ライフサイエンスコーパス: omeprazole

1 iod of heartburn-free days (23 vs 12 days on omeprazole).

2 ith or without inhibition of gastric acid by omeprazole.

3 increased (from 55% to 97%, P = 0.03) after omeprazole.

4 rchlorhydria) and control of all symptoms by omeprazole.

5 0, prevented inhibition of acid transport by omeprazole.

6 in PBMCs when compared with lansoprazole and omeprazole.

7 nificant difference between lansoprazole and omeprazole.

8 te, 36% would add antacid, and 13% would add omeprazole.

9 ridyl methylsulfinyl benzimidazoles, such as omeprazole.

10 cleavage of progastrin at Lys residues after omeprazole.

11 ncentrations in melanocytes was inhibited by omeprazole.

12 -92 were not influenced by pretreatment with omeprazole.

13 laparoscopic Nissen fundoplication (LNF) vs. omeprazole.

14 t determine the specificity of P450 2C19 for omeprazole.

15 a drug interaction that was attributable to omeprazole.

16 tion in upper gastrointestinal bleeding with omeprazole.

17 an drug substrate, the proton pump inhibitor omeprazole.

18 or lansoprazole rather than esomeprazole or omeprazole.

19 trial when clopidogrel was coprescribed with omeprazole.

20 n by the coadministration of esomeprazole or omeprazole.

21 ents when clopidogrel was co-prescribed with omeprazole.

22 ough the risk of diarrhea was increased with omeprazole.

23 en with an SIL-IS through a case study using omeprazole.

24 en PHOPDT plus omeprazole compared with only omeprazole.

25 n FVB/N mice rendered hypergastrinemic using omeprazole.

26 lansoprazole (25 microg/mL); c) control plus omeprazole (0.35 microg/mL); and d) control plus ranitid

27 with placebo at 180 days (hazard ratio with omeprazole, 0.34, 95% confidence interval [CI], 0.18 to

28 ole and 5.7% with placebo (hazard ratio with omeprazole, 0.99; 95% CI, 0.68 to 1.44; P = 0.96); high-

29 4 +/- 1.8 vs 2.1 +/- 2.2 hours, P = 0.0001), omeprazole (1.1 +/- 1.1 vs 4.4 +/- 1.3 hours, P < 0.0001

30 hetic CSF) was added to VCP in group II, and omeprazole (10(-5) mol/l of synthetic CSF) was added to

31 38.4 +/-94.2; lansoprazole 14.6+/-84.4; and omeprazole 15.1+/-48.9.

32 -2-pyridyl)methylsulfinyl]-1H-benzimidazole (omeprazole), 2-[(4-trifluoroethoxy-3-methyl-2-pyridyl)me

33 D were randomly allocated to either group 1 (omeprazole 20 mg + domperidone 30 mg) or group 2 (omepra

34 All patients received omeprazole 20 mg once daily for 3 weeks until endoscopy,

35 lofenac slow-release 75 mg twice a day (with omeprazole 20 mg twice a day for gastroprotection) for a

36 azole 20 mg + domperidone 30 mg) or group 2 (omeprazole 20 mg) in an equal ratio; 2 capsules daily in

37 285 patients were randomly assigned omeprazole 20 mg, amoxycillin 1000 mg, and clarithromyci

38 nts were randomly assigned active treatment (omeprazole 20 mg, clarithromycin 250 mg, and tinidazole

39 he NSAID diclofenac (75 mg twice daily) plus omeprazole (20 mg once daily), and either rifaximin-EIR

40 ly), metronidazole (400 mg twice daily), and omeprazole (20 mg twice daily).

41 ly), metronidazole (400 mg twice daily), and omeprazole (20 mg twice daily); or (3) azithromycin (500

42 ial compared Gaviscon(R) (4 x 10 mL/day) and omeprazole (20 mg/day) in patients with 2-6 day heartbur

43 an alginate (Gaviscon(R), 4 x 10 mL/day) and omeprazole (20 mg/day) on GERD symptoms in general pract

44 pH monitoring after 7 days of treatment with omeprazole, 20 mg twice daily, followed by different tre

45 supplements at bedtime: placebo; additional omeprazole, 20 mg; ranitidine, 150 mg; and ranitidine, 3

46 Patients were randomized to 20 mg omeprazole, 250 mg clarithromycin, and 500 mg tinidazole

47 atients were randomized to either placebo or omeprazole (40 mg AM and 20 mg PM) groups for 7 days.

