Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori is a unique organism which is pathogenic for stomach-duodenum (chronic gastritis, duodenal ulcer, gastric ulcer, gastric malignancy, mucosa-associated lymphoid tissue (MALT) lymphoma) and protective for oesophagus (Barrett's oesophagus, oesophageal adenocarcinoma) at the same time in an individual. For prevention of diseases, the necessity of presence of some bacteria throughout the gastrointestinal lumen needs to be emphasized. The concept--only good Helicobacter pylori is a dead Helicobacter pylori, is dangerous and humans should learn to live in harmony with a few bacteria throughout the gastrointestinal tract.
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PMID:Is the presence or absence of Helicobacter pylori in gastric mucosa a greater risk? 1664 44

A 58-year-old man underwent upper gastrointestinal surveillance endoscopy for Barrett's oesophagus. This showed a possible gastric ulcer, although histological examination was normal. Follow-up endoscopy showed white ridges in the distal duodenum and these were subjected to biopsy. Histological examination of the biopsy specimens showed polypoid duodenal mucosa showing features similar to those of a hyperplastic polyp of the colon. In addition, the mucosal surface was focally of gastric surface type. The features were interpreted overall as most likely to represent an unusual form of regenerative change in the setting of previous chronic inflammatory mucosal damage. The case is presented as an unusual histological phenomenon at this site; it would be important not to overdiagnose neoplasia in this situation.
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PMID:Hyperplastic polyps of the duodenum: an unusual histological finding. 1714 71

NICE recommends immediate referral for patients with dyspepsia and significant acute GI bleeding and urgent specialist referral for investigation if any of the following alarm symptoms are present: progressive difficulty swallowing; chronic GI bleeding; unintentional weight loss; persistent vomiting; abdominal mass; iron deficiency anaemia; suspicious findings on barium meal. Patients aged > 55 with unexplained and persistent dyspepsia, despite H. pylori testing and acid suppression therapy, should also be considered for endoscopy, as should those with previous gastric ulcer or surgery, continuing need for NSAIDs or raised risk of gastric cancer. Patients with uninvestigated dyspepsia should be managed by empirical treatment with a PPI or testing for and treating H. pylori if present. Testing by urea breath test, stool antigen test, or locally validated lab-based serology is suggested. H. pylori eradication is usually given as triple therapy, for seven days, involving a PPI, clarithromycin and either amoxicillin or metronidazole. It is important to take a thorough history and to enquire about any medication the patient is taking. Drugs that are common culprits for dyspepsia include: NSAIDs; calcium antagonists; bisphosphonates; steroids; theophyllines; nitrates. NSAIDs can also cause GI bleeding. Absence of dyspepsia in patients taking NSAIDs does not indicate a reduced risk of bleeding. Peptic ulcers fall into three categories: H. pylori associated ulcers; drug-induced ulcers (particularly NSAIDs); and ulcers in H. pylori-negative patients not taking causative medication. H. pylori is associated with both gastric and duodenal ulcer disease but it is in the duodenum where the closest relationship exists. In any 6-12 month period, 20-40% of healthy people, more commonly men, will experience symptoms of heartburn. Oesophageal reflux can progress to more serious disease such as erosive oesophagitis, stricture or Barrett's oesophagus.
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PMID:Managing dyspepsia in primary care. 1993 59

A 75-year-old man underwent endoscopic hemostatic therapy for hemorrhagic gastric ulcer in September 2002. After healing of the gastric ulcer, he underwent Helicobacter pylori eradication therapy in February 2003. In August 2007, an irregular tumor was detected in the lower esophagus at annual checkup for gastric cancer screening using X-ray. Endoscopic examination showed that the lower margin of the tumor almost coincided with the esophagogastric junction and that a short segment of Barrett's epithelium existed near the tumor. Biopsies of the tumor showed moderately to poorly differentiated adenocarcinoma. Mild reflux esophagitis and minor hiatal hernia was also observed, and the previously treated gastric ulcer was not recurrent. Absence of H. pylori was confirmed by serum antibody and urea breath test. Surgical resection of the lower esophagus and proximal stomach was performed. The tumor invaded into the muscularis propria of the esophageal wall but had no evidence of lymph node metastasis. Based on macroscopic and pathological findings, the tumor was recognized as esophageal adenocarcinoma. Previous endoscopic examination did not detect any apparent signs of tumor in the esophagogastric junction. As far as we know, this is the first report documenting a newly developed esophageal adenocarcinoma after the successful eradication of H. pylori.
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PMID:Esophageal Adenocarcinoma Developing after Eradication of Helicobacter pylori. 2176 87


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