ライフサイエンスコーパス: paroxetine

1 sma was made (single oral dose of 37.5 mg of paroxetine).

2 rval, 1.4 to 4.2) that among those receiving paroxetine.

3 ceived two years of maintenance therapy with paroxetine.

4 hodology was applied to the synthesis of (-)-Paroxetine.

5 d is reversed by propranolol, clonidine, and paroxetine.

6 with efficacy and tolerability comparable to paroxetine.

7 men were less likely to discontinue low-dose paroxetine.

8 hydrochloride ER and 46.0 mg (SD, 7.9 mg) of paroxetine.

9 nescent female Sprague-Dawley rats using [3H]paroxetine.

10 bated with the high-affinity SERT antagonist paroxetine.

11 terans with PTSD were treated with the SSRI, paroxetine.

12 treatment with a maximally tolerated dose of paroxetine.

13 und to the antidepressants (S)-citalopram or paroxetine.

14 commercial serotonin reuptake inhibitor (-)-paroxetine.

15 reast-feeding during maternal treatment with paroxetine.

16 re subject to site differences than those of paroxetine.

17 am and in humans with nonsaturating doses of paroxetine.

18 jection of clorgyline combined with the SSRI paroxetine.

19 elective synthesis of the antidepressant (-)-paroxetine.

20 responsive to prophylactic administration of paroxetine.

21 (1.41, 1.35, 1.30, and 1.27, respectively), paroxetine (1.35, 1.30, 1.27, and 1.22, respectively), a

22 trolled trial to investigate the efficacy of paroxetine 10 mg and 20 mg compared to placebo in reduci

23 Women were randomly assigned to 4 weeks of paroxetine 10 mg or 20 mg followed by placebo for 4 week

24 4 weeks, or placebo for 4 weeks followed by paroxetine 10 mg or 20 mg for 4 weeks.

25 Paroxetine 10 mg reduced hot flash frequency and composi

26 Paroxetine 10 mg was associated with a significant impro

27 le patients were randomized (1:1) to receive paroxetine (10-50 mg/d) or placebo.

28 ine 104, maprotiline 109, nortriptyline 114, paroxetine 118, sertraline 124, suloctidil 125, and terf

29 nt as usual (psychotherapy, $976 [SD, $984]; paroxetine, $1252 [SD, $1616]; and treatment as usual, $

30 tivity in HYP persisted during HYP + CPAP on paroxetine (183% versus 182% of placebo, respectively).

31 h the selective serotonin reuptake inhibitor paroxetine; 2 psychiatrist visits and 2 telephone calls

32 Paroxetine 20 mg reduced hot flash frequency and composi

33 h the selective serotonin reuptake inhibitor paroxetine (20 mg/d), the patients with depression were

34 venlafaxine hydrochloride ER (75-225 mg/d), paroxetine (20-50 mg/d), or placebo for 12 weeks or less

35 ndomly assigned to 8 weeks of treatment with paroxetine, 20 or 40 mg/day, or placebo.

36 omponent scores, 4.7 [2.03] for those taking paroxetine; 4.7 [1.96] for the PST-PC treatment; P =.02

37 were statistically significantly greater for paroxetine (77.6% response [125/161]) than for placebo (

38 mpared the widely prescribed antidepressants paroxetine (a selective serotonin reuptake inhibitor [SS

39 Treatment of wild type mice with paroxetine, a chemical inhibitor of SERT, also resulted

40 Follow-up studies focused on paroxetine, a clinically used antidepressant compound th

41 his randomized clinical trial tested whether paroxetine, a selective serotonin reuptake inhibitor ant

42 g kinase 1 (ROCK1) inhibitor, the other from paroxetine, a selective serotonin-reuptake inhibitor.

43 at the expense of affinity for serotonin or paroxetine, a selective SERT inhibitor.

44 We report that administration of paroxetine, a widely prescribed antidepressant drug that

45 sions appear less responsive to prophylactic paroxetine administration.

