1. The main, unsolved clinical problem is chronic duodenal ulcer.

2. Discussion Duodenal ulcer disease has traditionally been associated with excess secretion of gastric acid.

3. There were eight smokers in the duodenal ulcer group and three in each of the other two groups.

4. Risk factors for delayed duodenal ulcer healing are mentioned in all textbooks as important considerations in the management of duodenal ulcer disease.

5. Epigastric pain was the main clinical symptom of duodenal ulcer disease: this was experienced by all patients before entering the study.

6. There are many models of duodenal ulcer - do we need a new one?

7. Thus, in addition to duodenal ulcer disease, H pylori eradication may also cure gastric ulcer disease.

8. Bonnevie reported that the incidence rate of duodenal ulcer was four times higher than that of gastric ulcer in Copenhagen County.

9. Duodenal ulcer patients were asked to stop any antisecretory treatment two weeks before the secretory studies.

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10. The high pepsinogen C concentrations in patients with duodenal ulcer are probably related to H pylori related chronic active gastritis.

11. A bacterium is identified as the cause for his duodenal ulcer.

12. Eighty unrelated controls, 61 patients with gastric ulcer, and 57 patients with duodenal ulcer were studied.

13. The role of the increased serum gastrin concentration induced by H pylori in the pathogenesis of duodenal ulcer disease is also unknown.

14. Only a minority of patients infected with H pylori will eventually develop a duodenal ulcer.

15. Indeed, there were fewer patients than expected taking NSAIDs, perhaps since intake had been reduced because of chronic duodenal ulcer disease.

16. Treatment failure was defined as evidence by endoscopy of a recurrent duodenal ulcer crater.

17. Thus H pylori infection combined with active ulceration may cause the increased basal acid secretion seen in duodenal ulcer disease.

18. No other model of chronic ulcer shows such morphological and behavioural similarity to the human duodenal ulcer.

19. The exaggerated acid response to gastrin can be explained by the increased parietal cell mass present in duodenal ulcer patients.

20. H pylori was not examined because its importance in duodenal ulcer disease was not widely recognised when this study was being planned.

21. All carriers of the bacterium, however, do not suffer from duodenal ulcer.

22. We conducted such a study in patients with active duodenal ulcer disease.

23. In addition, the phospholipid composition of gastric mucosa was compared with that of duodenal mucosa in 10 patients with duodenal ulcer.

24. Endoscopy in the nine H pylori positive non-uraemic patients showed oesophagitis in one patient and active duodenal ulcer in another.

25. The finding of enhanced fasting gastrin concentrations in H pylori positive subjects and in duodenal ulcer disease can not easily be explained.

26. Pepsin measurements were not performed in two of the 10 duodenal ulcer patients after treatment.

27. Models of mucosal damage in which a noxious agent such as ethanol is employed are simply not relevant to chronic duodenal ulcer.

28. Phosphatidylglycerol was detectable in patients with chronic atrophic gastritis, but not in controls or in patients with duodenal ulcer.

29. This finding provides support for the belief that adequate treatment of H pylori infection will give longterm protection from duodenal ulcer recurrence.

30. Kothary etal have reported that terminally extended forms of gastrin in conjunction with G14 are more prevalent in duodenal ulcer patients.

1. A bacterium is identified as the cause for his duodenal ulcer.

31. The difference between mean rates of secretion of acid and pepsin in control subjects and patients with duodenal ulcer is about 190%.

32. The phosphatidylethanolamine value was higher in duodenal ulcer and lower in chronic atrophic gastritis compared with the control group.

33. After eradication of H pylori in the duodenal ulcer patients both their basal acid output and basal gastrin fell by 50%.

34. Five patients had additional selective gastric vagotomy because of excessive gastric acid or a history of duodenal ulcer.

35. Cyclical changes in H pylori infection may cause the variations in basal acid secretion that are seen in duodenal ulcer disease.

36. The aim of our study was to find out if the more potent prokinetic drug cisapride could prevent duodenal ulcer relapse.

37. There was no significant difference in phospholipid composition between antral and duodenal sites in duodenal ulcer patients.

38. Lysolecithin was the smallest component in the duodenal ulcer and chronic atrophic gastritis groups.

39. The complications of duodenal ulcer that require surgical management are hemorrhage , perforation, obstruction,(http:///duodenal ulcer.html) and intractability.

40. In a duodenal ulcer, a long post parricidal interval of two to three hours offend exists before pain is apparent and it may then occur immediately before next meal.

41. Objectives Discussing the effect of highly selective vagotomy (HSV) and repair treatment in perforation of duodenal ulcer.

42. Conclusion:Positive family history, engorgement, smoking, irregular eating, depression and anxiety can induce gastric and duodenal ulcer and thus increase its incidence.

43. Objective To evaluate the effect of modi fied highly selective vagotomy for the treatment of perforated duodenal ulcer.

44. This is a retrospective summary of the curative effect of highly selective vagotomy for treating 50 Patients with duodenal ulcer.

45. Objective To evaluate the long-term results of extended parietal cell vagotomy (EPCV) for the treatment of acutely perforated duodenal ulcer.

46. An duodenal ulcer is seen in two views on upper endoscopy.

47. Objective To study the efficiency of endoscope-guided Savary bougie dilatation ( ESBD ) for strictured duodenal ulcer.

48. D: According to your symptoms, it looks like you have duodenal ulcer.

49. Gastritis, duodenitis and duodenal ulcer were in the order of incidence in the middle-aged group.

50. Objective To conclude the effect of parietal cell vagotomy for duodenal ulcer and its complications.

51. The old people with gastric and duodenal ulcer are not suitable to drink tea with limosis in the morning.

52. Pregnant women and stomach, duodenal ulcer patients not take it.

53. Objective To discuss the effects and the main operative techniques of laparoscopic highly selective vagotomy (LHSV) in the treatment of perforating duodenal ulcer.

54. Methods: The efficacy of omeprazole and famotidine in treating 82 duodenal ulcer patients were analysed.

55. Objective:To compare and evaluate the short term effect of laparoscopic neoplasty and open neoplasty in the perforated duodenal ulcer.

56. Objective To investigate the effect calcitonin gene - related peptide ( CGRP ) 、 endothelin ( ET ) on duodenal ulcer ( DU ).

57. Previous duodenal ulcer but quiescent for years - no contraindications to thrombolysis?

58. Objective: To clarify the relationship between blood group ABO and duodenal ulcer ( DU ) in patients with H. pylori ( Hp ) infection.

59. Objective To study the long term results of extended parietal cell vagotomy (EPCV) in the treatment of patients with duodenal ulcer and their complications.

60. An acute duodenal ulcer is seen in two views on upper endoscopy.

61. Gastritis, duodenal ulcer and duodenitis were in the turn in younger-aged group.