ライフサイエンスコーパス: peptic ulcer

1 astric adenocarcinoma, gastric lymphoma, and peptic ulcer.

2 placebo as endoscopic treatment for bleeding peptic ulcer.

3 tting in patients at risk of rebleeding from peptic ulcer.

4 g after hemostasis in patients with bleeding peptic ulcer.

5 astritis, especially in H. pylori-associated peptic ulcer.

6 ts, and back and an increased hazard rate of peptic ulcer.

7 a triple treatment or being diagnosed with a peptic ulcer.

8 such markers and can identify patients with peptic ulcers.

9 9.3-18.0] per 1000 person-years; P = .40) or peptic ulcers (10.9 [95% CI, 7.7-15.5] vs 11.4 [95% CI,

10 BCC sequence was more frequently observed in peptic ulcer (64.1%, 25/39) and gastric cancer patients

11 ensive care unit at risk for rebleeding from peptic ulcers after hemostasis.

12 Patients with high-risk bleeding peptic ulcers after successful endoscopic therapy were r

13 er-related bleeding or prevent rebleeding in peptic ulcers after successful hemostasis?

14 confounders, the relative risks for bleeding peptic ulcer among current users of calcium channel bloc

15 eased risk for hospitalization with bleeding peptic ulcer among users of calcium channel blockers.

16 Fifty-one patients had peptic ulcer and 56 were diagnosed as functional dyspeps

17 thogen responsible, with acid secretion, for peptic ulcer and a 20-fold increase in the risk of gastr

18 us disease and was proximal in patients with peptic ulcer and Crohn disease.

19 vacA s2/m2 strains are associated with lower peptic ulcer and gastric cancer risk and are non-toxic.

20 variety of pathological sequelae, including peptic ulcer and gastric cancer, resulting in significan

21 s work has shown which features of vacA make peptic ulcer and gastric cancer-associated type s1/m1 an

22 world's population and is a leading cause of peptic ulcer and gastric cancer.

23 ssociation of cagA EPIYA motif patterns with peptic ulcer and gastric cancer.

24 current hemorrhage in patients with bleeding peptic ulcers and adherent clots.

25 rsistent, and has various outcomes including peptic ulcers and cancer.

26 2)-receptor antagonist, in the prevention of peptic ulcers and erosive oesophagitis in patients recei

27 in a spectrum of gastric diseases, including peptic ulcers and gastric cancer.

28 disorders ranging from chronic gastritis to peptic ulcers and gastric cancer.

29 ontrolled cell proliferation, and eventually peptic ulcers and gastric cancer.

30 nce and forming a recognized risk factor for peptic ulcers and gastric cancer.

31 pathogen to survive in the stomach and cause peptic ulcers and gastric cancer.

32 d between the number of EPIYA-C segments and peptic ulcers and gastric cancer.

33 PIYA-ABCC motif patterns are associated with peptic ulcers and gastric cancer.

34 shed as the etiologic agent of gastritis and peptic ulcers and is a major risk factor for gastric ade

35 It is responsible for most peptic ulcers and is an important risk factor for gastri

36 bacter pylori infection causes gastritis and peptic ulcers and is linked epidemiologically to gastric

37 f 75 patients with gastric IM (30 cancer, 26 peptic ulcer, and 19 chronic gastritis patients) and was

38 of these, 402 had chronic gastritis, 77 had peptic ulcer, and 20 had gastric cancer.

39 ection is associated with chronic gastritis, peptic ulcer, and gastric cancer.

40 ticosteroid or anticoagulant use, history of peptic ulcer, and high average daily dose of NSAIDs.

41 Alcohol consumption, smoking, prior peptic ulcer, and history of gastric cancer in parents w

42 the world's population, causes gastritis and peptic ulcer, and is strongly associated with gastric ad

43 wide range of diseases, including gastritis, peptic ulcer, and two forms of gastric cancer.

44 anxiety, dementia, migraine, heart disease, peptic ulcers, and arthritis are up to eight times more

45 infections are known to cause gastritis and peptic ulcers, and dramatically enhance the risk of gast

46 spectrum of disease that includes gastritis, peptic ulcers, and gastric adenocarcinoma.

47 rious gastric diseases, including gastritis, peptic ulcers, and gastric cancer.

48 Gastrointestinal bleeding, peptic ulcers, and polyps were self-reported during exte

49 Thus, incident peptic ulcers are common in the United States but repres

50 ociated with a range of pathology, including peptic ulcer, atrophic gastritis, and gastric cancer.

