ライフサイエンスコーパス: duodenal ulcer

1 toris, bronchial asthma, herpes simplex, and duodenal ulcer.

2 al with severe abdominal pain and a ruptured duodenal ulcer.

3 ting the risk of gastric cancer from that of duodenal ulcer.

4 gastric ulcer and 2.6 (95% CI: 1.1, 5.8) for duodenal ulcer.

5 astric ulcer and 5.8 (95% CI: 1.1, 30.0) for duodenal ulcer.

6 gastric ulcer and 2.5 (95% CI: 0.8, 7.4) for duodenal ulcer.

7 they documented 138 newly diagnosed cases of duodenal ulcer.

8 gastritis and the development of stomach and duodenal ulcers.

9 cag(-) H. pylori strain for both gastric and duodenal ulcers.

10 are paradoxically protected from developing duodenal ulcers.

11 ith diarrhea, heartburn, abdominal pain, and duodenal ulcers.

12 ative role in the development of gastric and duodenal ulcers.

13 f H. pylori in infected patients with active duodenal ulcers.

14 associated with absence of gastric ulcer or duodenal ulcer (0.21 [0.05 to 0.94] and 0.31 [0.12 to 0.

15 ing present in 60%-80% of gastric and 95% of duodenal ulcers.(1)H pylori is also the first bacterium

16 ts), gastric ulcer (14), gastritis (12), and duodenal ulcer (10).

17 cured patients (6% vs. 67% for patients with duodenal ulcers; 4% vs. 59% for patients with gastric ul

18 ees for all procedures (surgery for bleeding duodenal ulcer, 42% versus 26%, adjusted odds ratio (AOR

19 71]) associated with gastric ulcer than with duodenal ulcer (86 versus 56%).

20 in 2006 (-29.9%), with a larger reduction in duodenal ulcers (95,552 in 1993 vs. 60,029 in 2006, -37.

21 r that could distinguish gastric cancer from duodenal ulcer (adjusted odds ratio, 3.033; 95% confiden

22 -twenty patients; 116 with gastritis, 3 with duodenal ulcer and 1 gastric ulcer, were studied.

23 of Helicobacter pylori as the major cause of duodenal ulcer and development of effective eradication

24 fectiveness studies of various approaches to duodenal ulcer and dyspeptic patients.

25 Fourteen duodenal ulcer and five gastric ulcer studies satisfied

26 as well as two mutually exclusive diseases, duodenal ulcer and gastric carcinoma.

27 s compared with that of age- and sex-matched duodenal ulcer and nonulcer dyspepsia patients (16 each)

28 n H. pylori may lead to the disappearance of duodenal ulcers and distal gastric cancers and toward a

29 subset of individuals to develop gastric or duodenal ulcers and even gastric cancer.

30 or contributing factor in the development of duodenal ulcers and is believed to be a significant risk

31 s showed numerous small (<10 mm) gastric and duodenal ulcers and multiple 10-15-mm polypoid gastric m

32 opsy samples was comparable in patients with duodenal ulcers and normal subjects without apparent rel

33 In patients with inactive, healed duodenal ulcers and normal subjects, the effect of H. py

34 and of age) were determined in patients with duodenal ulcers and normal subjects.

35 does not appear to be an association between duodenal ulcers and pancreatic cancer.

36 of the birth-cohort patterns of gastric and duodenal ulcers and their identical appearance in countr

37 total of 150 men with gastric ulcer, 65 with duodenal ulcer, and 14 with both diseases were identifie

38 le gastritis, 40 with gastric ulcer, 35 with duodenal ulcer, and 30 with gastric cancer.

39 ian populations (126 with gastritis, 96 with duodenal ulcer, and 64 with gastric cancer) by PCR.

40 significantly associated with gastric ulcer, duodenal ulcer, and gastric cancer (odds ratios [95% con

41 tory protein A may have predictive value for duodenal ulcer, and host alleles for interleukin-1beta,

42 ut significance) in mucus from patients with duodenal ulcer, and increased five times (with high sign

43 s for sustaining an NSAID-induced gastric or duodenal ulcer, and there has been progress in further u

44 onia, congestive heart failure, dehydration, duodenal ulcer, and urinary tract infection, were signif

45 ad gastritis, 92 had gastric ulcers, 108 had duodenal ulcers, and 65 had gastric cancer.

46 s effective in the prevention of gastric and duodenal ulcers, and erosive oesophagitis in patients ta

47 three patients had tumor-associated bleeding duodenal ulcers, and one had a contained duodenal perfor

48 t of diseases such as gastritis, gastric and duodenal ulcers, and two types of gastric cancers.

49 gastric pathogen associated with gastric and duodenal ulcers as well as specific gastric cancers.

50 ion, the best markers of gastric cancer- and duodenal ulcer-associated strains are the vacA s1 and i1

51 pneumatosis after endoscopic hemostasis for duodenal ulcer bleeding.

52 He also had a duodenal ulcer, blood in the gastric lumen and a large p

53 ases gastric acid secretion in patients with duodenal ulcers but diminishes acid output in patients w

54 r were also inversely related to the risk of duodenal ulcer, but vitamin A from all sources combined

55 me trends of gastric ulcer preceded those of duodenal ulcer by 10-30 years.

56 s gastritis and atrophy, may protect against duodenal ulcers by decreasing acid output.

57 Whereas incident duodenal ulcer cases represented only 2.4 percent of all

58 nts undergoing surgery (surgery for bleeding duodenal ulcer, cholecystectomy, appendectomy, and colec

59 aired bicarbonate secretion in patients with duodenal ulcers could be caused by a cellular and/or phy

60 al relationship between the dupA cluster and duodenal ulcer development is not proved, the presence o

61 n of Helicobacter pylori, is associated with duodenal ulcer development.

