Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the causative role of Helicobacter pylori in peptic ulcer and gastritis was established, a number of advances have been made. Helicobacter virulence factors have been identified, the changes it causes in gastric acid secretion has been elucidated, and the entire genome of H. pylori has been mapped. Multiple lines of evidence indicate a strong link between the bacterium and noncardia gastric cancer. The infection can be confidently diagnosed by noninvasive serologic tests and the urea breath test. Triple therapy is almost always curative, and the infection almost never recurs in Canadian adults, but eradicating the bacteria in the absence of peptic ulcer only rarely leads to resolution of dyspepsia. New studies suggest that treating Helicobacter may increase the risk of peptic esophagitis and adenocarcinoma of the esophagus and cardia.
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PMID:Helicobacter and disease: still more questions than answers. 1104 91

Barrett's esophagus (BE) is an acquired disease of the esophagus, in which esophageal squamous epithelium is changed by injury from reflux to metaplastic intestinal type columnar epithelium. BE is the premalignant lesion of adenocarcinoma of the esophagus. It is widely accepted that the long-standing reflux of gastric acid is a catalyst for the development of BE. More recent work points toward the reflux of duodenal secretions as a catalyst in this disease process as well. Moreover, the time course for the development of BE once a patient has reflux is not known. Our case challenges the currently defined time course of "long-standing" reflux symptoms for the development of BE, and supports the role of duodenal secretions alone in the development of BE. A 68-yr-old Caucasian man was admitted with weight loss, left upper quadrant pain, a hemoglobin of 6.8, and heme-positive stool. Esophagogastroduodenoscopy (EGD) revealed normal esophageal mucosa and a mass in the gastric cardia. Biopsies showed moderately differentiated gastric adenocarcinoma. The patient underwent a total gastrectomy, distal esophagectomy, and a Roux-en-Y esophagojejunostomy. Pathology confirmed gastric adenocarcinoma (T1 N0 Mx). The distal esophagus and gastroesophageal junction in the resected specimen were grossly and microscopically normal. Six months later an EGD, prompted by new complaints of regurgitation and dyspepsia, revealed distal esophageal mucosa lined by red-colored columnar tissue. Biopsies showed intestinal type epithelium. Thus, our case report's contribution to the current literature is twofold. It provides evidence of development of BE solely from duodenal reflux, and it documents a relatively short time span to development of BE.
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PMID:Development of Barrett's esophagus six months after total gastrectomy. 1555 10

The article presents an analysis of results of 24 384 endoscopic examinations of the upper gastrointestinal tract in population of the Leningrad oblast with symptoms of gastric dyspepsia during the period from 2007 to 2011. The detection of the columnar-celled metaplasia was 1.1%, adenocarcinoma of the esophagus--0.045%. Esophageal adenocarcinoma occurred in 3.95% of cases of the column-celled esophagus. Barrett's esophagus was revealed in males more often than in women (56.5% and 54.5% respectively). The peak incidence of esophageal adenocarcinoma in males was at the age from 46 to 60 years (36.4% of patients), in females--from 61 to 75 years (27.3% of patients). Intestinal metaplasia was detected in 72.7% of cases with esophageal adenocarcinoma: The diagnosis of long and short segment of column-celled esophagus revealed no significant difference in the development of esophageal adenocarcinoma.
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PMID:[Columnar-celled metaplasia and adenocarcinoma of the esophagus in inhabitants of the Leningrad oblast (by the data of esophagogastroduodenoscopy)]. 2348 70