ライフサイエンスコーパス: escitalopram

1 difference in the scores with placebo versus escitalopram.

2 ive behavior therapy, and 6 nonresponders to escitalopram.

3 ign with 8 wk of standardized treatment with escitalopram.

4 ed 8 wk of standardized pharmacotherapy with escitalopram.

5 r the selective serotonin reuptake inhibitor escitalopram.

6 subjects who completed phase 1 responded to escitalopram.

7 s after 8 weeks of open-label treatment with escitalopram.

8 nt selection in depression, particularly for escitalopram.

9 serotonin reuptake inhibitors fluoxetine and escitalopram.

10 s after 8 weeks of open-label treatment with escitalopram.

11 measures of executive function more than the escitalopram.

12 3 points higher with nortriptyline than with escitalopram.

13 ctions than historical controls treated with escitalopram.

14 Patients were randomized 1:1 to receive escitalopram (10-20 mg) or matching placebo in addition

15 Among healthy women, the use of escitalopram (10-20 mg/d) compared with placebo resulted

16 igned to one of four conditions: 16 weeks of escitalopram (10-20 mg/day) plus modular CBT, followed b

17 ual likelihood to 12 weeks of treatment with escitalopram (10-20 mg/day), duloxetine (30-60 mg/day),

18 cale (HAM-D) score of 18 or greater received escitalopram, 10 mg daily, for 12 weeks.

19 Escitalopram, 10 mg/d (n = 90), or placebo (n = 91) admi

20 lop depression than individuals who received escitalopram (11 major and 2 minor cases of depression [

21 cantly differ between treatments (CBT: 10.2, escitalopram: 11.1, duloxetine: 11.2).

22 ompare nCCR-GD to a gold-standard treatment (escitalopram: 20 mg per 12 weeks) in 11 treatment-resist

23 At the end of 6 weeks, more patients taking escitalopram (34.2% [95% CI, 25.4%-43.0%]) had absence o

24 , 51 given amitriptyline (53%), and 37 given escitalopram (38%) (P = .05, after treatment, adjusted f

25 antly differ between treatments (CBT: 41.9%, escitalopram: 46.7%, duloxetine: 54.7%).

26 cognitive behavior therapy, 11 remitters to escitalopram, 9 nonresponders to cognitive behavior ther

27 ent randomization, with 91 being assigned to escitalopram, 94 to tDCS, and 60 to placebo.

28 lammation, predicts differential response to escitalopram (a serotonin reuptake inhibitor) and nortri

29 n this study, we investigated the effects of escitalopram, a selective serotonin reuptake inhibitor (

30 wed by 28 weeks of maintenance escitalopram; escitalopram alone, followed by maintenance escitalopram

31 pram plus CBT, followed by pill placebo; and escitalopram alone, followed by placebo.

32 Hamilton Anxiety Rating Scale compared with escitalopram alone.

33 Phase 2 relapse proportions were 18% for escitalopram and 40% for placebo.

34 MDD patients were treated with citalopram or escitalopram and blood was drawn at baseline, 4 and 8 we

35 Both escitalopram and CBT prevented relapse compared with pla

36 ional 12 weeks of treatment with combination escitalopram and cognitive behavior therapy.

37 py (CBT) and two antidepressant medications (escitalopram and duloxetine) in patients with major depr

38 nce in mean cumulative response rate between escitalopram and placebo (57%; 95% CI, 46%-67%; vs 45%;

39 5% CI, 2.24-4.15) hot flashes per day in the escitalopram and placebo groups, respectively.

40 rmetabolism was associated with remission to escitalopram and poor response to cognitive behavior the

41 the selective serotonin reuptake inhibitors escitalopram and sertraline and the serotonin-norepineph

42 Escitalopram and sertraline showed the best profile of a

43 the selective serotonin reuptake inhibitors escitalopram and sertraline than did A allele carriers.

44 both efficacy and acceptability in favour of escitalopram and sertraline.

45 onded better and had fewer side effects with escitalopram and sertraline.

