ライフサイエンスコーパス: peptic ulcer

1 astric adenocarcinoma, gastric lymphoma, and peptic ulcer.

2 % in these cases, so that 33.65% of whom had peptic ulcer.

3 placebo as endoscopic treatment for bleeding peptic ulcer.

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

5 g after hemostasis in patients with bleeding peptic ulcer.

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

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

8 tion of esophagus, small or large bowel, and peptic ulcer.

9 ure, chronic kidney disease, or a history of peptic ulcer.

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

11 such markers and can identify patients with peptic ulcers.

12 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,

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

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

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

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

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

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

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

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

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

22 derwent emergent laparotomy for a perforated peptic ulcer and died from sepsis.

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

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

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

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

27 r pylori (Hp) infection is the main cause of peptic ulcer and gastric cancer.

28 particular, the most important of them i.e. peptic ulcer and gastric cancer.

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

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

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

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

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

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

35 ic mucosa by Helicobacter pylori can lead to peptic ulcers and gastric cancer.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 acterial infection that can cause gastritis, peptic ulcers, and cancer.

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

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

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

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

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

58 ominal pain in a primary care setting have a peptic ulcer as the cause of their symptoms.

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

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

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

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

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

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

65 Peptic ulcer bleeding leads to substantial morbidity and

66 Mortality in peptic ulcer bleeding remains high, especially in patien

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

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

69 surgery regarding prognosis after refractory peptic ulcer bleeding, and the shorter length of hospita

70 dication protects against aspirin-associated peptic ulcer bleeding, but this might not be sustained i

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

72 nagement of hospitalized patients with acute peptic ulcer bleeding.

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

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

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

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

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

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

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

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

81 etic factors are recognized to contribute to peptic ulcer disease (PUD) and other gastrointestinal di

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

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

84 (GC), the impact on other diseases, such as peptic ulcer disease (PUD), dyspepsia, and gastric lymph

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

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

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

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

89 71 (36%), intestinal obstruction 11 (6%) and peptic ulcer disease 9 (5%).

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

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

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

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

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

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

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

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

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

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

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

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

102 Peptic ulcer disease and gastric cancer are caused most

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 r pylori (HP), a known major risk factor for peptic ulcer disease and gastric cancer.

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

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

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

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

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

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

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

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

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

127 of gastric diseases like gastric cancer and peptic ulcer disease attributed to Helicobacter pylori i

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

129 Peptic ulcer disease has been associated with an increas

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

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

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

133 Annually, 10 000 people die of peptic ulcer disease in the US.

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

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

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

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

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

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

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

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

142 Globally, peptic ulcer disease occurs in 3.5-32% of patients with

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

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

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

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

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

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

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

150 h a higher risk of gastric adenocarcinoma or peptic ulcer disease than cag PAI-negative strains.

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

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

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

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

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

156 Explanatory variables associated with peptic ulcer disease were analyzed by applying logistic

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

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

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

160 Peptic ulcer disease, although declining in prevalence,

161 Peptic ulcer disease, although declining in prevalence,

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

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

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

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

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

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

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

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

170 nificant association observed in vacA s1 and peptic ulcer disease, as well as vacA s1/m2 and gastric

171 e human stomach and induces acute gastritis, peptic ulcer disease, atrophic gastritis, and gastric ad

172 edical history (smoking, diabetes, bleeding, peptic ulcer disease, cancer, chronic liver disease, chr

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

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

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

176 ns of the PCSK9 T allele were also seen with peptic ulcer disease, depression, asthma, chronic kidney

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

197 refractory NVUGIB, the etiology of bleeding (peptic ulcer disease, unknown source, post surgical); pa

198 s1m1, and s2m1 genotypes and development to peptic ulcer disease.

199 nfected congenital anomalies, and perforated peptic ulcer disease.

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

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

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

203 tes to the development of gastric cancer and peptic ulcer disease.

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

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

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

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

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

209 es to the pathogenesis of gastric cancer and peptic ulcer disease.

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

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

212 rden due to chronic liver diseases (CLD) and peptic ulcer disease.

213 Endoscopy definitively diagnoses peptic ulcer disease.

214 infectious disease, autoimmune disorders, or peptic ulcer disease.

215 e considered the top-ranked risk factors for peptic ulcer disease.

216 < 0.001) were identified as risk factors for peptic ulcer disease.

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

218 s requiring emergency surgery for perforated peptic ulcer disease.

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

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

221 ction is a major cause of chronic gastritis, peptic ulcer diseases and cancer.

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

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

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

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

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

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

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

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

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

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

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

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

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

235 (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

236 1m1, s1m2, s2m1 and s2m2) and development to peptic ulcer in Iranian population.

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

238 Acid blockers, such as omeprazole, can heal peptic ulcers in approximately 80% to 100% of patients w

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

240 copy in 105 of the 158 patients (66.4%) with peptic ulcers in the urgent-endoscopy group and in 76 of

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

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

243 Complications of peptic ulcer include bleeding (73% of patients), perfora

244 Gastric ulcer or peptic ulcer is a common disease worldwide.

245 Perforated peptic ulcer is a common emergency condition worldwide,

246 Among causes, peptic ulcer is the casuistic one.

247 A decisive factor in the pathogenesis of peptic ulcers is gastric acid, the secretion of which is

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

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

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

251 Pseudoachalasia, peptic ulcer, normal gastric emptying scintigraphy (GES)

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

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

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

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

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

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

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

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

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

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

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

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

264 e strains significantly increase the risk of peptic ulcer (OR 1.36; 1.07-1.72 with 95% CIs), especial

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

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

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

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

269 perforation (OR 6.97, 95% CI 6.60-7.37), and peptic ulcer perforation (OR 3.67, 95% CI 3.40-3.96).

270 perforation (OR 4.33, 95% CI 4.12-4.56), and peptic ulcer perforation (OR 4.63, 95% CI 4.27-5.02).

271 ith laparoscopic surgery (LS) for perforated peptic ulcer (PPU) disease using a National dataset BACK

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

273 with Roux-en-Y reconstruction for nonhealing peptic ulcer presented to the emergency department and r

274 in thrombosis prophylaxis (0.74 [0.68-0.81), peptic ulcer prophylaxis (0.46 [0.38-0.57]), spontaneous

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

276 duodenal wall of the patient with perforated peptic ulcer, real time reverse transcriptase polymerase

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

278 Eradication of H pylori decreases peptic ulcer recurrence rates from approximately 50% to

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

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

281 mall intestine, excision of large intestine, peptic ulcer repair, lysis of peritoneal adhesions, and

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

283 section, appendicitis, perforated esophagus, peptic ulcer, small bowel or large bowel, and incarcerat

284 section, appendicitis, perforated esophagus, peptic ulcer, small bowel or large bowel, and incarcerat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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