48 ve 3 and 4 were higher with rabeprazole than omeprazole (46 [37-55] vs. 30 [15-55] %, 9 [5-11] % for

49 160-383 (SRS-2-SRS-5) of P450 2C19 conferred omeprazole 5-hydroxylase activity to P450 2C9.

50 residues 160-227 of P450 2C19 also exhibited omeprazole 5-hydroxylase activity which was dramatically

51 A single mutation Ile99 --> His increased omeprazole 5-hydroxylase to approximately 51% of that of

52 0 2C9 to an enzyme with a turnover number of omeprazole 5-hyrdroxylation, which resembled that of P45

53 he alternative PPIs (8/52 pantoprazole, 6/52 omeprazole, 5/52 esomeprazole, 3/52 rabeprazole).

54 r presence of the H(+),K(+)-ATPase inhibitor omeprazole (60 mg kg(-1) I.P.), indomethacin blocked sim

55 elevated 5-6-fold by oral administration of omeprazole (75 mg/kg).

56 teraction and demonstrate assay sensitivity, omeprazole 80 mg) was given daily for 9 days.

57 germ-free mice that were either treated with omeprazole, a proton-pump inhibitor that suppresses acid

58 Omeprazole abolished RX 77368-induced acid secretion but

59 Pantoprazole and omeprazole accounted for 62% and 9% of concurrent PPI us

60 ial acid and nonacid reflux before and after omeprazole administration.

61 peridone combination was more effective than omeprazole alone in providing complete cupping of reflux

62 In addition, mice were treated with omeprazole alone or in combination with either YF476 or

63 Omeprazole also elevated VMAT2 expression in rats fasted

64 Omeprazole, an intravenous proton pump inhibitor, signif

65 ndomly to groups given hybrid therapy (40 mg omeprazole and 1 g amoxicillin, twice daily for 14 days;

66 testinal event; the event rate was 1.1% with omeprazole and 2.9% with placebo at 180 days (hazard rat

67 ascular event, with event rates of 4.9% with omeprazole and 5.7% with placebo (hazard ratio with omep

68 e to aryl hydrocarbon receptor (AhR) agonist omeprazole and a 10-fold induction in response to PXR ag

69 acid secretion is approximately 28 hours for omeprazole and approximately 46 hours for pantoprazole.

70 We found that omeprazole and its closely related congeners inhibited m

71 age was blocked by the proton pump inhibitor omeprazole and mediated by the acid-activated protease p

72 Omeprazole and pantoprazole have no activity.

73 gnificantly lower with rabeprazole than with omeprazole and placebo (22 [14-53] vs. 54 [19-130] and 9

74 single oral dose of 20 mg rabeprazole, 20 mg omeprazole and placebo in obese subjects.

75 We investigated the effects of omeprazole and Sch 28080, a more specific and a more pot

76 o inhibitors of the apical H(+)/K(+) ATPase (omeprazole and SCH28080), thereby unmasking a stable, lo

77 ith a proton-pump inhibitor (lansoprazole or omeprazole) and bismuth subsalicylate.

78 ns for 5 consecutive days concomitantly with omeprazole, and 4 weeks later during cycle 2 patients re

79 line Beecham, Philadelphia, PA), the antacid omeprazole, and dexamethasone was most effective in amel

80 dical therapies with somatostatin analogues, omeprazole, and locoregional tumor ablation have made a

81 al ambulatory pH monitoring with response to omeprazole, and provides additional insights into the pa

82 Atorvastatin, omeprazole, and several other drugs have been shown in p

83 ior ulcer disease; antimicrobial therapy and omeprazole are prescribed when H. pylori is present.