46 Escitalopram and tDCS were both superior to placebo (dif

47 Participants received 12 weeks of open-label escitalopram and were then randomly assigned to one of f

48 thiazines, fluoxetine, citalopram (including escitalopram), and methadone were significantly more fre

49 fluoxetine and cognitive behavioral therapy, escitalopram, and collaborative care demonstrated benefi

50 talopram than those treated with placebo and escitalopram, and median time to onset of anxiolytic res

51 Neither amitriptyline nor escitalopram appeared to affect GE or meal-induced satie

52 Amitriptyline, but not escitalopram, appears to benefit some patients with FD,

53 nt scores were improved with eszopiclone and escitalopram at every point (P < .02), while CGI of Seve

54 Escitalopram augmented with CBT increased response rates

55 s a randomized double-blind 12-week trial of escitalopram, bupropion, or the combination of the two i

56 med significantly above chance in a combined escitalopram-buproprion treatment group in COMED (n=134;

57 effective at reducing depressive symptoms as escitalopram but does so in 4 weeks instead of 12.

58 curacy specifically following treatment with escitalopram but not the other medications.

59 and depression, 18 months of treatment with escitalopram compared with placebo did not significantly

60 the TPJ showed increased activity in IED on escitalopram compared with placebo.

61 heart disease and baseline MSIMI, 6 weeks of escitalopram, compared with placebo, resulted in a lower

62 whether pretreatment with the antidepressant escitalopram could reduce IL-2-induced neuroendocrine, i

63 Continuation-phase escitalopram delayed time to relapse, and fewer escitalo

64 Ziprasidone as an adjunct to escitalopram demonstrated antidepressant efficacy in adu

65 e difference in the decrease for tDCS versus escitalopram (difference, -2.3 points; 95% confidence in

66 participants were randomized 1:1 to receive escitalopram (dose began at 5 mg/d, with titration to 20

67 l to achieve remission as a result of CBT or escitalopram, either alone or in combination, have a dis

68 placebo or the serotonin reuptake inhibitor, escitalopram (ESC) 10-20 mg/day, 2 weeks before, and dur

69 ersely, early exposure to the antidepressant escitalopram (ESC; Lexapro) results in decreased anxiety

70 lar CBT, followed by 28 weeks of maintenance escitalopram; escitalopram alone, followed by maintenanc

71 escitalopram alone, followed by maintenance escitalopram; escitalopram plus CBT, followed by pill pl

72 Furthermore, escitalopram, fluoxetine, and cocaine induced a very sim

73 n adults: bupropion, citalopram, duloxetine, escitalopram, fluoxetine, fluvoxamine, milnacipran, mirt

74 pram, clomipramine, desipramine, duloxetine, escitalopram, fluoxetine, imipramine, mirtazapine, nefaz

75 given placebo, 50 mg amitriptyline, or 10 mg escitalopram for 10 weeks.

76 body dysmorphic disorder received open-label escitalopram for 14 weeks (phase 1); 58 responders were

77 ividuals treated with citalopram (STAR*D) or escitalopram (GENDEP) identified an intergenic region on

78 ity scores were significantly greater in the escitalopram group (-0.52; 95% CI, -0.64 to -0.40 vs -0.

79 chemia were slightly lower at 6 weeks in the escitalopram group (45.8% [95% CI, 36.6%-55.0%]) than in

80 cantly among those whose mothers were in the escitalopram group (compared with those whose mothers we

81 pation time of 18.4 months (n = 185) for the escitalopram group and 18.7 months (n = 187) for the pla

82 n was diagnosed in 8% of the patients in the escitalopram group and 19% in the placebo group (absolut

83 20.2 at baseline to 11.2 at 12 weeks in the escitalopram group and from 21.4 to 12.5 in the placebo

84 (95% CI, 21% to 43%) of the patients in the escitalopram group developed a MADRS score of 13 or high

85 Participants in the escitalopram group produced more effort and thereby achi

86 ee weeks after treatment ended, women in the escitalopram group reported a mean 1.59 (95% CI, 0.55-2.

87 nges in parental functioning: Mothers in the escitalopram group reported significantly greater improv

88 Fifty-five percent of women in the escitalopram group vs 36% in the placebo group reported

89 Only in the escitalopram group was significant improvement of mother

90 ore (P < .01, adjusted mean change in score: escitalopram group, 10.0; nonescitalopram group, 3.1) an

91 ore (P < .01, adjusted mean change in score: escitalopram group, 11.3; nonescitalopram group, 2.5).