51 and high-dose PPI groups who had a high risk peptic ulcer bleeding (n = 104 in each group), and these

52 ifferent stages of cirrhosis following acute peptic ulcer bleeding (PUB).

53 all patients (n = 271,030) hospitalized for peptic ulcer bleeding between January 1997 and December

54 association between cirrhosis and recurrent peptic ulcer bleeding by analyzing the Taiwan National H

55 pump inhibitor after endoscopic therapy for peptic ulcer bleeding has been recommended as adjuvant t

56 Peptic ulcer bleeding leads to substantial morbidity and

57 d forty-seven patients presenting with major peptic ulcer bleeding were randomized to heater probe pl

58 associated with long-term risk of recurrent peptic ulcer bleeding, although the risk declines with a

59 apy has become the mainstay of treatment for peptic ulcer bleeding, with current consensus guidelines

60 nagement of hospitalized patients with acute peptic ulcer bleeding.

61 ri cure as the primary efficacy end point in peptic ulcer clinical trials.

62 6), myocardial infarction (1.34; 1.07-1.69), peptic ulcer disease (1.27; 1.03-1.58), peripheral vascu

63 y was oesophageal varices (57%), followed by peptic ulcer disease (18%) and gastritis (10%).

64 cluded diverticulitis (5), pancreatitis (4), peptic ulcer disease (4), and cholecystitis (2).

65 by paralysis (90% increase), dementia (60%), peptic ulcer disease (53%), other neurological disorders

66 in patients developing the complications of peptic ulcer disease (eg, obstruction and perforation),

67 m2) was associated with an increased risk of peptic ulcer disease (PUD) (P = 0.003).

68 Gastric biopsy specimens of 68 peptic ulcer disease (PUD) and 327 chronic gastritis (CG

69 udy was to analyse the risk of uncomplicated peptic ulcer disease (PUD) in a cohort of new users of l

70 Despite progress in diagnosis and treatment, peptic ulcer disease (PUD) remains a common reason for h

71 tion in 1994 of guidelines for management of peptic ulcer disease (PUD), trends in physician practice

72 i to activate neutrophils is associated with peptic ulcer disease (PUD).

73 (s1a) allele of the underlying vacA gene to peptic ulcer disease (PUD).

74 astrointestinal bleeding (UGIB) secondary to peptic ulcer disease (PUD).

75 n gastric mucosa, and it is a major cause of peptic ulcer disease and a principal risk factor for gas

76 luids of a 64-year-old man with a history of peptic ulcer disease and alcohol abuse.

77 phenotypic subgroup has been associated with peptic ulcer disease and an increased bleeding tendency.

78 e H. pylori are more closely associated with peptic ulcer disease and cancer.

79 lori varies in severity from asymptomatic to peptic ulcer disease and cancer.

80 Helicobacter pylori, a cause of peptic ulcer disease and certain types of gastric cancer

81 ylori is the strongest known risk factor for peptic ulcer disease and distal gastric adenocarcinoma,

82 s and is the strongest known risk factor for peptic ulcer disease and distal gastric cancer, yet only

83 ter pylori, a human pathogen associated with peptic ulcer disease and gastric adenocarcinoma, we clon

84 n that may contribute to the pathogenesis of peptic ulcer disease and gastric adenocarcinoma.

85 A (CagA) into host cells are associated with peptic ulcer disease and gastric adenocarcinoma.

86 er pylori infection is the leading cause for peptic ulcer disease and gastric adenocarcinoma.

87 Peptic ulcer disease and gastric cancer are caused most

88 Helicobacter pylori, the main cause of peptic ulcer disease and gastric cancer in adult populat

89 Gastric diseases, including peptic ulcer disease and gastric cancer, affect 10% of t

90 an cells, contributes to the pathogenesis of peptic ulcer disease and gastric cancer, and is a candid

91 tant virulence factor in the pathogenesis of peptic ulcer disease and gastric cancer.

92 ch and may contribute to the pathogenesis of peptic ulcer disease and gastric cancer.

93 use of most gastric diseases, including both peptic ulcer disease and gastric cancer.

94 ) that may contribute to the pathogenesis of peptic ulcer disease and gastric cancer.

95 tence increases the risk of diseases such as peptic ulcer disease and gastric cancer.

96 to persistence of the bacterium and risk for peptic ulcer disease and gastric cancer.

97 tant virulence factor in the pathogenesis of peptic ulcer disease and gastric cancer.

98 tients is known to prevent the occurrence of peptic ulcer disease and gastric cancer.

