ライフサイエンスコーパス: SSRI

1 SSRI and non-SSRI monotherapy use during the 90 days bef

2 SSRI exposure was confirmed in a subset of participants

3 SSRI treatment decreased plasma serotonin concentrations

4 SSRI treatment increased activation in both the left dor

5 SSRI treatment significantly increased rolipram binding

6 SSRIs inhibit serotonin's transporter, and in doing so,

7 SSRIs may exert their effects by remediating emotion reg

8 SSRIs selectively inhibited hippocampal long-term depres

9 SSRIs with high and intermediate, but not low, affinity

10 1R antagonism is sufficient to prevent acute SSRI-induced enhancements in aversive learning.

11 isk of upper gastrointestinal bleeding after SSRI exposure was 1.67 (95% CI=1.23-2.26) for the 7-day

12 unmedicated MDD patients and increased after SSRI treatment.

13 do not show any improvement during or after SSRI treatment.

14 -2.60]; 13 trials and 831 patients), and all SSRIs (class effect -3.49 [95% credible interval -5.12 t

15 SSRI treatment alone, the combined use of an SSRI and a statin was associated with a significantly lo

16 ts late in pregnancy: 102,179 (2.7%) used an SSRI and 26,771 (0.7%) a non-SSRI.

17 am PET scan ~8 weeks after treatment with an SSRI.

18 am PET scan 8 weeks after treatment with an SSRI.

19 faces predicted greater response to CBT and SSRI treatment.

20 Infants in the SSRI and SSRI plus benzodiazepine groups had lower motor scores a

21 ebo (SMD -0.56, 95% CrI -1.00 to -0.11), and SSRIs and SNRIs compared with pill placebo (-0.44, -0.67

22 5] vs. 0.0/1000 PY [95 % CI: 0.0 - 0.3]) and SSRIs (0.4/1000 PY [95 % CI: 0.1 - 1.0] vs. 0.0/1000 PY

23 idence supports the effectiveness of CBT and SSRIs for reducing childhood anxiety symptoms.

24 Yet, how serotonin (5-HT) and SSRIs cause changes in prolactin secretion is not known.

25 Limited doses of aspirin, NSAIDs, and SSRIs might not increase the risk, although higher doses

26 Is), SSRIs with concomitant benzodiazepines (SSRI plus benzodiazepine), and no maternal depression or

27 lly significant positive association between SSRI dose and efficacy.

28 nequalities modified the association between SSRI use and suicide.

29 re used to determine the association between SSRI use and upper gastrointestinal bleeding.

30 rences may exist in the relationship between SSRI use and upper gastrointestinal bleeding.

31 n differentially predicted remission between SSRI and SNRI medications, with SSRI remitters showing g

32 ls, there was an overall association between SSRIs and violent crime convictions (hazard ratio [HR] =

33 The association between SSRIs and violent crime convictions and violent crime ar

34 there was a significant association between SSRIs and violent crime convictions for individuals aged

35 there was a significant association between SSRIs and violent crime convictions for males aged 15 to

36 tions for understanding associations between SSRIs and child development.

37 harmacological treatment for depression, but SSRIs are effective in only half of the patients and typ

38 was decoupled from behavioral adaptation by SSRI administration in the LL group.

39 vioral despair model, which was prevented by SSRI treatment.

40 termine the modulation of Ca(2+) channels by SSRIs.

41 The inhibition of long-term depression by SSRIs was mediated by a direct block of voltage-activate

42 After chronic SSRI treatment, 5-HT(1A) autoreceptors desensitize, whic

43 pumps, 5-HTP IR with injections, and chronic SSRI with dietary fluoxetine.

44 Our results suggest that chronic SSRI treatment differentially affects purine and pyrimid

45 inephrine reuptake inhibitors (collectively: SSRIs), SSRIs with concomitant benzodiazepines (SSRI plu

46 Current SSRI use was associated with an increased risk for ICH (

47 The neural basis of this early SSRI effect is not known.

48 disruptive contaminants in the environment, SSRIs affect reproduction in aquatic organisms.

49 We provide strong evidence that exogenous SSRI fluoxetine selectively increases serotonin-immunore

50 Duration of SSRI exposure, SSRI exposure at conception, and family history of depre

51 eurobehavioral development was different for SSRI exposure than depression alone.