84 trointestinal bleeding was also reduced with omeprazole as compared with placebo (hazard ratio, 0.13;

85 breakthrough with placebo at bedtime; 7 with omeprazole at bedtime (P = NS); 4 with ranitidine, 150 m

86 Additional omeprazole at bedtime reduced the percentage of time wit

87 We compared the effect of a third dose of omeprazole at bedtime with that of a dose of ranitidine

88 A series of omeprazole-based analogues was synthesized and assessed

89 Mice were injected with either IL-1beta or omeprazole before measuring Shh mRNA expression and acid

90 lyacrylamide gel electrophoresis showed that omeprazole bound covalently to one of the two cysteines

91 vascular interaction between clopidogrel and omeprazole, but our results do not rule out a clinically

92 Regimen 1, omeprazole + clarithromycin (O/C), was supported by two

93 vergrowth between patients given PHOPDT plus omeprazole compared with only omeprazole.

94 from randomized controlled trials evaluating omeprazole compared with placebo showed no difference in

95 surgery and 6 months of once- or twice-daily omeprazole (controls, n = 42).

96 At 10 years, LNF and omeprazole costs were similar.

97 in the canine model, physiological doses of omeprazole decrease CSF production by about 26%.

98 Prior mechanistic studies reported that omeprazole decreases the platelet inhibitory effects of

99 cokinetic and pharmacodynamic responses with omeprazole demonstrated assay sensitivity.

100 ice, were almost completely restored through omeprazole, demonstrating that urease production in L. r

101 jects taking a hydrogen pump blocking agent (omeprazole) develop bacterial overgrowth of the small in

102 metabolizing enzymes (caffeine, tolbutamide, omeprazole, dextromethorphan, and oral and intravenous m

103 y, since Sch 28080 which is more potent than omeprazole did not significantly affect CSF production.

104 AIM: To compare the efficacy and safety of omeprazole-domperidone combination vs omeprazole monothe

105 Omeprazole-domperidone combination was more effective th

106 diet for 35 d were randomly assigned to take omeprazole during the first period of study or starting

107 t patients take no more than low-dose (20-mg omeprazole equivalents) PPI daily.

108 in which hypergastrinemia was induced using omeprazole, following gamma-radiation, 5-fluorouracil, a

109 and PAM were unchanged after treatment with omeprazole for 5 days, whereas gastrin, PC1/3 and PC2 mR

110 ), was increased 3-fold after treatment with omeprazole for either 1 or 5 days.

111 , incubated in vitro, from rats treated with omeprazole for up to 5 days.

112 uded in the Gaviscon(R) group and 121 in the omeprazole group for the per protocol non-inferiority an

113 days by D7 was significantly greater in the omeprazole group: 3.7 +/- 2.3 days vs. 3.1 +/- 2.1 (p =

114 centration of clopidogrel active metabolite (omeprazole > esomeprazole > lansoprazole > dexlansoprazo

115 Omeprazole had no significant inhibitory effect on the a

116 Omeprazole has shown remarkable efficacy and safety in t

117 tagastrin (pH 3.5 +/- 0.2) and eliminated by omeprazole, implicating parietal cell H,K-ATPase as the

118 Nausea resolved after treatment with omeprazole in 7 patients, after treatment with cisapride

119 Gaviscon(R) was non-inferior to omeprazole in achieving a 24-h heartburn-free period in

120 nt literature discusses the use of high-dose omeprazole in diagnosing and treating chest pain associa

121 ease in intraluminal pH that was reversed by omeprazole in fundic organoids and indicated functional

122 a more potent inhibitor of K+,H+-ATPase than omeprazole, in canine cerebrospinal fluid (CSF) producti

123 cid secretion by proton pump inhibitors like omeprazole increases the synthesis and secretion of the

124 We report here how omeprazole influences the conversion of the gastrin prec

125 inhibited ATPase activity and SCH 28080- and omeprazole-inhibited 86Rb uptake.

126 Only removal of Cys822 blocked omeprazole inhibition of 86Rb transport.

127 d omeprazole suspension (containing 40 mg of omeprazole) initially, followed by a second 20-mL dose 6

128 Omeprazole is a proton pump inhibitor used in the treatm

129 Thermolysin digestion of the isolated omeprazole-labeled fifth and sixth transmembrane pair sh

130 ality-adjusted life years per patient), with omeprazole less expensive than LNF ($6053 vs. $9482 per

131 Omeprazole may predispose to small intestinal bacterial

132 gnificantly lower with rabeprazole than with omeprazole (median 1 [1,2] vs. 2 [1-3], p = 0.04).