46 Among patients taking paroxetine, adverse events during placebo substitution c

47 ity SSRIs, racemic citalopram ((RS)-CIT) and paroxetine, affect the outgrowth of embryonic thalamic a

48 to 56-fold) whilst ibogaine, imipramine and paroxetine all bound with lower affinity (up to 90-fold)

49 Paroxetine also improved SBP response to exercise.

50 euticals, such as treatments for depression (paroxetine, amitifadine), diabetes (gliclazide), leukaem

51 ared prolonged exposure therapy (a CBT) plus paroxetine (an SSRI) with prolonged exposure plus placeb

52 , SERT Met172 mice maintained sensitivity to paroxetine, an antidepressant that is unaffected by the

53 ctility at 20-fold lower concentrations than paroxetine, an inhibitor with more modest selectivity fo

54 The indazole-paroxetine analogs were indeed more potent than their re

55 f GRK2 compared with previous complexes with paroxetine analogs.

56 rse events were infrequent (5.5% [9/163] for paroxetine and 1.3% [2/156] for placebo).

57 ed 20 patients to receive the antidepressant paroxetine and 20 to receive placebo.

58 A total of 244 patients treated with paroxetine and 235 patients treated with placebo provide

59 f the 41 patients who started treatment with paroxetine and 29 of the 40 patients who started treatme

60 t in cardiomyocyte contractility assays over paroxetine and a plasma concentration higher than its IC

61 We directly measured the K(D) for paroxetine and assessed its mechanism of inhibition for

62 We treated DBA/2J mice for 28 days with paroxetine and assessed their behavioral response with t

63 3 for the interaction between treatment with paroxetine and baseline severity of medical illness).

64 .85) and -9.6% per year (P = .21) during the paroxetine and black box warning study periods, respecti

65 The paroxetine and black box warnings had modest and relativ

66 psychotherapy, 37 percent of those receiving paroxetine and clinical-management sessions, 68 percent

67 However, both paroxetine and imipramine were superior to placebo for p

68 is study compared the efficacy and safety of paroxetine and imipramine with that of placebo in the tr

69 r 2005 rates for all antidepressants, except paroxetine and imipramine, started to rise again.

70 changes with 2 distinct forms of treatment (paroxetine and interpersonal psychotherapy).

71 We tested the efficacy of maintenance paroxetine and monthly interpersonal psychotherapy in pa

72 ed the efficacy, tolerability, and safety of paroxetine and nortriptyline in depressed patients with

73 For the paroxetine and placebo groups, the 6 visits over 11 week

74 For minor depression, both paroxetine and PST-PC improved mental health functioning

75 who had a response to initial treatment with paroxetine and psychotherapy were less likely to have re

76 g patients with a response to treatment with paroxetine and psychotherapy, 116 were randomly assigned

77 ears in 35 percent of the patients receiving paroxetine and psychotherapy, 37 percent of those receiv

78 x that now were significantly enhanced under paroxetine and reduced under bupropion.

79 13 exposed subjects) and between the use of paroxetine and right ventricular outflow tract obstructi

80 o significant association between the use of paroxetine and right ventricular outflow tract obstructi

81 comparisons showed possible associations of paroxetine and sertraline with other specific defects.

82 curring at an incidence of 5% or greater for paroxetine and twice that for placebo were insomnia (14.

83 Published results from one trial of paroxetine and two trials of sertraline suggest equivoca

84 own improvements with oestrogen, gabapentin, paroxetine, and clonidine, but little or no benefit with

85 hepatotoxicity are citalopram, escitalopram, paroxetine, and fluvoxamine.

86 Nortriptyline, paroxetine, and sertraline may be preferred choices in b

87 Nortriptyline, paroxetine, and sertraline usually produce undetectable

88 s with malignant melanoma, pretreatment with paroxetine appears to be an effective strategy for minim

89 Paroxetine appears to have a specific pharmacological ef

90 Doses of 20 and 40 mg/day of paroxetine are effective and well tolerated in the treat

91 encies of the antidepressants tianeptine and paroxetine are unchanged.