52 For SSRIs, odds ratios were 1.51 (95% CI, 1.35-1.69) unadjus

53 h antidepressant treatment, particularly for SSRIs, and may be a potential substrate of the clinical

54 to primary PPHN, the adjusted odds ratio for SSRIs was 1.28 (95% CI, 1.01-1.64) and for non-SSRIs 1.1

55 Yet, many patients withdraw from SSRI therapy due to sexual side effects (e.g., infertili

56 Furthermore, SSRIs protected both wild-type and SERT knockout mice fr

57 follow-up of 22.8 months, 79285 [66.3%] had SSRI or SNRI exposure.

58 Higher SSRI use was associated with lower suicide rates among U

59 Precisely how SSRIs induce long-term modifications in serotonin transm

60 However, it remains unclear how SSRIs, which inhibit the plasma membrane serotonin trans

61 In contrast, in SSRI-treated mothers, the risk was higher for offspring

62 s became available in 1988, a 1% increase in SSRI usage was associated with a 0.5% lower suicide rate

63 However, with each 1% increase in SSRI use, a 1-standard deviation (SD) higher SES was ass

64 Pregnancy outcomes in SSRI users were compared with those in the unexposed gro

65 otonin concentrations and may have a role in SSRI treatment outcomes.

66 The authors identified 872,216 incident SSRI users, of whom 113,108 (13.0%) used a statin concom

67 wide cohort study that included all incident SSRI users in Denmark between 1997 and 2012, the authors

68 of a selective serotonin reuptake inhibitor (SSRI) and a statin may have superior antidepressant effe

69 ween selective serotonin reuptake inhibitor (SSRI) antidepressant use during pregnancy and risk of pe

70 y to selective serotonin reuptake inhibitor (SSRI) antidepressants, all other non-SSRI antidepressant

71 the selective serotonin reuptake inhibitor (SSRI) antidepressants, has been thought to be effective

72 the selective serotonin reuptake inhibitor (SSRI) citalopram (10 mg) intravenously in a double-blind

73 the selective serotonin reuptake inhibitor (SSRI) citalopram decreases amyloid-beta generation and p

74 the selective serotonin reuptake inhibitor (SSRI) citalopram downregulates the expression of the hum

75 hydroxytryptamine (5-HT) reuptake inhibitor (SSRI) effectiveness in vivo.

76 The selective serotonin reuptake inhibitor (SSRI) fluoxetine (FLX), the active ingredient of the ant

77 on a selective serotonin reuptake inhibitor (SSRI) initially experience increased anxiety, which can

78 the selective serotonin reuptake inhibitor (SSRI) sertraline or cognitive behavior therapy (CBT), pa

79 d to selective serotonin reuptake inhibitor (SSRI) therapy.

80 atal selective serotonin reuptake inhibitor (SSRI) treatment and pregnancy complications, accounting

81 evidence-based serotonin reuptake inhibitor (SSRI) treatment.

82 the selective serotonin reuptake inhibitor (SSRI), (S)-citalopram (1).

83 m, a selective serotonin reuptake inhibitor (SSRI), on brain activation during face processing.

84 e, a selective serotonin reuptake inhibitor (SSRI), provided the most substantial benefit.

85 ical selective serotonin reuptake inhibitor (SSRI).

86 th a selective serotonin reuptake inhibitor (SSRI).

87 th a selective serotonin reuptake inhibitor (SSRI).

88 of a selective serotonin reuptake inhibitor (SSRI, citalopram) are studied over longer timescales, le

89 Selective serotonin reuptake inhibitors (SSRI) are aimed at increasing brain 5-HT tone; however,

90 een selective serotonin receptor inhibitors (SSRIs) and risk of upper gastrointestinal bleeding remai

91 erotonin-norepinephrine reuptake inhibitors (SSRIs and SNRIs; -0.91, -1.23 to -0.60), and anticonvuls

92 of selective serotonin-reuptake inhibitors (SSRIs) and other antidepressants during pregnancy is ass

93 by selective serotonin reuptake inhibitors (SSRIs) and the tricyclic class of antidepressant (TCA) a

94 Selective serotonin reuptake inhibitors (SSRIs) are a first-line treatment for PTSD, but treatmen

95 bo, selective serotonin reuptake inhibitors (SSRIs) are associated with better response and remission

96 Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed for depression, but sexua

97 Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed to treat these disorders,

98 Selective Serotonin Reuptake Inhibitors (SSRIs) are commonly used drugs for the treatment of psyc

99 Selective serotonin reuptake inhibitors (SSRIs) are the most commonly used class of antidepressan

100 Selective serotonin reuptake inhibitors (SSRIs) are the primary pharmacological treatment for dep

101 ugh selective serotonin reuptake inhibitors (SSRIs) are widely prescribed, associations with violence