99 tomach and contributes to the development of peptic ulcer disease and gastric cancer.

100 ects half of the world population and causes peptic ulcer disease and gastric cancer.

101 acter pylori infection of the stomach causes peptic ulcer disease and gastric cancer.

102 cells and contributes to the pathogenesis of peptic ulcer disease and gastric cancer.

103 tric epithelial cells and has been linked to peptic ulcer disease and gastric carcinoma.

104 the human stomach and increases the risk for peptic ulcer disease and gastric carcinoma.

105 oton pump inhibitor used in the treatment of peptic ulcer disease and gastrosophageal reflux disease

106 class it is fraught with the risk of serious peptic ulcer disease and its complications.

107 isms by which H pylori increases the risk of peptic ulcer disease and noncardia gastric adenocarcinom

108 rove to lessen the morbidity associated with peptic ulcer disease and other benign conditions.

109 ploratory laparotomy and gastric surgery for peptic ulcer disease approximately 10 years ago.

110 A small proportion of patients have peptic ulcer disease as cause and this can be treated em

111 atients who underwent gastrectomy for benign peptic ulcer disease between 1960 and 1975, 163 patients

112 Peptic ulcer disease has been associated with an increas

113 pylori in the pathogenensis of gastritis and peptic ulcer disease has been shown in adults and childr

114 roscopic surgery for treatment of perforated peptic ulcer disease has now been validated, with subseq

115 Incidence and risk factors for peptic ulcer disease in the United States have not been

116 Partial gastrectomy for benign peptic ulcer disease is associated with an increased ris

117 H. pylori-induced peptic ulcer disease is associated with inadequate regul

118 ts for children in whom H. pylori-associated peptic ulcer disease is diagnosed.

119 he risk for development of gastric cancer or peptic ulcer disease is higher among humans infected wit

120 Upper gastrointestinal bleeding from peptic ulcer disease is not a new clinical problem.

121 Gastric surgery for benign peptic ulcer disease is not a risk factor for either sho

122 greatest effect on surgical intervention in peptic ulcer disease is the Centers for Disease Control

123 Dumping, bile gastritis, or peptic ulcer disease occurred in three patients after PP

124 lly asymptomatic but sometimes progresses to peptic ulcer disease or gastric adenocarcinoma.

125 ommon in strains isolated from patients with peptic ulcer disease or gastric cancer, rather than asym

126 face, evade host immune clearance, and cause peptic ulcer disease or gastric neoplasia in a significa

127 d with chronic gastritis and, in some cases, peptic ulcer disease or gastric neoplasms.

128 ns of Helicobacter pylori from patients with peptic ulcer disease or intestinal-type gastric cancer c

129 s of the peptide; and the role of gastrin in peptic ulcer disease pathogenesis secondary to Helicobac

130 in the pathogenesis of chronic gastritis or peptic ulcer disease remain unclear.

131 g(+)/type s1-vacA strains from patients with peptic ulcer disease than in cag-negative/s2-vacA strain

132 ri causes diseases ranging from gastritis to peptic ulcer disease to gastric cancer.

133 History of peptic ulcer disease was assessed at baseline in 1986 an

134 Peptic ulcer disease was believed to be caused by acid a

135 ergency operation for bleeding or perforated peptic ulcer disease was performed to determine the asso

136 Prevalences of heart or peptic ulcer disease were not significantly higher.

137 an early proponent of an infectious cause of peptic ulcer disease were recently discovered.

138 our patients without previous GI bleeding or peptic ulcer disease who were enrolled in a multicenter,

139 Peptic ulcer disease, although declining in prevalence,

140 Peptic ulcer disease, although declining in prevalence,

141 in various degrees of gastric inflammation, peptic ulcer disease, and a predisposition to gastric ca

142 ion, psychiatric disorders, anemia, obesity, peptic ulcer disease, and cancer but a lower prevalence

143 s the risk of developing atrophic gastritis, peptic ulcer disease, and gastric adenocarcinoma.

144 its etiologic role in symptomatic gastritis, peptic ulcer disease, and gastric adenocarcinoma.

145 estive diseases including chronic gastritis, peptic ulcer disease, and gastric cancer.

146 elium is strongly associated with gastritis, peptic ulcer disease, and gastric cancer.

147 major role in the development of gastritis, peptic ulcer disease, and gastric cancer.