92 In the escitalopram group, 56% (CI, 46% to 66%) of patients ach

93 e from baseline was 11.3+/-6.5 points in the escitalopram group, 9.0+/-7.1 points in the tDCS group,

94 tly only for those whose mothers were in the escitalopram group.

95 Remitters to escitalopram had 33% higher baseline 5-HT1A binding in t

96 Older adults with GAD randomized to escitalopram had a higher cumulative response rate for i

97 Patients taking eszopiclone and escitalopram had greater improvements in total Hamilton

98 Patients receiving escitalopram had more frequent sleepiness and obstipatio

99 These findings do not support the use of escitalopram in patients with chronic systolic heart fai

100 r example, high-dose duloxetine outperformed escitalopram in treating core emotional symptoms (effect

101 ude that nCCR-GD may be equally effective as escitalopram in treating GD.

102 Escitalopram increased amygdala activation in controls,

103 ake inhibitors (SSRIs) such as fluoxetine or escitalopram inhibit SERT and are currently the principa

104 data analysis sample received treatment with escitalopram (n = 22) or duloxetine (n = 14) for 10 week

105 ouble-blind placebo-controlled comparison of escitalopram (n = 43) with placebo (n = 45), and a nonbl

106 ouble-blind placebo-controlled comparison of escitalopram (n = 59) with placebo (n = 58), and a nonbl

107 Of 127 participants randomized to receive escitalopram (n = 64) or placebo (n = 63), 112 (88.2%) c

108 Twelve weeks of 10 to 20 mg/d of escitalopram (n = 85) or matching placebo (n = 92).

109 randomly allocated to 12-week treatment with escitalopram (N=115) or nortriptyline (N=126).

110 n ancestry treated for major depression with escitalopram (N=394) or nortriptyline (N=312) over a 12-

111 Women received 10 to 20 mg/d of escitalopram or a matching placebo for 8 weeks.

112 with a 2-way analysis of variance treatment (escitalopram or cognitive behavior therapy) x outcome (r

113 ssigned to 12 weeks of treatment with either escitalopram or cognitive-behavioral therapy (CBT).

114 ssociated with the outcome of treatment with escitalopram or nortriptyline at suggestive levels of si

115 iagnosis of GAD randomized to receive either escitalopram or placebo and conducted between January 20

116 ssed patients with recent stroke, the use of escitalopram or problem-solving therapy resulted in a si

117 ceive tDCS plus oral placebo, sham tDCS plus escitalopram, or sham tDCS plus oral placebo.

118 ts who achieve remission as a result of CBT, escitalopram, or their combination.

119 of depression did not show noninferiority to escitalopram over a 10-week period and was associated wi

120 ignment to 12 weeks of treatment with either escitalopram oxalate (10-20 mg/d) or 16 sessions of manu

121 y prior to treatment randomization to either escitalopram oxalate or cognitive behavior therapy for 1

122 pram hydrobromide, duloxetine hydrochloride, escitalopram oxalate, fluoxetine hydrochloride, mirtazap

123 ted with the FDA-approved drugs tramadol and escitalopram oxalate, they release or uptake serotonin i

124 Patients received 10 mg of escitalopram oxolate for 10 weeks and were randomized to

125 flashes per day at week 8 among women taking escitalopram (P < .001), with mean reductions of 4.60 (9

126 Adverse effects of escitalopram (P < .05 vs placebo) were fatigue or somnol

127 potential for hepatotoxicity are citalopram, escitalopram, paroxetine, and fluvoxamine.

128 pression after an 8-week open-label trial of escitalopram (phase 1), randomly assigned in a 1:1 ratio

129 alone, followed by maintenance escitalopram; escitalopram plus CBT, followed by pill placebo; and esc

130 were treated with an additional 12 weeks of escitalopram plus CBT.

131 se of intolerance, compared with none in the escitalopram plus placebo group.

132 us ziprasidone, N=71) or adjunctive placebo (escitalopram plus placebo, N=68), with 8 weekly follow-u

133 The escitalopram plus ziprasidone group also showed signific

134 Ten (14%) patients in the escitalopram plus ziprasidone group discontinued treatme

135 [SD=6.2]) were significantly greater for the escitalopram plus ziprasidone group.

