or surgical anastomosis strictures( Fig. 24.1 ). There is an association between CD, eosinophilic esophagitis (EoE), and lymphocytic esophagitis, particularly in the pediatric population . In histology, CD of the esophagus is featured with chronic active inflammation, and rarely granulomas . The histologic hallmark of EoE is the increased number of eosinophils in the esophageal epithelium with at least 15 eosinophils per high-power field . Lymphocytic esophagitis is characterized by the prominence of peripapillary intraepithelial lymphocytes without remarked granulocytosis. True esophageal CD is rare in adult patients. However, CD-associated esophagitis should be distinguished from reflux esophagitis, EoE, and lymphocytic esophagitis ( Fig. 24.2 ). Classic histologic features of esophageal CD include the infiltration of mononuclear cells with clusters and occasional granuloma formation. CD patients with severe malnutrition and iron deficiency anemia may present with esophageal strictures (i.e., Plummer–Vinson syndrome) . Long-term use of antibiotics or corticosteroids, particularly in the presence of partial gastric outlet obstruction from small bowel obstruction in IBD, may predispose the patient to the development of Candida esophagitis ( Fig. 24.3 ). Esophageal varices can occur in patients with IBD. The patients often have concurrent PSC, porto-mesenteric vein thrombosis, or nonalcoholic fatty liver disease–associated cirrhosis ( Fig. 24.4 ).

Various forms of gastritis may be found in patients with CD or UC, ranging from nonspecific gastritis, nonsteroidal antiinflammatory drug (NSAID)–associated gastritis, Helicobacter pylori –associated gastritis , and proton pump inhibitor–associated nodular gastric mucosa or gastric pseudopolyps ( Fig. 24.5 ) . Nonspecific antral gastritis that is not associated with the use of NSAIDs or H. pylori infection is common in patients with CD. The association between H. pylori infection and CD is not settled .

Isolated pyloric stenosis can occur in patients with CD . Pyloric stenosis in this setting typically shows no ulceration or inflammation in the stenosis site, gastric antrum or body, or duodenum ( Figs. 24.6–24.8 ). These patients may or may not have CD in the small bowel or colon. The pattern may share a similar pathogenesis of immune-mediated achalasia. Another pattern in CD may be observed in the ileocecal valve (ICV) (see next). Pyloric stenosis in CD typically responds poorly to medical therapy or endoscopic balloon dilation ( Fig. 24.6 ). These patients may be treated with endoscopic stricturotomy with a needle knife or insulated-tip knife ( Fig. 24.7 ). Topical injection of botulinum toxin A ( Fig. 24.6B and D ) and gastric peroral endoscopic myotomy may be attempted ( Fig. 24.8 ). Some patients may even require pyloroplasty surgery ( Fig. 24.9 ). Peroral endoscopic gastrostomy tube has been used for a supplement of enteral nutrition, relief of symptoms of gastric outlet obstruction, or decompression of the stomach ( Fig. 24.10 ).

Gastric lesions may present with gastric antral vascular ectasia (GAVE) or portal hypertensive gastropathy in PSC patients with portal hypertension and liver cirrhosis. Gastric varices may develop in IBD patients with portal hypertension from concurrent PSC, primary biliary cirrhosis, AIH-associated cirrhosis, porto-mesenteric vein thrombosis, or even nonalcoholic fatty liver disease ( Figs. 24.11–24.13 ).