102 Selective serotonin reuptake inhibitors (SSRIs) are widely used antidepressants, but the mechanis

103 Selective serotonin reuptake inhibitors (SSRIs) are widely used antidepressants.

104 Selective serotonin reuptake inhibitors (SSRIs) display a delayed onset of action of several week

105 to selective serotonin reuptake inhibitors (SSRIs) during pregnancy influences susceptibility to the

106 of selective serotonin reuptake inhibitors (SSRIs) has been associated with an increased cataract ri

107 of selective serotonin-reuptake inhibitors (SSRIs) has been associated with an increased risk of bon

108 by selective serotonin reuptake inhibitors (SSRIs) in hippocampal brain slices from wild-type rats a

109 to selective serotonin reuptake inhibitors (SSRIs) in major depressive disorder follows a flat respo

110 of selective serotonin reuptake inhibitors (SSRIs) in some treatment-resistant patients; however, it

111 Selective serotonin reuptake inhibitors (SSRIs) may increase the risk for spontaneous intracrania

112 ity with selective 5-HT reuptake inhibitors (SSRIs) remains the most widely used treatment for mood d

113 bo, selective serotonin reuptake inhibitors (SSRIs) significantly reduced primary anxiety symptoms an

114 hat selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine ((+/-)-N-methyl-gamma-[4-(trif

115 Selective 5-HT reuptake inhibitors (SSRIs) such as fluoxetine or escitalopram inhibit SERT a

116 ith selective serotonin reuptake inhibitors (SSRIs) was 1.6, whereas that from use of COX-2 inhibitor

117 of selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SN

118 or selective serotonin reuptake inhibitors (SSRIs).

119 otonin (5-HT) selective reuptake inhibitors (SSRIs).

120 to selective serotonin reuptake inhibitors (SSRIs).

121 and selective serotonin reuptake inhibitors (SSRIs).

122 of selective serotonin reuptake inhibitors (SSRIs).

123 to selective serotonin reuptake inhibitors (SSRIs).

124 ing selective serotonin reuptake inhibitors (SSRIs).

125 ith selective serotonin reuptake inhibitors (SSRIs; e.g., Prozac).

126 ine (serotonin-specific reuptake inhibitors [SSRI]), or venlafaxine-extended release (serotonin and n

127 se (selective serotonin reuptake inhibitors [SSRIs] or serotonin-norepinephrine reuptake inhibitors [

128 or selective serotonin reuptake inhibitors [SSRIs], and individuals with pharmacologically untreated

129 In monocyte-derived macrophages, SSRI treatment decreased expression of CD4 (p < .0001) a

130 In the water flea Daphnia magna, SSRIs increase offspring production in a food ration-dep

131 ey residue for high-affinity binding of many SSRIs, including (S)-citalopram.

132 xpenditure Panel Survey were used to measure SSRI use.

133 mptoms and least improvement), and Michelson SSRI (Selective SRI) Withdrawal Symptoms Scale scores (r

134 erences in symptomatic days or the Michelson SSRI Withdrawal Symptoms Scale.

135 ith no history of maternal depression and no SSRI exposure (18% vs 2%, p=0.003, OR estimate 10.32, 95

136 ith no history of maternal depression and no SSRI exposure in occurrence of CIM (7% vs 5%, p=0.75, OR

137 ith no history of maternal depression and no SSRI exposure.

138 (2.7%) used an SSRI and 26,771 (0.7%) a non-SSRI.

139 SSRI and non-SSRI monotherapy use during the 90 days before delivery

140 s from analyses of SSRI antidepressants, non-SSRI antidepressants, and nonantidepressant psychotropic

141 ibitor (SSRI) antidepressants, all other non-SSRI antidepressants, or other nonantidepressant psychot

142 RIs was 1.28 (95% CI, 1.01-1.64) and for non-SSRIs 1.14 (95% CI, 0.74-1.74).

143 For non-SSRIs, the odds ratios were 1.40 (95% CI, 1.12-1.75) and

144 0,000 births), and 78 infants exposed to non-SSRIs (29.1; 95% CI, 23.3-36.4 per 10,000 births).

145 within individuals who received CBT but not SSRIs.

146 Drugs, notably SSRIs, that elevate brain extracellular 5-HT (5-HTExt) a

147 Results from analyses of SSRI antidepressants, non-SSRI antidepressants, and nona

148 dose among youths with more than 150 days of SSRI or SNRI use (RR, 2.39; 95% CI, 1.04-5.52 for >15.0

149 ) but not among youths with 1 to 150 days of SSRI or SNRI use.

