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Rational Medical Therapy of Functional GI Disorders
Published in Kevin W. Olden, Handbook of Functional Gastrointestinal Disorders, 2020
Richard M. Sperling, Kenneth R. McQuaid
Endoscopic Duodenitis The prevalence of endoscopic duodenitis is greater in NUD than in matched controls. The etiology is unclear, but it does not appear to progress to peptic ulcer disease. Patients with erosive duodenitis may respond more favorably to antisecretory therapy.
Metagonimus
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Jong-Yil Chai, Bong-Kwang Jung
Unless the host is immunocompromised, the habitat of the adult flukes is confined to the mucosa (villus and crypt), and the worms never invade deeper layers of the submucosa, muscularis mucosa, or serosa.22,66 They become adult flukes within 5 days after infection.22,66 Living in the mucosa of the small intestine, the adult worms give mechanical, chemical, and immunological stimuli to the host; these stimuli together elicit local and systemic inflammatory responses of the host.22 Thus, mild to severe mucosal inflammation, that is, duodenitis, jejunitis, or ileitis, occurs according to locations in the small intestine. An increase in the permeability of intestinal mucosa was reported in experimentally infected mice.149 Poor absorption of intestinal secretions from secretory crypt cells seems to lead to watery diarrhea.150 Decreased enzyme activities may be associated with malabsorption and diarrhea in acute infections.146
The Extent of the Problems and the Epidemiological Aspects of Alcohol Drinking
Published in Victor R. Preedy, Ronald R. Watson, Alcohol and the Gastrointestinal Tract, 2017
Although excessive alcohol intake is described as an important cause ot acute gastritis, little evidence is available from epidemiological studies. In a clinical survey on hemorrhagic gastritis in Sweden, bleeding episodes were frequently associated with alcohol intake (35%).69 For all types of gastritis and duodenitis combined, a significantly increased hospitalization rate was observed in alcoholics compared with controls.49 More epidemiological data are available for chronic gastritis. In an earlier study by Edwards and Coghill, the prevalence of chronic gastritis, analyzed by drinking habit, was highest in regular and irregular heavy drinkers.70 Fontham et al. found that patients with chronic atrophic gastritis consumed more alcohol than controls diagnosed with normal gastric mucosa or superficial gastritis by gastric biopsy.71 An endoscopic survey in seven areas of France also found that the proportion of heavy drinkers was twice as high in patients with chronic gastritis as in those without.72 In support of these findings, decreased gastric secretory capacity has been demonstrated in alcoholics compared with controls.73
Frequency and clinical significance of histologic upper gastrointestinal tract findings in children with inflammatory bowel disease
Published in Scandinavian Journal of Gastroenterology, 2022
Marleena Repo, Johanna Pessi, Eelis Wirtanen, Pauliina Hiltunen, Heini Huhtala, Laura Kivelä, Kalle Kurppa
Children with CD and UGI findings had perianal disease less often, whereas in UC the findings predicted complications at the time of diagnosis. In contrast, no significant difference between UGI and no UGI groups were seen in the number of strictures, fistulas or abscesses, or in the frequency of later initiation of biological therapy or surgery, although this could be partly due to rather low number of cases. Previously, Kim et al. found no difference in severe complications between CD children with and without UGI findings [16], whereas such an association has been reported in adults [24–26]. Sullivan et al. found the presence of active gastritis and duodenitis to predict inadequate treatment response in UC [27]. These discrepancies could be explained by the differences in the rate and nature of complications between children and adults, by inconsistent definitions, or by variable length of follow-up. In light of our findings, UGI investigations could be used to determine the intensity of initial treatment.
Histopathologic ─ Endoscopic Concordance of Pediatric Duodenal Biopsy; How to Be Improved?
Published in Fetal and Pediatric Pathology, 2021
Khadiga Mohamed Ali, Khaled R Zalata, Tarik Barakat
We report the prevalence, clinical, endoscopic, and pathological characteristics of duodenitis in a vast cohort of Egyptian children. There are few pediatric studies on this subject [1,2,16,17]. We observed duodenal pathology in 72.3% of children underoing UGE. This finding is higher than any previous studies on pediatric population mostly due to uniform and accurate histopathologic assessment of duodenal specimens giving special care to any minor changes in the duodenal structure; keeping in mind that focal changes can be found in variety of diseases and that taking patient clinical presentation in consideration. However; it is of notice to say that there were 446 cases diagnosed as non specific duodenitis with free gross endoscopy without further categorization.
Upper gastrointestinal symptoms and associated endoscopic and histological features in patients receiving immune checkpoint inhibitors
Published in Scandinavian Journal of Gastroenterology, 2019
Tenglong Tang, Hamzah Abu-Sbeih, Wenyi Luo, Phillip Lum, Wei Qiao, Robert S. Bresalier, David M. Richards, Yinghong Wang
The histopathological slides for all patients were re-reviewed by a GI pathologist to minimize inter-observer variation after confirmation with previous histology reports. Inflammation in the stomach and duodenum is classified as active or chronic inactive in histology, and we grouped patients according to these standard classifications. Signs of active inflammation in the stomach and duodenum include increased neutrophil and eosinophil counts in the lamina propria and epithelium, collection of neutrophils in the lamina of crypts, edema and vascular congestion in the lamina propria, erosion and ulceration of the epithelium. Signs of chronic inflammation in the stomach include increased counts of intraepithelial lymphocytes and plasma cells (more than 5 cells in 1 cluster), deep lymphoid aggregates, granulomatous inflammation with absence of fungi (by Gomori Methenamine silver stain) and acid-fast bacilli (by Fite stain), glandular atrophy, reactive epithelial changes, intestinal metaplasia, and neuroendocrine cell hyperplasia. Signs of chronic inflammation in the duodenum include architecture distortion of the crypts, crypt dropout, lamina propria expansion by lymphoplasmacytic infiltrate, increased counts of intraepithelial lymphocytes, villous blunting, crypt hyperplasia, gastric metaplasia, Paneth cell metaplasia/hyperplasia, and granulomatous inflammation when infectious etiology was excluded. If the duodenal inflammation has only features of chronicity in the absence of active inflammation, it is classified as chronic inactive duodenitis. If the inflammation has only active inflammation or features of both, it is classified as active duodenitis. The presence of Helicobacter pylori was ruled out histologically or immunohistochemically.