92 identifies a novel pharmacological action of paroxetine as a protector of endothelial cells against h

93 (HPLC-MS/MS) assay has been validated using paroxetine as a tool compound (range 0.2-200 ng/mL human

94 identified the serotonin reuptake inhibitor paroxetine as an inhibitor of G protein-coupled receptor

95 ted after 10 days of maternal treatment with paroxetine at a stable daily dose (10-50 mg/day).

96 Paroxetine attenuated motor dysfunction and body weight

97 Paroxetine augmented systolic blood pressure (SBP) durin

98 Time of day influenced [3H]paroxetine binding in the SCN and the paraventricular th

99 The density of specific [3H]paroxetine binding in various brain regions was compared

100 ng independently increased the number of [3H]paroxetine binding sites.

101 nly region that displayed a reduction in [3H]paroxetine binding with age was the suprachiasmatic nucl

102 n contrast, Cl(-) did not enhance cocaine or paroxetine binding.

103 depressants, particularly those who received paroxetine, but was reduced in older adults.

104 of: (1) switch to a second, different SSRI (paroxetine, citalopram, or fluoxetine, 20-40 mg); (2) sw

105 cal trials of nortriptyline hydrochloride or paroxetine combined with interpersonal psychotherapy (N

106 provement score of 1) was 47.8% (77/161) for paroxetine compared with 14.9% (23/154) for placebo.

107 ater baseline suicidal ideation treated with paroxetine compared with bupropion appeared to experienc

108 mong users of amitriptyline, fluoxetine, and paroxetine compared with the risk among users of dothiep

109 fluoxetine, and 1.29 (95% CI, 0.97-1.70) for paroxetine compared with those using dothiepin.

110 t gradient effect was observed, with greater paroxetine concentrations found in later portions of bre

111 Breast milk paroxetine concentrations were highly variable (2-101 ng

112 ter than 85% inhibition) of control at these paroxetine concentrations.

113 placebo or receive 12.5 mg/d or 25.0 mg/d of paroxetine CR (in a 1:1:1 ratio) for 6 weeks.

114 ean reduction, 3.2) for those in the 25-mg/d paroxetine CR groups and from 6.6 to 4.8 (mean reduction

115 .5-mg/d and 64.6% for those in the 25.0-mg/d paroxetine CR groups compared with 37.8% for those in th

116 Paroxetine CR may be an effective and acceptable alterna

117 ly significantly greater for those receiving paroxetine CR than for those receiving placebo.

118 l, -6.8 to -0.4; P =.03) comparing 25.0-mg/d paroxetine CR with placebo.

119 - 8.1 to -1.3; P =.007) comparing 12.5-mg/d paroxetine CR with placebo; and -3.6 (95% confidence int

120 ive 12.5 mg/d and 58 to receive 25.0 mg/d of paroxetine CR.

121 Paroxetine, currently classified as a selective 5-HT reu

122 ast milk was demonstrated, although maternal paroxetine daily dose reliably predicted both trough and

123 e that the SSRIs fluoxetine, sertraline, and paroxetine decrease the K(m) of the conversion of 5alpha

124 Paroxetine decreased norepinephrine uptake to 73% of con

125 potency when substituted for benzodioxole in paroxetine derivatives.

126 Paroxetine did not show statistical superiority to desip

127 lthough all patient groups received the same paroxetine dose for the same duration, regional metaboli

128 ion, after recovery sleep (after the initial paroxetine dose), and after 2 weeks of paroxetine treatm

129 ol t.i.d. or placebo for 4 weeks to a steady paroxetine dose.

