ライフサイエンスコーパス: duodenal ulcer

1 they documented 138 newly diagnosed cases of duodenal ulcer.

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

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

4 ors in the development of gastric cancer and duodenal ulcer.

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

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

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

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

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

10 gastritis and the development of stomach and duodenal ulcers.

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

12 antly associated with gastritis, gastric and duodenal ulcers.

13 are paradoxically protected from developing duodenal ulcers.

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

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

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

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

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

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

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

21 71]) associated with gastric ulcer than with duodenal ulcer (86 versus 56%).

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

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

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

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

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

27 Fourteen duodenal ulcer and five gastric ulcer studies satisfied

28 causative agent of stomach diseases such as duodenal ulcer and gastric cancer, in this regard incomp

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

30 There were two grade 4 toxicities: duodenal ulcer and hyponatremia.

31 One (1%) patient developed an acute grade 4 duodenal ulcer and late grade 4 gastritis.

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

33 The association between acute gastric/duodenal ulcer and opium use has been previously propose

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

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

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

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

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

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

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

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

42 d gastrointestinal syndrome characterized by duodenal ulcers and strictures was observed in a subset

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

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

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

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

47 13 for H. heilmannii (three gastritis, five duodenal ulcer, and five gastric ulcer samples), and 7 f

48 for H. bizzozeronii (zero gastric ulcer, two duodenal ulcer, and five gastritis samples).

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

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

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

52 ples), 10 for H. felis (one gastritis, three duodenal ulcer, and six gastric ulcer samples), 20 for H

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

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

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

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

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

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

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

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

61 pneumatosis after endoscopic hemostasis for duodenal ulcer bleeding.

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

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

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

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

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

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

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

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

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

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

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

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

74 Patients with duodenal ulcer disease have impaired proximal duodenal m

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

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

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

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

79 inical outcomes including gastric cancer and duodenal ulcer disease.

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

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

82 dy, Vietnamese patient H. pylori samples (46 duodenal ulcer (DU), 51 non-cardia gastric cancer (NCGC)

83 cers (GU) were diagnosed in 2095 (8%) cases, duodenal ulcers (DU) in 2276 (9%) cases and 239 (1%) had

84 y mimic acute diverticulitis, cholecystitis, duodenal ulcer, duodenitis, enteritis, or adnexal or tes

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

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

87 ic ulcer samples), 20 for H. salomonis (four duodenal ulcer, five gastritis, and 11 gastric ulcer sam

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

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

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

91 erall burden of PUD in Africa, its patterns (duodenal ulcers, gastric ulcers, and coexisting ulcers),

92 Gastric and duodenal ulcers (GDUs) are decreasing both in frequency

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

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

95 Most patients with duodenal ulcers have impaired proximal duodenal mucosal

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

97 sociations have been previously reported for duodenal ulcer, here replicated trans-ancestrally.

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

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

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

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

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

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

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

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

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

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

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

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

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

111 43%, respectively, for surgery for bleeding duodenal ulcer, P < 0.0001 for all comparisons).

112 om a non-cardia gastric cancer patient and a duodenal ulcer patient, respectively, and their virulenc

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

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

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

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

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

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

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

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

121 12 months) was not significantly related to duodenal ulcer recurrence.

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

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

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

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

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

127 ome of 21 captive marmosets diagnosed with a duodenal ulcer/stricture (57 samples).

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

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

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

131 2.4 percent of all persons with a history of duodenal ulcer, the corresponding value for gastric ulce

132 y of NHPGH species was 10 for H. suis (three duodenal ulcer, three gastritis, and four gastric ulcer

133 rk-up revealed many clean-based non-bleeding duodenal ulcers to the third portion of the duodenum and

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

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

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

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

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

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

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

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