Malabsorption and Gastrointestinal Dysmotility in Inflammatory Bowel Disease

A special issue of Gastrointestinal Disorders (ISSN 2624-5647).

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 3410

Special Issue Editor

Department of Laboratory Medicine & Pathology, Division of Anatomical Pathology, Children’s Hospital of Eastern Ontario, University of Ottawa, Ottawa, ON K1H 8L1, Canada
Interests: gastrointestinal/biliary diseases; metabolic diseases; congenital heart disease; mitochondrial DNA-related cardiomyopathies; carcinogenesis (bone/liver)
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Inflammatory bowel disease (IBD) and ROMA III-supported inflammatory bowel syndrome (IBS) can present acutely, but their problematic occurrence in health is characterized by the unambiguous character of chronicity, which is associated with long-term follow-up and challenging therapeutic protocols for most patients. Two critical symptoms associated with IBD are malabsorption and gastrointestinal dysmotility. If it is true that celiac disease or gluten-sensitive enteropathy (GSE) and congenital megacolon or Hirschsprung disease (HSCR) are rare diseases, it seems that they may occur much more often in patients with IBD than they do in the general population. However, both GSE and HSCR occurrences in individuals affected with IBD may have a predisposing genetic background. Their relationship with IBD is not clear-cut and remains a topic of intense investigation. Dyssynergic defecation is a common disease encountered in patients with IBD that may experience abdominal discomfort, constipation, distention, bloating, diarrhea, the sensation of incomplete evacuation, straining, and urgency. This special issue will focus on malabsorption and gastrointestinal dysmotility in IBD. Other than GSE, HSCR, and dyssynergic defecation, we would be grateful if we could receive articles on the following topics: bile acid malabsorption, exocrine pancreatic insufficiency, carbohydrate intolerance, small intestinal bacterial/fungal overgrowth, Ehlers-Danlos syndromes hypermobility type, mast cell activation syndrome, eosinophilic gastroenteritis, intra-abdominal adhesions, and giardiasis.

Prof. Dr. Consolato M. Sergi
Guest Editor

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7 pages, 236 KiB  
Article
Disaccharidase Deficiency in Pediatric Patients with Inflammatory Bowel Disease
by Chance S. Friesen, William San Pablo, Julie Bass, Uttam Garg and Jennifer M. Colombo
Gastrointest. Disord. 2022, 4(1), 1-7; https://0-doi-org.brum.beds.ac.uk/10.3390/gidisord4010001 - 11 Jan 2022
Viewed by 2744
Abstract
Background: Disaccharidase (DS) deficiencies have been reported in pediatric patients with inflammatory bowel disease (IBD), but the relationship between duodenal inflammation and DS deficiency has not been evaluated outside of lactase deficiency. Methods: This study assessed DS levels and DS deficiencies in pediatric [...] Read more.
Background: Disaccharidase (DS) deficiencies have been reported in pediatric patients with inflammatory bowel disease (IBD), but the relationship between duodenal inflammation and DS deficiency has not been evaluated outside of lactase deficiency. Methods: This study assessed DS levels and DS deficiencies in pediatric IBD patients who underwent endoscopy with assessment of DS activity. Records were reviewed for IBD subtype, pathology findings, and the results of DS analysis. Results: A total of 136 patients were identified. Overall, 89 (65.4%) patients had a diagnosis of Crohn’s disease (CD), 31 (22.8%) patients had a diagnosis of ulcerative colitis (UC), and 16 (11.8%) patients had a diagnosis of indeterminant colitis. Lactase deficiency was identified in 55.9% of patients, followed by maltase deficiency (19.9%), sucrase and palatinase deficiency (14%), and pan-deficiency (12.5%). When analyzing only patients with CD, patients with duodenitis were more likely to exhibit sucrase deficiency, palatinase deficiency, and pan-deficiency with a trend towards maltase deficiency. Conclusions: The most common DS deficiency was lactase deficiency; however, this was not related to duodenal inflammation. Pediatric patients with CD and duodenal inflammation exhibit DS deficiencies, namely, sucrase, palatinase, and pan-deficiency. Dietary adjustments may be warranted temporarily until duodenal inflammation is healed in patients with CD and duodenitis. Full article
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