148 can lead to gastroesophageal reflux disease, peptic ulcer disease, and stress-related erosion/ulcer d

149 ylori has been implicated in the etiology of peptic ulcer disease, chronic gastritis, gastric carcino

150 In patients with bleeding related to peptic ulcer disease, combination therapy (epinephrine i

151 tic significance among CAD patients, whereas peptic ulcer disease, connective tissue disease, and lym

152 chronic active gastritis, which can lead to peptic ulcer disease, gastric adenocarcinoma, and mucosa

153 a resultant decline in H. pylori-associated peptic ulcer disease, gastric cancer remains the second

154 ronic gastritis and plays a critical role in peptic ulcer disease, gastric carcinoma, and gastric lym

155 ses chronic gastritis and is associated with peptic ulcer disease, gastric carcinoma, and gastric lym

156 acterial pathogens, often causing gastritis, peptic ulcer disease, gastric mucosa-associated lymphati

157 s, in whom it is a key etiological factor in peptic ulcer disease, gastric mucosa-associated lymphoid

158 ndications for PPI use, including history of peptic ulcer disease, gastroesophageal reflux disease, o

159 on, cholecystectomy, operative management of peptic ulcer disease, lysis of peritoneal adhesions, app

160 Compared with those with report of no peptic ulcer disease, men with gastric ulcer had an incr

161 nistering therapy include active or inactive peptic ulcer disease, mucosa-associated lymphoid tissue

162 intestinal tract, such as chronic gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue

163 ic gastritis and leading in some patients to peptic ulcer disease, mucosa-associated lymphomas, and g

164 at a variety of gastric disorders, including peptic ulcer disease, neoplasia, and autoimmune gastriti

165 Of patients with peptic ulcer disease, nine of 37 (24%) had stigmata of r

166 lays an etiologic role in the development of peptic ulcer disease, only a small number of these child

167 Peptic ulcer disease, present in 56% of patients, was th

168 cter pylori is the main etiologic factor for peptic ulcer disease, recent studies have explored a pot

169 d contraindication to aspirin use, including peptic ulcer disease, renal insufficiency, and use of no

170 cobacter pylori, implicated in gastritis and peptic ulcer disease, Streptococcus agalactiae, implicat

171 ding after successful hemostasis of bleeding peptic ulcer disease, the following questions should be

172 d areas: morbid obesity, gastric cancer, and peptic ulcer disease.

173 or for the development of gastric cancer and peptic ulcer disease.

174 the bacterium in pathogenesis and relapse of peptic ulcer disease.

175 IDA regardless of the presence or absence of peptic ulcer disease.

176 and that contributes to the pathogenesis of peptic ulcer disease.

177 ggest a relationship between lung cancer and peptic ulcer disease.

178 oeconomic status, added salt, and history of peptic ulcer disease.

179 episodes of acute distress that can lead to peptic ulcer disease.

180 much lower than for patients with idiopathic peptic ulcer disease.

181 plications of gastrin in the pathogenesis of peptic ulcer disease.

182 superior result for H. pylori eradication in peptic ulcer disease.

183 s requiring emergency surgery for perforated peptic ulcer disease.

184 ndrome, gastroesophageal reflux disease, and peptic ulcer disease.

185 nfected congenital anomalies, and perforated peptic ulcer disease.

186 ith Helicobacter pylori is the main cause of peptic-ulcer disease.

187 Using solid state NMR methods, a peptic ulcer drug analogue has been described at atomic

188 ing triple treatment or being diagnosed with peptic ulcer during the following 33 months more than tw

189 ients with different clinical presentations (peptic ulcer, gastric cancer, and atrophic gastritis).

190 ponsible for severe gastric diseases such as peptic ulcers, gastric adenocarcinoma, and gastric lymph

191 The association between stress and peptic ulcers has been questioned since the discovery of

192 patients who had bleeding associated with a peptic ulcer (hazard ratio, 0.70; 95% CI, 0.26 to 1.25)

193 nducted on 235 cirrhotic patients with acute peptic ulcer hemorrhage who underwent therapeutic endosc

194 Among 20,294 GBP patients, diabetes and peptic ulcer history entailed statistically significantl

195 Diabetes and peptic ulcer history seem to be risk factors for MU, but

196 We studied peptic ulcer hospitalizations in a cohort of Tennessee M

197 ctive cotherapy had an adjusted incidence of peptic ulcer hospitalizations of 5.65 per 1000 person-ye

198 h 363,037 person-years of follow-up and 1223 peptic ulcer hospitalizations.

199 ing triple treatment or being diagnosed with peptic ulcer (HR 2.24; CI 95% 1.16:4.35) after adjustmen

200 (HR, 1.14 [CI, 1.06 to 1.22]; P < 0.001) and peptic ulcers (HR, 1.17 [CI, 1.09 to 1.27]; P < 0.001) o

201 with an increased risk of gastric cancer and peptic ulcers in adults.