130 Pretreatment with paroxetine dramatically altered the metabolism and kinet

131 SSRIs citalopram, sertraline and especially paroxetine dropped dramatically after 2002, while rates

132 After 5 d of paroxetine, EMGgg activity increased significantly withi

133 No clear time course of paroxetine excretion into breast milk was demonstrated,

134 Paroxetine exhibits up to 50-fold selectivity for GRK2 v

135 atients treated with prolonged exposure plus paroxetine experienced significantly greater improvement

136 The SSRI antidepressants paroxetine, fluoxetine, and sertraline were similar in e

137 ansporter affinity, all of which were SSRIs (paroxetine, fluoxetine, and sertraline).

138 ctive serotonin reuptake inhibitors (SSRIs) (paroxetine, fluoxetine, fluvoxamine, and sertraline) and

139 islets or Min6 beta cell line with the SSRIs paroxetine, fluoxetine, or sertraline inhibited insulin-

140 o were all then treated with 30-60 mg/day of paroxetine for 8-12 weeks.

141 Our results suggest that the selectivity of paroxetine for GRK2 largely reflects its lower affinity

142 s study evaluated the efficacy and safety of paroxetine for the treatment of patients with chronic po

143 Several of the analogues displaced [(3)H]paroxetine from serotonin transporters with moderate to

144 ression developed in 2 of 18 patients in the paroxetine group (11 percent) and 9 of 20 patients in th

145 fore 12 weeks in 1 of the 20 patients in the paroxetine group (5 percent), as compared with 7 patient

146 d to psychotherapy and 43 of 86 (50%) of the paroxetine group completed the full course of treatment.

147 inical effects with brain drug levels in the paroxetine group suggests that relationships between dru

148 Summary score at 9 months was + 15.8 in the paroxetine group, + 15.1 in the fluoxetine group, and +

149 ificantly greater for the venlafaxine ER and paroxetine groups (58.6% and 62.5%, respectively) vs the

150 30% and 36% of patients in the 20- and 40-mg paroxetine groups, respectively, compared with 20% given

151 ty scale were significantly greater for both paroxetine groups.

152 order of potency: sertraline > fluoxetine > paroxetine > fluvoxamine > citalopram.

153 Paroxetine had no influence on fatigue in patients recei

154 ryptophan and, more recently, fluoxetine and paroxetine, have been tested as pharmacologic treatments

155 aining complexes confirmed that the indazole-paroxetine hybrids form stronger interactions with the h

156 e effect of the serotonin reuptake inhibitor paroxetine hydrochloride (Paxil, SmithKline Beecham) on

157 mly assigned to receive either 20 mg of oral paroxetine hydrochloride daily or placebo for 8 weeks.

158 d Drug Administration (FDA) recommended that paroxetine hydrochloride not be used to treat young peop

159 s were randomly assigned to pharmacotherapy (paroxetine hydrochloride or bupropion hydrochloride) (n

160 tpatients under protocolized conditions with paroxetine hydrochloride or nortriptyline hydrochloride,

161 = 0.98 (95% confidence interval, 0.63-1.51); paroxetine hydrochloride, hazard ratio = 1.02 (95% confi

162 lective serotonin reuptake inhibitor (SSRI), paroxetine hydrochloride, may increase genioglossal elec

163 e, mirtazapine, nortriptyline hydrochloride, paroxetine hydrochloride, venlafaxine hydrochloride, and

164 re and after 8 to 12 weeks of treatment with paroxetine hydrochloride.

165 the selective serotonin reuptake inhibitor, paroxetine hydrochloride.

166 ents with severe IBS, both psychotherapy and paroxetine improve health-related quality of life at no

167 For dysthymia, paroxetine improved mental health functioning vs placebo

168 e behavioral effects of both desipramine and paroxetine in Dbh(-/-) mice, thus demonstrating that the

169 The low concentrations of paroxetine in infant serum and lack of any observable ad

170 hed that (1) fluoxetine was more potent than paroxetine in inhibiting agonist-activated Ca(2+) influx

171 However, the binding site and orientation of paroxetine in SERT remain controversial.

172 evious data by demonstrating the presence of paroxetine in the breast milk of nursing women treated w

173 serotonin-selective reuptake inhibiting drug paroxetine in the incubation medium.