133 performed by human CYP2C19, the major human omeprazole-metabolizing P450 enzyme.

134 H. pylori eradication therapy using omeprazole, metronidazole, and clarithromycin was admini

135 ety of omeprazole-domperidone combination vs omeprazole monotherapy in gastroesophageal reflux diseas

136 ntoprazole (n = 9), rabeprazole (n = 2), and omeprazole (n = 1).

137 utilized for the sensitive determination of omeprazole (OME).

138 me ranitidine is more effective than bedtime omeprazole on residual nocturnal acid secretion in patie

139 ce a day for the following 3 weeks and 20 mg omeprazole once daily for a further 4 weeks.

140 6 of whom were treated for 8 days with 20 mg omeprazole or 20 mg rabeprazole in a 2-way crossover fas

141 iple Doses of Dexiansoprazole, Lansoprazole, Omeprazole or Esomeprazole on the Pharmacokinetics and P

142 ical therapy or requiring daily therapy with omeprazole or high-dose H2 antagonists.

143 on of ATPase following inhibition in vivo by omeprazole or its enantiomers was seen with dithiothreit

144 527,364 lansoprazole initiators and 923,500 omeprazole or pantoprazole initiators.

145 ears; 95% confidence interval 8.1-12.4) than omeprazole or pantoprazole users (n = 193; 15.3 cases pe

146 rs have a lower incidence of TB disease than omeprazole or pantoprazole users.

147 ceive clopidogrel in combination with either omeprazole or placebo, in addition to aspirin.

148 t decrease (reduced-function CYP2C19 allele; omeprazole) or increase (cigarette smoking) the metaboli

149 udied a cohort of new users of lansoprazole, omeprazole, or pantoprazole from the United Kingdom Clin

150 gnificantly lower with rabeprazole than with omeprazole (p < 0.0001).

151 ity of pain relief was slightly in favour of omeprazole (p = 0.049).

152 s for Gaviscon(R) and 2.0 (+/- 2.3) days for omeprazole (p = 0.93); mean intergroup difference was 0.

153 Prescription of omeprazole, pantoprazole, lansoprazole, esomeprazole, or

154 rough nanoindentation studies on a series of omeprazole polymorphs, in which the proportions of the 5

155 During treatment with omeprazole, postprandial reflux becomes predominantly no

156 cessed by the cationic sulfenamide formed by omeprazole, presumably the turn between M5 and M6.

157 Subjects were given omeprazole, rabeprazole or placebo in a randomized order

158 th either saline or an antisecretory dose of omeprazole, ranitidine, or cimetidine, were intragastric

159 In addition, omeprazole reduced tyrosinase protein abundance in the p

160 ings are consistent with the hypothesis that omeprazole reduces melanogenesis by inhibiting ATP7A and

161 imens 1 and 2; n = 6) or in combination with omeprazole (regimen 3; n = 4), or bismuth subsalicylate

162 of PPIs and randomized controlled trials of omeprazole seem to provide conflicting results for the e

163 able to activate acid secretion through the omeprazole-sensitive H+,K+ -ATPase even in the absence o

164 Patients received 20 mL of simplified omeprazole suspension (containing 40 mg of omeprazole) i

165 Patients were randomized to treatment with omeprazole suspension (two 40-mg doses on day 1, via oro

166 in the per-protocol population was 4.5% with omeprazole suspension and 6.8% with cimetidine, meeting

167 e, phase 3, double-blind trial with parallel omeprazole suspension and cimetidine treatment groups.

168 In the omeprazole suspension group, median gastric pH was >4 on

169 Immediate-release omeprazole suspension is effective in preventing upper g

170 Simplified omeprazole suspension prevented clinically significant u

171 astric pH was > or =6 on all trial days with omeprazole suspension treatment and on 50% of days with

172 Simplified omeprazole suspension was administered through a nasogas

173 er gastrointestinal bleeding after receiving omeprazole suspension.

174 eting the criteria for the noninferiority of omeprazole suspension.