136 1:1 ratio to receive adjunctive ziprasidone (escitalopram plus ziprasidone, N=71) or adjunctive place

137 e, phenothiazines, and citalopram (including escitalopram) remained statistically significant.

138 ects then received 8 weeks of treatment with escitalopram; remission was defined as a posttreatment 2

139 escitalopram, treatment with eszopiclone and escitalopram resulted in significantly improved sleep an

140 enzofuran-5-carboni trile), and its eutomer, escitalopram (S-(+)-1) are selective serotonin reuptake

141 Participants were randomized to 1 of 3 arms: escitalopram, sertraline (serotonin-specific reuptake in

142 eks of randomized open-label treatment ADMs: escitalopram, sertraline or venlafaxine-extended release

143 mes for three commonly used antidepressants (escitalopram, sertraline, and extended-release venlafaxi

144 ndomly assigned to 8 weeks of treatment with escitalopram, sertraline, or extended-release venlafaxin

145 whom 576 completed 8 weeks of treatment with escitalopram, sertraline, or extended-release venlafaxin

146 ment with one of three antidepressant drugs (escitalopram, sertraline, or venlafaxine extended-releas

147 pressed participants were then randomized to escitalopram, sertraline, or venlafaxine-extended releas

148 Participants treated with escitalopram showed greater improvement than with placeb

149 olving Therapy, stroke patients who received escitalopram showed improvement in global cognitive func

150 iority margin of -2.75 (50% of placebo minus escitalopram), so noninferiority could not be claimed.

151 Mental Stress-Induced Myocardial Ischemia to Escitalopram) study underwent psychometric assessments,

152 her in patients treated with eszopiclone and escitalopram than those treated with placebo and escital

153 on the MADRS score was 3 points higher with escitalopram than with nortriptyline.

154 ime to relapse was significantly longer with escitalopram than with placebo treatment (hazard ratio=2

155 h the selective serotonin reuptake inhibitor escitalopram; this is consistent with data from a separa

156 owing acute response; more than one-third of escitalopram-treated subjects experienced further improv

157 italopram delayed time to relapse, and fewer escitalopram-treated subjects relapsed than did placebo-

158 Among escitalopram-treated subjects, body dysmorphic disorder

159 (Responses of Myocardial Ischemia to Escitalopram Treatment [REMIT]; NCT00574847).

160 antly improved during 6 additional months of escitalopram treatment following acute response; more th

161 We externally validated the model in the escitalopram treatment group (n=151) of an independent c

162 The model was externally validated in the escitalopram treatment group (N=151) of COMED (accuracy

163 ith treatment outcome following standardized escitalopram treatment in MDD.

164 nfounders, there was a significant effect of escitalopram treatment on the change in RBANS total scor

165 l biomarker for remission after standardized escitalopram treatment.

166 Compared with treatment with placebo and escitalopram, treatment with eszopiclone and escitalopra

167 Mirtazapine, escitalopram, venlafaxine, and sertraline were significa

168 to double-blind continuation treatment with escitalopram versus switch to placebo for 6 months (phas

169 f dropout, mean cumulative response rate for escitalopram was 69% (95% confidence interval [CI], 58%-

170 Response to escitalopram was best predicted by a marker in the inter

171 Noninferiority of tDCS versus escitalopram was defined by a lower boundary of the conf

172 e level, but an association with response to escitalopram was detected in the interleukin-6 gene, whi

173 Prophylactic antidepressant treatment with escitalopram was effective in reducing the incidence and

174 Escitalopram was given at a dose of 10 mg per day for 3

175 This beneficial effect of escitalopram was independent of its effect on depression

176 8 weeks, 95% CI, 1.6 to 3.1; P < .001), but escitalopram was not significantly different from placeb

177 A significant difference favoring escitalopram was observed (odds ratio, 2.62 [95% CI, 1.0

178 rolling for prior history of mood disorders, escitalopram was superior to placebo (23.1% vs 34.5%; ad

179 Coadministration of eszopiclone and escitalopram was well tolerated and associated with sign

180 nausea, and adverse effects associated with escitalopram were not significantly different between th

181 nitive behavior therapy and poor response to escitalopram, while insula hypermetabolism was associate

182 We expected that escitalopram would reduce amygdala activity in IED and i

183 We hypothesized that patients who received escitalopram would show improved performance in neuropsy