174 tribute to the broad therapeutic efficacy of paroxetine in the treatment of depression, panic disorde

175 assessed the efficacy of two fixed doses of paroxetine in the treatment of generalized anxiety disor

176 sovagal syncope (propranolol, clonidine, and paroxetine) in a double-blind crossover study.

177 ival analysis showed discontinuations due to paroxetine-induced side effects were strongly associated

178 5-HT, d-amphetamine, cocaine, and paroxetine inhibit transport more potently at lower expr

179 The study examined whether paroxetine inhibits the human norepinephrine transporter

180 han pharmacokinetic variation in determining paroxetine intolerance.

181 Paroxetine is an effective treatment for hot flashes in

182 Paroxetine is an effective, generally well-tolerated tre

183 This study demonstrates that paroxetine is an efficacious and well-tolerated treatmen

184 ogen bond formed by the benzodioxole ring of paroxetine is better accommodated by GRKs.

185 ng those starting the newest antidepressant, paroxetine, is of a magnitude that could readily be due

186 elease venlafaxine was more efficacious than paroxetine, lithium augmentation more than phenelzine, a

187 Paroxetine maintained the ability of vascular rings to r

188 in controls but declined significantly after paroxetine monotherapy to levels comparable with those o

189 moderate to severe MDD randomized to receive paroxetine (n = 120), placebo (n = 60), or cognitive the

190 of mirtazapine (n = 124) or 20 to 40 mg/d of paroxetine (n = 122).

191 Patients were randomly assigned to receive paroxetine (n = 137) or placebo (n = 140), starting at 1

192 Patients were randomly assigned to receive paroxetine (n = 189), fluoxetine (n = 193), or sertralin

193 g/day of paroxetine (N=183), or 40 mg/day of paroxetine (N=182) for 12 weeks.

194 signed to take placebo (N=186), 20 mg/day of paroxetine (N=183), or 40 mg/day of paroxetine (N=182) f

195 t with prolonged exposure (10 sessions) plus paroxetine (N=19) or prolonged exposure plus placebo (N=

196 ha and ribavirin received the antidepressant paroxetine (n=28) or a placebo (n=33).

197 se, were randomly assigned to treatment with paroxetine (N=35), imipramine (N=39), or placebo (N=43)

198 e-blind, randomized, clinical pilot trial of paroxetine (N=36) or bupropion (N=38) in DSM IV major de

199 cluded in the intention-to-treat population (paroxetine, n = 163; placebo, n = 156).

200 uble-blind conditions to one of four groups: paroxetine+naltrexone; paroxetine+placebo; desipramine+n

201 We studied the effects of paroxetine on EMGgg using an intraoral surface electrode

202 the determination of whether this effect of paroxetine on platelet function is caused by a direct ef

203 ior to placebo for augmenting the effects of paroxetine on social anxiety symptoms.

204 model selection showed modest advantages for paroxetine on: (1) mHDRS-17 (p=0.02); and (2) in a separ

205 , subjects with MDD were treated with either paroxetine or interpersonal psychotherapy (based on pati

206 omly assigned to double-blind treatment with paroxetine or nortriptyline for 6 weeks.

207 four maintenance-treatment programs (either paroxetine or placebo combined with either monthly psych

208 content of the hippocampus was unaffected by paroxetine or sertraline treatment, ruling out neurotoxi

209 ective serotonin reuptake inhibitors (SSRIs) paroxetine or sertraline, the selective norepinephrine r

210 in reuptake inhibitor (SSRI) antidepressant, paroxetine, or routine care by a gastroenterologist and

211 regnant women taking citalopram, fluoxetine, paroxetine, or sertraline participated.

