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

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

33. As a result, the inflamed duodenal mucosa may then become susceptible to acid and this may ultimately lead to ulceration.

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

35. Patients after acute pancreatitis had slower duodenal juice protein and amylase turnover rates but trypsin turnover was not different with controls. Sentencedict.com

36. A positive provocation test was documented if upper abdominal pain was present with or without nausea after introduction of duodenal contents.

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

38. Gastrin levels may also be elevated by pernicious anemia. duodenal ulcers, and after a meal.

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

40. When food leaves the stomach or duodenal during the night, the ulcer is bathed in acid.

41. Decreased concentrations of activated pepsinogen were found in H pylori positive patients only. Duodenal biopsies were tested in 76 patients.

42. Diets rich in polyunsaturated fatty acids enhance the phenomenon of adaptive cytoprotection and render the duodenal mucosa more resistant to acid.

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

44. In our previous study, the ratio of gastric to duodenal ulcers was 1.69 in Kinki district where Kyoto Prefecture is located.

45. H pylori positive gastritis, and the combination of active duodenitis and gastric metaplasia were independent predictors of duodenal ulceration.

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

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

48. The absence of a low folate value should not deter the physician from obtaining a duodenal biopsy specimen.

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

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

51. To determine the extent of gastric metaplasia, multiple biopsy specimens were collected from standardised sites of the duodenal bulb.

52. Both factors may be part of a complex cascade of events that ultimately leads to the development of duodenal ulceration.

53. Laparotomy showed duodenal scarring with enlarged lymph nodes in the pyloric and duodenal areas and white nodules in the liver.

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

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

56. Five out of 10 patients had a positive result on provocation with their duodenal aspirate, developing epigastric pain.

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

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

59. Six patients had gastric ulcers and five had duodenal ulcers.

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