Disease relevance of Duodenal Ulcer

• Ranitidine and recurrent hemorrhage from duodenal ulcer [1].
• Helicobacter pylori augments the pH-increasing effect of omeprazole in patients with duodenal ulcer [2].
• Cimetidine, therefore, may help to prevent haemorrhage from gastric ulcer but not duodenal ulcer [3].
• H. pylori density, gastric urease activity, and severity of gastritis were studied in patients with duodenal ulcer who were positive for H. pylori before, during, and after 4 weeks' treatment with sucralfate (2 g twice daily) [4].
• In this study, 30 patients (10 with endoscopically verified duodenal ulcers, 10 with verified nonulcer dyspepsia, and 10 healthy volunteers) participated in a double-blind crossover study of the effects of ranitidine on pain reports after an injection of pentagastrin [5].

Psychiatry related information on Duodenal Ulcer

• Previous structure-activity and pharmacologic studies with duodenal ulcerogens cysteamine and propionitrile implicating catecholamines in the pathogenesis of duodenal ulceration have now been followed up by dose- and time-response biochemical investigations to assess the importance of monoamines in the development of duodenal ulcers [6].
• Cholecystokinin (CCK) plays an important role in the regulation of postprandial gastric motor activity which was found to be abnormal in duodenal ulcer patients [7].

High impact information on Duodenal Ulcer

• Healing rates among patients with duodenal ulcers were higher with either dose of omeprazole than with misoprostol, whereas healing rates among patients with erosions alone were higher with misoprostol [8].
• Famotidine for the prevention of gastric and duodenal ulcers caused by nonsteroidal antiinflammatory drugs [9].
• Hemorrhage is the most common complication of duodenal ulcer disease, but there is little information about the effectiveness and safety of long-term maintenance therapy with histamine H2-receptor blockers [10].
• To study the effect of the eradication of H. pylori on the recurrence of duodenal ulcer, we treated 104 patients with H. pylori infection and recurrent duodenal ulcer with either amoxicillin (750 mg three times daily) plus metronidazole (500 mg three times daily) or identical-appearing placebos, given orally for 12 days [11].
• Effect of omeprazole and cimetidine on duodenal ulcer. A double-blind comparative trial [12].

Chemical compound and disease context of Duodenal Ulcer

• Placebos, antacids and cimetidine for duodenal ulcer [13].
• Ranitidine to prevent recurrence of duodenal ulcer [14].
• Nine patients with duodenal ulcer were studied after a low dose (15 mg) and after a near toxic dose (averaging 48 mg) of the anticholinergic, propantheline [15].
• Increased sensitivity to stimulation of acid secretion by pentagastrin in duodenal ulcer [16].
• We calculated gastric HCO3- and H+ secretion, as well as nonparietal and parietal volume secretion, in 15 duodenal ulcer patients who had previously undergone successful proximal gastric vagotomy, 15 unoperated duodenal ulcer patients, and 15 normal control subjects [17].

Biological context of Duodenal Ulcer

• The effect of an H2-receptor antagonist on food-stimjlated acid secretion, serum gastrin, and gastric emptying in patients with duodenal ulcers. Comparison with an anticholinergic drug [18].
• Comparison of acid secretory responsiveness to gastrin heptadecapeptide and of gastrin heptadecapeptide pharmacokinetics in duodenal ulcer patients and normal subjects [19].
• Although oipA status was closely linked to specific cag PAI, vacA, and babA2 genotypes, only oipA status remained in the final model to discriminate duodenal ulcer from gastritis (adjusted odds ratio [OR] = 5 and 95% confidence interval [CI] = 2.1-11.9) [20].
• These data suggest that abnormally low levels of synaptic transmission in serotonergic and possibly noradrenergic neurons play an important role in the pathogenesis of duodenal ulcer while the role of dopamine may be limited to modulation of ulcer severity [21].
• To test this, a maximally tolerated dose of bethanechol (50 micrograms/kg/hr) or saline was infused intravenously in nine duodenal ulcer patients who had been treated by proximal gastric vagotomy [22].

Anatomical context of Duodenal Ulcer

• Inhibition of gastric acid secretion by cimetidine in patients with duodenal ulcer [23].
• Studies were designed (a) to determine whether somatostatin is released into the circulation after meals in sufficient amounts to regulate gastric or pancreatic islet function in humans and (b) to investigate the possible role of somatostatin in the pathogenesis of duodenal ulcer disease [24].
• Endoscopic biopsy specimens of fundic and antral mucosa were obtained from duodenal ulcer patients before and after 4 wk of therapy with cimetidine 1.2 g/day or misoprostol 800 micrograms/day [25].
• We conclude that even though duodenal ulcer patients deliver more acid into the duodenum, this does not cause increased luminal acid aggression [26].
• The healing of acetic acid-induced gastric and duodenal ulcers was examined together with biochemical indices of growth in gastric and duodenal mucosa in rats with intact or removed salivary glands after treatment with epidermal growth factor (EGF) or somatostatin, or both [27].

Gene context of Duodenal Ulcer

• Helicobacter pylori infection may be associated with duodenal ulcer (DU) and accompanied by enhanced gastrin release but the mechanism of this H pylori related hypergastrinaemia in DU patients is unclear [28].
• As these peptides may be important in ulcer healing, this study investigated the possibility that the expression of pS2 and hSP is increased in gastric metaplasia at the margin of duodenal ulcers [29].
• However, a strong allelic association between IL-1B and IL-1RN genes was found in duodenal ulcer patients (P < 0.0006) [30].
• Changes in the interleukin-1 and interleukin-2 generation in duodenal ulcer patients during cimetidine treatment [31].
• Omeprazole, a proton pump inhibitor used widely for the treatment of gastric and duodenal ulcers, is predominantly metabolized by CYP2C19 and CYP3A4 [32].

Analytical, diagnostic and therapeutic context of Duodenal Ulcer

• Controlled comparison of two dosage regimens of cimetidine in duodenal ulcer: a multicenter study [33].
• Cimetidine in the treatment of duodenal ulcer: a multicenter double blind study [34].
• Pancreatic-polypeptide response to food in duodenal-ulcer patients before and after vagotomy [35].
• This study was designed to compare the rates of duodenal ulcer healing and recurrence after treatment with cimetidine or antacid [36].
• Healing of duodenal ulcer was assessed biweekly up to 12 wk by endoscopy, during which procedures at least two antral and two fundal biopsy specimens were taken [37].

References