212 The advantage of paroxetine over placebo in antidepressant efficacy was n

213 rdiac disease) received greater benefit from paroxetine (P=0.03 for the interaction between treatment

214 Lithium and the antidepressant (AD) paroxetine (PAR) functionally synergize with FKBP51, as

215 e with the antidepressants reboxetine (REB), paroxetine (PAROX) and clomipramine (CLOM) on extracellu

216 Paroxetine patients showed greater (difference in mean [

217 ptake inhibitors (SSRI)-fluoxetine (Prozac), paroxetine (Paxil), and citalopram (Celexa)-substantiall

218 oactive agents, including the antidepressant paroxetine (Paxil), the most potent selective serotonin

219 the antidepressants sertraline (Zoloft) and paroxetine (Paxil).

220 o one of four groups: paroxetine+naltrexone; paroxetine+placebo; desipramine+naltrexone; desipramine+

221 uate response to standardized treatment with paroxetine plus interpersonal psychotherapy.

222 Initial treatment with paroxetine plus prolonged exposure was more efficacious

223 % (SD=17%) of the brain fluorine signal from paroxetine (plus fluorinated metabolites).

224 and a baboon with reduced SERT availability (paroxetine pretreatment).

225 We conclude that paroxetine produces an augmentation in EMGgg in normal s

226 21) decreased the cerebrocortical binding of paroxetine (PXT), a marker for the serotonin (5HT) trans

227 tinuations than did duloxetine, fluvoxamine, paroxetine, reboxetine, and venlafaxine.

228 tine, fluvoxamine, milnacipran, mirtazapine, paroxetine, reboxetine, sertraline, and venlafaxine.

229 Paroxetine reduced hyperglycemia-induced mitochondrial R

230 l trial we have previously demonstrated that paroxetine reduces hot flashes.

231 Patients taking paroxetine reported 6.8 times as much change on neurotic

232 Patients who took paroxetine reported greater personality change than plac

233 8% of the patients receiving 20 and 40 mg of paroxetine, respectively, compared with a 46% response r

234 reatment predicted lower relapse rates among paroxetine responders (P = .003) but not among cognitive

235 Compared to imipramine, paroxetine resulted in a lower incidence of adverse even

236 Paroxetine reversed paradoxical vascular responses durin

237 [125I]iodocyanopindolol ([125I]ICYP) and [3H]paroxetine, selective radioligands for the 5-HT(1B) rece

238 derstand the molecular mechanisms underlying paroxetine selectivity among GRKs.

239 ine, mirtazapine, nefazodone, nortriptyline, paroxetine, sertraline, and venlafaxine.

240 concentrations up to 50 microM, fluoxetine, paroxetine, sertraline, norfluoxetine, carbamazepine, cl

241 served were the antidepressants (citalopram, paroxetine, sertraline, venlafaxine, and bupropion, and

242 ndicated that S allele carriers treated with paroxetine showed a small impairment in antidepressant r

243 Paroxetine showed moderate benefit for depressive sympto

244 Our data suggest that the orientation of paroxetine, specifically its fluorophenyl ring, in SERT'

245 Under paroxetine, subjects showed significantly decreased acti

246 depressant medication intervention (trial of paroxetine switched to buproprion, if lack of response)

247 nificantly greater improvement was seen with paroxetine than placebo.

248 ext, we designed a benzolactam derivative of paroxetine that has optimized interactions with the hing

249 ects study design and administering the SSRI paroxetine, the dopamine/norepinephrine reuptake inhibit

250 The lowest ratios were for sertraline and paroxetine; the highest were for citalopram and fluoxeti

251 ture-based drug design approach, we modified paroxetine to generate a small compound library.

252 The ability of paroxetine to improve hyperglycemic endothelial cell inj

253 number of patients needed to be treated with paroxetine to prevent one recurrence was 4 (95 percent c

254 melanogaster dopamine transporter and docked paroxetine to these models.