175 is study was to evaluate the efficacy of the omeprazole test (OT) in diagnosing gastroesophageal refl

176 ridyl-methylsulfinyl-benzimidazoles, such as omeprazole, that convert to thiophilic probes of luminal

177 ally used drugs including the antiulcer drug omeprazole, the anxiolytic drug diazepam, the beta-block

178 Long-term omeprazole therapy in H. pylori-positive patients with Z

179 as started, and the lowest gastric pH during omeprazole therapy.

180 Omeprazole topically applied to the skin of UV-irradiate

181 e percent decreases in CSF production in the omeprazole treated group were 26 +/- 17 and 24 +/- 13 at

182 ) were invited to be randomly assigned to an omeprazole-treated (hypochlorhydric) group or a non-omep

183 ole-treated (hypochlorhydric) group or a non-omeprazole-treated group, but 6 subjects chose not to pa

184 nomas from the small and large intestines of omeprazole-treated mice were increased 35 and 29%, respe

185 ed within 240 min of the labelling period in omeprazole-treated samples, but secretion of labelled ga

186 episodes were detected before and 261 after omeprazole treatment (P > 0.05).

187 n the period when the diet was combined with omeprazole treatment (P > 0.05).

188 weeks in the controls to 10 weeks following omeprazole treatment (P < 0.00001, log-rank test).

189 line (P < 0.05); however, the combination of omeprazole treatment and the phylloquinone-restricted di

190 Omeprazole treatment increased the proportion of EndoH s

191 recovery of acid secretion in rats following omeprazole treatment is approximately 15 hours, whereas

192 ression, similar to the levels obtained with omeprazole treatment of wild-type mice.

193 In contrast, omeprazole treatment resulted in mild progression of gas

194 icted diet or during the period of diet plus omeprazole treatment.

195 g tinidazole twice a day for 1 week or 20 mg omeprazole twice a day and identical placebos.

196 egative patients were given open label 20 mg omeprazole twice a day for 1 week.

197 All patients received 20 mg omeprazole twice a day for the following 3 weeks and 20

198 ned (2:1) to receive PHOPDT (n=138) or 20 mg omeprazole twice daily (n=70).

199 cturnal acid secretion in patients receiving omeprazole twice daily is most likely histamine related.

200 with 150 mg and 6% with 300 mg (P <0.01 vs. omeprazole twice daily plus bedtime).

201 <4 from 48% to 31% (P < 0.005) compared with omeprazole twice daily with placebo at bedtime.

202 ithout medication, session 2 after 7 days of omeprazole twice daily.

203 cturnal acid secretion in patients receiving omeprazole twice daily.

204 cturnal acid secretion in patients receiving omeprazole twice daily.

205 They then took PPIs for 4 weeks (40 mg omeprazole, twice daily) and fecal samples were collecte

206 o 5 days with the H(+)-K(+)-ATPase inhibitor omeprazole, VMAT2, histidine decarboxylase and chromogra

207 en lansoprazole vs. ranitidine (p< .01), and omeprazole vs. ranitidine (p< .05), and no significant d

208 s 6.8, and the mean lowest pH after starting omeprazole was 5.6.

209 was 7.1, the mean gastric pH after starting omeprazole was 6.8, and the mean lowest pH after startin

210 parietal cell Shh expression by IL-1beta and omeprazole was additive.

211 Omeprazole was discontinued at 8 weeks and patients were

212 easures were gastric pH measured 4 hrs after omeprazole was first administered, mean gastric pH after

213 ested, and ion enhancement of about 500% for omeprazole was observed in one lot but not in the other.

214 as first administered, mean gastric pH after omeprazole was started, and the lowest gastric pH during

215 response to a single dose of rabeprazole and omeprazole was strong and not significantly different be

216 and 1 observational) assessed the effect of omeprazole when added to DAPT; the other 30 (observation

217 he H2-antagonist failed, 52% would change to omeprazole, whereas 67% would change to an H2-antagonist

218 tion of S-mephenytoin and 5-hydroxylation of omeprazole, while the structurally homologous P450 2C9 h

219 (n=142, H. pylori eradication treatment), or omeprazole with placebo antibiotics (n=143, controls) fo