Disease relevance of Peptic Ulcer

• Eradication of Helicobacter pylori from the stomach by triple therapy with bismuth, tetracycline, and metronidazole cures peptic ulcer disease [1].
• None of the 19 patients with chronic gastritis who did not recognise the 120 kDa protein had peptic ulcers, whereas 25 of 57 with positive recognition had peptic ulcers (p less than 0.001) [2].
• Thus, somatostatin at a dose which has been used in the treatment of acute peptic ulcer hemorrhage (250 microgram/h) failed to influence estimated hepatic blood flow and wegded hepatic venous pressure in patients with cirrhosis but lowered splanchnic blood flow in normal subjects [3].
• We hypothesized that COX-2-specific inhibition with rofecoxib (25 mg once daily) in the treatment of patients with osteoarthritis would cause fewer gastroduodenal ulcers than an equally effective dose of ibuprofen (800 mg 3 times a day), a nonspecific COX inhibitor [4].
• Prednisone significantly increased the occurrence rate of peptic ulcer in males and in patients without chronic active hepatitis [5].

Psychiatry related information on Peptic Ulcer

• The more convenient dosage schedule of ranitidine may be important for patient compliance with initial therapy of peptic ulcer disease, and the greater duration of ranitidine antisecretory effects may enhance effectiveness of long-term maintenance therapy by providing more complete inhibition of nocturnal acid secretion [6].
• Proton-pump inhibitor treatment resulted in an absolute risk reduction of peptic ulcer by 36.6% in acute and 34.6% in chronic non-steroidal anti-inflammatory drugs/aspirin users; indeed, the number needed to treat to avoid one peptic ulcer in elderly non-steroidal anti-inflammatory drugs/aspirin users was three both in acute and chronic users [7].
• Over the followup period, patients with RA had a higher likelihood of developing congestive heart failure, chronic pulmonary disease, dementia, and peptic ulcer disease, while cases with OA had a significantly higher risk of developing peptic ulcer disease and renal disease [8].
• The following factors seemed to have no influence on rates of ulcer healing: age, sex, duration of ulcer disease, duration (beyond four weeks) of cimetidine therapy, family history of peptic ulcer, alcohol consumption, and coffee consumption [9].
• OBJECTIVE: The evolution of views regarding the impact of psychosocial factors on peptic ulcer was traced by examining all articles related to the upper gastrointestinal tract published in Psychosomatic Medicine since its inception [10].

High impact information on Peptic Ulcer

• CONCLUSIONS: After endoscopic treatment of bleeding peptic ulcers, a high-dose infusion of omeprazole substantially reduces the risk of recurrent bleeding [11].
• Famotidine to prevent peptic ulcer caused by NSAIDs [12].
• Misoprostol for the treatment of peptic ulcer and antiinflammatory-drug-induced gastroduodenal ulceration [13].
• Side effects were minimal in all treated patients except two, who were dropped from the study because of peptic ulcer and gastric intolerance to chlorambucil [14].
• Of 3064 steroid-treated patients evaluated for peptic ulcer, 55 (1.8 per cent) had ulcers, as compared with 23 of 2897 controls (0.8 per cent) (relative risk, 2.3; 95 per cent confidence interval, 1.4 to 3.7) [15].

Chemical compound and disease context of Peptic Ulcer

• A comparison of omeprazole and placebo for bleeding peptic ulcer [16].
• These effects of caffeine have been used as evidence that regular coffee should not be used by patients with peptic-ulcer disease or gastroesophageal reflux [17].
• However, NSAIDs produce gastroduodenal ulcers in about 25% of users (often with bleeding and/or perforations) and delay ulcer healing, presumably by blocking prostaglandin synthesis from cyclooxygenase (COX)-1 and COX-2 (ref. 10) [18].
• Histamine has been implicated in the pathogenesis of gastroduodenal ulcers [19].
• Aminophylline should be used with caution, if at all, in patients with peptic ulcer disease [20].

Biological context of Peptic Ulcer

• In all parts of the world, vacA s1/cagA-positive genotypes were associated with peptic ulcer disease (P < 0.001) [21].
• The vacuolating cytotoxin VacA is a major virulence factor of Helicobacter pylori, a bacterium responsible for gastroduodenal ulcers and cancer [22].
• The use of omeprazole may prevent rebleeding by elevating intragastric pH in patients with bleeding peptic ulcer after hemostasis has been achieved [23].
• A 52 year old man with a long history of marked hypertension, peptic ulcer disease, nephrocalcinosis and intermittent hypercalcemia was referred to be evaluated for primary aldosteronism suspected on the basis of low plasma renin activity, hypokalemia and blood pressure responsive to spironolactone [24].
• Since 1979, it has been the policy of the gastroenterology department at Ninewells Hospital in Tayside to recommend long-term, continuous therapy with H2-receptor antagonists for patients with peptic ulcer; in contrast, prophylactic therapy is less commonly used in the rest of Scotland [25].

Anatomical context of Peptic Ulcer

• CONTEXT: Nonsteroidal anti-inflammatory drug (NSAID)-induced gastrointestinal (GI) toxic effects, such as upper GI tract perforations, symptomatic gastroduodenal ulcers, and upper GI tract bleeding (PUBs), are thought to be attributable to cyclooxygenase 1 (COX-1) inhibition [26].
• The role of gastric acid in the development of gastroduodenal ulcers in prostaglandin-deficient conditions is unclear [27].
• Bacteriological studies were carried out on samples of gastric juice obtained from 31 patients with peptic ulcer before and immediately after a month's course of cimetidine [28].
• Repeated administration of EGF either subcutaneously or orally accelerated the healing of gastroduodenal ulcers in rats with intact salivary glands and completely reversed the delay in ulcer healing in sialoadenectomized animals [29].
• Reduced tissue type plasminogen activator activity of the gastroduodenal mucosa in peptic ulcer disease [30].

Gene context of Peptic Ulcer

• Thus, stomach- and subunit-specific inhibitors of KCNQ1 might offer new therapeutical perspectives for peptic ulcer disease [31].
• The significance of gastrin in the pathogenesis and therapy of peptic ulcer disease [32].
• Cyclooxygenase-2 (COX-2) represents the inducible key enzyme of arachidonic acid metabolism and contributes to the pathogenesis of gastroduodenal ulcers and gastric cancer [33].
• Furthermore, clinical reports also show elevated plasma and gastric mucosal endothelin-1 levels in patients suffering from peptic ulcers [34].
• The polymorphic IL-1B and IL-1RN genes in the aetiopathogenesis of peptic ulcer [35].

Analytical, diagnostic and therapeutic context of Peptic Ulcer

• In addition, estrogens, orchiectomy, or both were associated with a decreased frequency of peptic ulcer, supporting reports of the efficacy of estrogen in the treatment of peptic ulcer [36].
• We conclude that there has been a dramatic decline in elective peptic ulcer surgery in Sweden that began long before the advent of fiberoptic endoscopy, highly selective vagotomy, or H2-receptor antagonists [37].
• AIMS: To assess the value of the 14C urea breath test as a predictor of peptic ulcer disease in patients presenting with dyspepsia [38].
• Transthoracic vagotomy for postoperative peptic ulcer. Effects on basal, sham feeding- and pentagastrin-stimulated acid secretion, and on clinical outcome [39].
• One hundred and nine patients presenting with severe haemorrhage from benign peptic ulcers were randomised to either endoscopic injection sclerotherapy using a combination of 1:100,000 adrenaline and 5% ethanolamine or to conservative treatment [40].

References