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Do I Have IBS?
Published in Melissa G. Hunt, Aaron T. Beck, Reclaim Your Life From IBS, 2022
Melissa G. Hunt, Aaron T. Beck
Celiac disease is an autoimmune disorder in which the body is unable to break down gluten, one of the major proteins in wheat, rye, and barley. When people with celiac disease eat foods containing gluten (like bread and pasta), their immune system treats gluten as a foreign invader and mounts a huge defensive response. Unfortunately, this results in damage to the wall of the small intestine. The small intestine is lined with villi – tiny, fingerlike projections that coat the lining of the small intestine and dramatically increase the surface area available for absorbing nutrients from food. In celiac disease, the villi are damaged or even destroyed. The most common symptoms of celiac disease are – you guessed it – abdominal pain and diarrhea (and sometimes constipation), although the stools in celiac disease are usually pale in color. The second most common symptom in adults is anemia, due to malabsorption of nutrients. Like inflammatory bowel diseases, celiac disease can also manifest itself in other parts of the body, leading to fatigue, joint pain, arthritis, canker sores in the mouth, or an itchy rash on the skin. People with celiac disease usually find that their symptoms get worse after eating certain foods – but so do people with IBS. You can see why celiac disease, inflammatory bowel diseases, and IBS can be very difficult to distinguish from one another on the basis of symptoms alone.
Gastrointestinal system
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
In coeliac disease gluten sensitivity is permanent and increases the risk of malignancy. The gluten-free diet should therefore be continued throughout life. The condition is familial and pancreatic dysfunction is minimal. Diagnosis is based on demonstrating villous atrophy, regeneration of the villi following a gluten-free diet and recurrence of villous atrophy after reintroduction of gluten. Clinical onset does not occur until some time after the introduction of gluten in the diet.
Diarrhea and Malnutrition
Published in Fima Lifshitz, Childhood Nutrition, 2020
Andrea Maggioni, Fima Lifshitz
In chronic diarrhea of infancy associated with acquired monosaccharide intolerance, the villous atrophy lesions were patchy, the crypt length was increased, and the villi were decreased in size. Many bacteria were observed in contact with the enterocyte surface of the jejunal mucosa. Some of them were overlying the microvilli; others were adherent.101 It has been postulated that bacteria, not only of ETEC or EPEC type, may be central to the pathogenesis of protracted diarrhea of infants by causing widespread histological and ultrastructural changes which are not confined to the enterocyte surface. The persistence of the bacteria on the surface of the mucosa may be related to the alteration of the immune system, which in turn could be influenced by nutritional status of the host.102 Several studies have shown that enteroadherent E. coli, especially those with an aggregative pattern of adherence to HEp-2 cells, and Cryptosporidium have an unusual capacity to cause persistent diarrhea. They may be associated with approximately half of the cases of persistent diarrhea. This is especially true for children with pre-existing malnutrition who are infected with Cryptosporidium.
Polysaccharide Fraction from Campomanesia adamantium and Campomanesia pubescens Attenuates 5-Fluorouracil-Induced Intestinal Mucosal Inflammation in Mice
Published in Nutrition and Cancer, 2023
Isabella Wzorek França dos Santos, Karien Sauruk da Silva, Laryssa Regis Bueno, Vanessa Suzane Schneider, Carolina Silva Schiebel, Natalia Mulinari Turin de Oliveira, Liziane Cristine Malaquias da Silva, Elizabeth Soares Fernandes, Marcelo Biondaro Gois, Lucimara Mach Cortes Cordeiro, Daniele Maria-Ferreira
Although tissue damage is similar throughout the digestive tract, the small intestine appears to be the most affected region (6), and apoptosis may occur more frequently in this region than in the colon (43, 68). On the other hand, the colon also suffers significant damage (69,70), including decreased cellularity and apoptosis, which contribute to decreased colon homeostasis (65,70). For this reason, both regions (duodenum and colon) were analyzed in our study. 5-FU induced brush border abruptions in the duodenum, decreased duodenal villi height, increased duodenal villi width, and increased mucosal thickness; caused decreased colon length, colon vacuolization, and decreased colon villi height. All these changes may occur in response to the intense intestinal inflammation. In addition, it is important to note that normally, villi in the duodenum and jejunum are long, with a villus-to-crypt length ratio on the order of 3:1–5:1, whereas villi in the ileum are typically shorter. Thus, the progressive widening and blunting of the villi to complete loss of villous structures clearly indicates pathological changes. In the group treated with 5-FU, we demonstrated that the ratio of villi to crypts was less than 3:1, consistent with blunting and atrophy of the villi and indicative of a loss of intestinal histoarchitecture. CPW treatment improved the previously mentioned histopathological measures and reduced the thickness of the mucosa. Furthermore, CPW treatment prevented shortening of the colon, and preserve mucin staining in both duodenum and colon; on the other hand, CPW did not prevent the reduction of colonic crypt depth.
A New Zealand White rabbit model of thrombocytopenia and coagulopathy following total body irradiation across the dose range to induce the hematopoietic-subsyndrome of acute radiation syndrome
Published in International Journal of Radiation Biology, 2021
Isabel L. Jackson, Ganga Gurung, Yannick Poirier, Mathangi Gopalakrishnan, Eric P. Cohen, Terez-Shea Donohue, Diana Newman, Zeljko Vujaskovic
Across all radiation doses, there was more damage to the small intestine than the colon. There were no significant differences in the radiation-induced effects on morphology along the duodenum, jejunum, and ileum. Six animals in the 6.5 Gy (4/5) and 7.5 Gy (2/5) arms survived to day 45 and these survivors exhibited significant dose-dependent damage to the small intestine (Figure 8(A)). Microscopic exam revealed dilation of submucosal blood vessels, elongation of crypts, loss of surface epithelial cells, and mucosal hemorrhage. Among animals expiring prior to the study endpoint, damage to the small intestine was variable. Intact villi, with loss of epithelial cells particularly at tips were observed along the length of the small intestine. There was a slightly greater radiation-induced effect on the distal versus the proximal colon with evidence of abnormal crypts and increased mucosal depth (Figure 8(B)).
Role of microbiota and related metabolites in gastrointestinal tract barrier function in NAFLD
Published in Tissue Barriers, 2021
Maria Victoria Fernandez-Cantos, Diego Garcia-Morena, Valeria Iannone, Hani El-Nezami, Marjukka Kolehmainen, Oscar P. Kuipers
The physical barrier in the GI tract consists of mucus layers, IECs and endothelial cells (ECs) (Figure 1). They physically avoid the invasion of microorganisms through the mucosa, preventing the translocation of bacteria and bacterial components to the bloodstream.28–30 However, their features vary between the small and large intestine. The small intestine has a smaller radius than the large intestine, and its epithelium is folded forming villi (evaginations projected toward the intestinal lumen) and crypts (invaginations occurring at the base of the villi). Intestinal stem cells found at the base of the crypts divide, migrate and differentiate continuously into enterocytes, goblet cells, Paneth cells or enteroendocrine cells, whose physiological roles are respectively the absorption, mucus production, antimicrobial production and hormone secretion. Besides, crypts contain mainly stem cells and Paneth cells, while enterocytes are predominantly present in the villi, and enteroendocrine and goblet cells are distributed in the upper crypt and the villi. In contrast, the large intestine lacks Paneth cells and villi, and only crypts are present along it.58 Moreover, the interaction of the different cell types with the microbiota will not be equal, as well as, the concentration of the molecules secreted by the host will differ along the radius of the intestine.