202 of Helicobacter pylori, the leading cause of peptic ulcers in humans.

203 ment or being diagnosed in a hospital with a peptic ulcer, in relation to quintiles of stress levels.

204 A total of 121 peptic ulcer incidents were recorded within 33 months of

205 Perforated peptic ulcer is a common emergency condition worldwide,

206 Among causes, peptic ulcer is the casuistic one.

207 elicobacter pylori strain is associated with peptic ulcer, it is uncertain whether the risk is greate

208 for murine atherosclerosis and that, unlike peptic ulcer, Koch's postulates cannot be fulfilled for

209 We summarise the evidence for perforated peptic ulcer management and identify directions for futu

210 ing triple treatment or being diagnosed with peptic ulcer of approximately 0.4%, whereas the highest

211 Upper gastrointestinal endoscopy revealed peptic ulcer of the duodenal bulb.

212 Patients with peptic ulcer or functional dyspepsia infected by H. pylo

213 proposed regimen in Brazilian patients with peptic ulcer or functional dyspepsia showed no significa

214 ts infected with H. pylori will ever develop peptic ulcer or gastric cancer.

215 ulcer complications (age 75 years or older, peptic ulcer or gastrointestinal bleeding in the past ye

216 ng-term users of NSAIDs with past or current peptic ulcer or troublesome dyspepsia led to impaired he

217 be associated with disease symptoms such as peptic ulcers or cardiovascular disorders, and epidemiol

218 astric ulcers and did not affect the rate of peptic ulcers or dyspepsia over 6 months.

219 is found more commonly in strains that cause peptic ulcers or gastric cancer, rather than asymptomati

220 pancreas and, if untreated, can cause severe peptic ulcers or metastatic disease.

221 Upper gastrointestinal bleeding from peptic ulcers or other nonvariceal causes generally stop

222 However, the risks of peptic ulcer (OR = 7.0, 95% CI = 3.3-15.1; p < 0.001) an

223 e disorders, POWs had higher hazard rates of peptic ulcer (P<.01).

224 Subgroup analysis of diagnosed peptic ulcer patients revealed the same pattern as the m

225 chronic gastritis patients, 73.6% (39/53) in peptic ulcer patients, and 78.6% (11/14) in gastric canc

226 obstruction or gangrene (PEH) and perforated peptic ulcer (PPU) was analyzed, independent of HV esoph

227 ption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular pancreas, and ev

228 cirrhosis was significantly associated with peptic ulcer rebleeding (adjusted hazard ratio, 3.19; 95

229 suppression status and acid-related disease (peptic ulcer, reflux esophagitis).

230 itor (PPI) therapies for patients with acute peptic ulcer-related bleeding of sufficient severity to

231 sident of the ACG, and a panel of experts in peptic ulcer, selected by the committee.

232 d assess whether the most recent behavior of peptic ulcer still fits the overall pattern governed by

233 reduced despite the decreasing incidence of peptic ulcers, strategies to eradicate Helicobacter pylo

234 nsity was much greater in H. pylori-infected peptic ulcer subjects than in the other gastritis groups

235 ry, 127 (2.8%) versus 2033 (2.4%), P > 0.05; peptic ulcer surgery, 22 (0.5%) versus 277 (0.3%), P > 0

236 The main side-effect of aspirin is peptic ulcers; therefore coadministration of aspirin wit

237 tion and produces a variety of diseases from peptic ulcer to cancer.

238 g in severity from superficial gastritis and peptic ulcer to gastric cancer and mucosal-associated ly

239 nued to influence the temporal variations of peptic ulcer until most recently.

240 pulmonary disease, perinatal conditions, and peptic ulcer was relatively underfunded.

241 Hospitalization for bleeding peptic ulcers was identified by hospital claims and veri

242 Long before the cause was discovered, peptic ulcers were known to occur preferentially in indi

243 The optimal management of bleeding peptic ulcer with adherent clot is controversial and may

244 robe plus placebo injection as treatment for peptic ulcers with active bleeding or nonbleeding visibl

245 SAIDs) prescribed to those with a history of peptic ulcer without co-prescription of a proton-pump in

246 non-selective NSAID if they had a history of peptic ulcer without gastroprotection (OR 0.58, 95% CI 0

247 (H2) receptor agonist commonly used to treat peptic ulcers, would be effective against lung adenocarc