255 =20 were randomly assigned to treatment with paroxetine (to 60 mg/day) or desipramine (to 30 mg/day)

256 udy compared the serotonin uptake inhibitor, paroxetine, to the norepinephrine uptake inhibitor, desi

257 d decreases in normalized prefrontal cortex (paroxetine-treated bilaterally and interpersonal psychot

258 Paroxetine-treated long-time floating (PLF) and paroxeti

259 lar pathways and biosignatures that stratify paroxetine-treated mouse sub-groups.

260 Paroxetine-treated patients in both dose groups demonstr

261 Side effect severity in paroxetine-treated patients with the C/C genotype was al

262 Such effects were not observed in paroxetine-treated SERT (-/-) mice.

263 oxetine-treated long-time floating (PLF) and paroxetine-treated short-time floating (PSF) groups were

264 After treatment, paroxetine-treated subjects had a greater mean decrease

265 Among paroxetine-treated subjects, S allele carriers experienc

266 : SAD=15, controls=17) and following 8-weeks paroxetine treatment (N: SAD=12, untreated controls=7).

267 itial paroxetine dose), and after 2 weeks of paroxetine treatment (patients only).

268 reductions may, however, not be specific to paroxetine treatment and could be due to a more general

269 er status, and was significantly superior to paroxetine treatment at weeks 1 and 2 for the Social Pho

270 tom dimension was significantly lower in the paroxetine treatment group (p=0.04); severity of the neu

271 sion symptom dimension is more responsive to paroxetine treatment in individuals undergoing concomita

272 es in pediatric OCD and further suggest that paroxetine treatment may be paralleled by a reduction in

273 on of platelet activation is associated with paroxetine treatment of patients with depression.

274 urine and pyrimidine metabolisms for chronic paroxetine treatment response in the mouse was further c

275 Moreover, paroxetine treatment resulted in statistically significa

276 Paroxetine treatment was significantly superior to place

277 After paroxetine treatment, the patients with depression exhib

278 greater than during RA for both placebo and paroxetine treatments (p = 0.006).

279 e compared the interaction of fluoxetine and paroxetine, two selective serotonin reuptake inhibitors

280 ere taking 20 mg/day of either fluoxetine or paroxetine underwent placebo substitution for 3 days.

281 Some study subjects received paroxetine, up to 50 mg daily, augmented by lithium carb

282 R, 1.17; 95% CI, 1.05 to 1.30; P = .01), and paroxetine use (RR, 1.29; 95% CI, 1.08 to 1.54; P = .01)

283 Youth paroxetine use also significantly increased during the p

284 oncerns about a possible association between paroxetine use and right ventricular outflow tract obstr

285 study results) of the newer antidepressants paroxetine, venlafaxine, fluoxetine, and sertraline decr

286 : prewarning (May 1, 2002 to June 19, 2003), paroxetine warning (June 20, 2003 to October 15, 2004),

287 ference in trends between the prewarning and paroxetine warning periods was significant (P < .001).

288 1) before significantly declining during the paroxetine warning study period (-44.2% per year; P < .0

289 Paroxetine was administered at a fixed-flexible dose of

290 ng the follow-up year, psychotherapy but not paroxetine was associated with a significant reduction i

291 Paroxetine was beneficial when treatment was initiated b

292 Paroxetine was better tolerated than nortriptyline and l

293 Paroxetine was effective for both men and women.

294 Binding to 5-HT transporters ([3H]paroxetine) was significantly increased (P<0.05) in both

295 The selective serotonin reuptake inhibitor, paroxetine, was previously identified as a GRK2 inhibito

296 hibitors (SSRIs) fluoxetine, sertraline, and paroxetine were also absent or severely attenuated in th

297 serum pairs, no detectable concentrations of paroxetine were found in the serum of the nursing infant

298 Both psychotherapy and paroxetine were superior to treatment as usual in improv

299 Both doses of paroxetine were well tolerated.

300 However, desipramine was superior to paroxetine with respect to study retention and alcohol u