62 uster but not dupA alone, is associated with duodenal ulcer development.

63 ori, who are known to have increased risk of duodenal ulcer disease and gastric cancer.

64 Patients with duodenal ulcer disease have impaired proximal duodenal m

65 e agent of chronic superficial gastritis and duodenal ulcer disease in humans, produces a unique cyto

66 e consistent with H. pylori infection (e.g., duodenal ulcer disease), rapid urease testing and DNA se

67 m of dogs, Trichuris vulpis, in a woman with duodenal ulcer disease, chronic diarrhea, and close cont

68 hough Helicobacter pylori is associated with duodenal ulcer disease, most patients infected with the

69 inical outcomes including gastric cancer and duodenal ulcer disease.

70 ex matched to 4 controls and with a parallel duodenal ulcer (DU) group.

71 rica, including 120 with gastritis, 140 with duodenal ulcer (DU), 110 with gastric ulcer (GU), and 13

72 In patients with duodenal ulcers, eradication of H. pylori normalized pro

73 s of gastric ulcer rose by 22 %, and that of duodenal ulcer fell by 14 % per decade.

74 n logistic regression models to discriminate duodenal ulcer from gastritis.

75 The age-specific death rates of gastric and duodenal ulcers from each individual country were plotte

76 whelm mucosal defense mechanisms, leading to duodenal ulcer, gastric ulcer, and gastroesophageal refl

77 In patients with duodenal ulcers, H. pylori eradication normalized proxim

78 atio [OR] 0.20, 95% CI 0.09-0.47; p=0.0002); duodenal ulcers had developed in one (0.5%) patient comp

79 Most patients with duodenal ulcers have impaired proximal duodenal mucosal

80 Eradication of Helicobacter pylori expedites duodenal ulcer healing and prevents recurrences.

81 en used to perform vagotomy in patients with duodenal ulcer; however, no direct comparisons are avail

82 . pylori eradication exclusively in inactive duodenal ulcer (iDU) or non-ulcer dyspepsia (NUD).

83 atic cancer and the occurrence of gastric or duodenal ulcer in a large US cohort.

84 ions between dietary factors and the risk of duodenal ulcer in a prospective cohort of 47,806 men, ag

85 es alike, the risk of dying from gastric and duodenal ulcer increased among consecutive generations b

86 In patients with duodenal ulcer, infection with Helicobacter pylori is as

87 to become accepted therapy for patients with duodenal ulcer managed presently with OPGV.

88 and stimulated acid outputs in patients with duodenal ulcer, most people infected with the organism a

89 d including gastroduodenitis (n=10), gastric/duodenal ulcer (n=2), and hemorrhagic esophagitis (n=1).

90 In 1 patient, a treatment-related duodenal ulcer occurred.

91 years, who were free of diagnosed gastric or duodenal ulcer or cancer.

92 ntly higher incidence of personal history of duodenal ulcer (P = .02).

93 versus 78% of 18 isolates from patients with duodenal ulcers (P = 0.344) and only 64% of 22 isolates

94 43%, respectively, for surgery for bleeding duodenal ulcer, P < 0.0001 for all comparisons).

95 c-cancer patients (71.9%) than in those from duodenal ulcer patients (52.1%) (P = 0.012).

96 ntral bacteria] density was 5-fold higher in duodenal ulcer patients than in others (P = .005).

97 nd vegetables, may reduce the development of duodenal ulcer, possibly due to their fiber content.

98 The duodenal ulcer promoting (dupA) gene, located in the pla

99 passed both jhp0917 and jhp0918 called dupA (duodenal ulcer promoting gene) was associated with a spe

100 the outer membrane inflammatory protein; the duodenal ulcer-promoting gene, and possibly the blood gr

101 y efficacy end point for reduced gastric and duodenal ulcer recurrence for the purpose of clinical tr

102 For H. pylori-cured patients, duodenal ulcer recurrence was higher in studies using tw

103 12 months) was not significantly related to duodenal ulcer recurrence.

104 vegetables was associated with lower risk of duodenal ulcer (relative risk (RR) = 0.67, 95% confidenc

105 resence of a complete dupA cluster increases duodenal ulcer risk compared to H. pylori infection with

106 strongly associated with a decreased risk of duodenal ulcer (RR = 0.40, 95% CI 0.22-0.74 for the high

107 ke was inversely associated with the risk of duodenal ulcer (RR = 0.55, 95% CI 0.31-0.96 for men in t

108 ion, and apoptosis in gerbil mucosa than did duodenal ulcer strain G1.1, and gastric ulceration and a

109 cephalic-vagal stimulation) in patients with duodenal ulcers, suggesting a generalized secretory defe

110 l inflammation and stricture, gastric ulcer, duodenal ulcer, suspected Barrett's esophagus (> or =2 c

111 ious clinical manifestations associated with duodenal ulcer than from patients with gastritis alone o

112 2.4 percent of all persons with a history of duodenal ulcer, the corresponding value for gastric ulce

113 In contrast, duodenal ulcer was not associated with pancreatic cancer

114 Observed in 88 (30.6%) of UGIB patients, duodenal ulcer was the most common cause, followed by va

115 Altered DMBS in patients with duodenal ulcers was unrelated to histopathologic abnorma

116 Eradication rates in patients with duodenal ulcer were 82% (n = 51; 95% CI, 70-92) and 77%

117 ared with none in the risedronate group, and duodenal ulcers were noted in 1 evaluable subject in the

118 Three patients developed gastric or duodenal ulcers with severe bleeding requiring transfusi

119 d the risk for developing gastric cancer and duodenal ulcer, with the presence of the homB gene actin

120 lammatory drugs, and a history of gastric or duodenal ulcer, women with RA and no history of cardiac