150 Duration of SSRI exposure, SSRI exposure at conception, and family h

151 categories in order to assess the effect of SSRI dosing on the efficacy and tolerability of SSRIs fo

152 findings indicate that the initial effect of SSRI treatment is to alter processing of aversive stimul

153 The authors evaluated the impact of SSRI treatment on CSF biomarkers and progression from mi

154 Exposure of interest was the number of SSRI prescriptions and prescriptions for other antidepre

155 offspring of unexposed mothers, offspring of SSRI-treated mothers and mothers unexposed to medication

156 s and statins with people who had periods of SSRI treatment alone.

157 alized to a more heterogeneous population of SSRI users.

158 ated several candidate genetic predictors of SSRI response in SAD.

159 Current long-term use of SSRI (>/=20 prescriptions) was not associated with an in

160 The use of SSRI less than or equal to median had a decreased risk o

161 In these data, use of SSRI was not associated with an increased risk of catara

162 is study identifies a dual mode of action of SSRIs on bone remodeling and suggests a therapeutic stra

163 anisms underlying the therapeutic actions of SSRIs.

164 The slightly increased benefits of SSRIs at higher doses are somewhat offset by decreased t

165 a consequence, lowers the effective dose of SSRIs.

166 Higher doses of SSRIs appear slightly more effective in major depressive

167 Higher doses of SSRIs were associated with an increased likelihood of dr

168 stimulation was necessary for the effects of SSRIs in a mouse model of anxiety/depression, and whethe

169 the efficacy or potential adverse effects of SSRIs in patients cannot be directly drawn from this stu

170 We tested the behavioral effects of SSRIs in the chronic behavioral despair model of depress

171 Its purpose was to investigate effects of SSRIs on brain development in nonhuman primates using an

172 d further elucidate the long-term effects of SSRIs on various social-emotional tasks in IED.

173 lieved to underlie the beneficial effects of SSRIs, but the identity of the specific RGS proteins inv

174 ics the antidepressant behavioral effects of SSRIs, suggesting that these cells may represent a novel

175 h SERT-dependent and -independent effects of SSRIs, we developed a knock-in mouse model whereby high-

176 activation is necessary for these effects of SSRIs.

177 -controlled trials examining the efficacy of SSRIs for treating adults with major depressive disorder

178 These findings suggest that the efficacy of SSRIs in treating depression and OCD may depend on ongoi

179 Thus, efficacy of SSRIs likely depends upon the brain's adaptive response

180 vide novel evidence for a protective role of SSRIs on some deleterious reproductive outcomes, possibl

181 I dosing on the efficacy and tolerability of SSRIs for major depressive disorder.

182 nd unpublished randomized clinical trials of SSRIs or SNRIs in youths with DD, AD, OCD, or PTSD were

183 The use of SSRIs and more generally of antidepressants with strong

184 SSRI treatment alone, the concomitant use of SSRIs and statins was not associated with significant in

185 people who had periods of concomitant use of SSRIs and statins with people who had periods of SSRI tr

186 Current use of SSRIs compared with TCAs and strong compared with weak s

187 the risk for ICH associated with the use of SSRIs compared with tricyclic antidepressants (TCAs) amo

188 Given the safe and widespread use of SSRIs in clinical practice, our study identifies an attr

189 risk of PPHN associated with maternal use of SSRIs in late pregnancy.

190 reater during current use than former use of SSRIs or SNRIs (absolute risk, 1.29 per 10000 person-mon

191 rt of youths insured by Medicaid, the use of SSRIs or SNRIs-the most commonly used antidepressant sub

192 risks of any cardiac defect with the use of SSRIs were 1.25 (95% confidence interval [CI], 1.13 to 1

193 findings suggest that clinical decisions on SSRI use during pregnancy should be individualized, taki

194 Once SSRIs became available in 1988, a 1% increase in SSRI us

195 days, after which either vehicle control or SSRI (10(-6) mol/L) was added for 2 hours.

196 ith 5-HT2A receptor (5-HT2AR) antagonists or SSRIs revealed that functional 5-HT2ARs, not SERTs, are

197 and 12 weeks later, following either CBT or SSRIs in the patient sample.

198 ent decisions regarding engagement in CBT or SSRIs, especially among individuals with an enhanced ERN

199 In PBMCs, SSRI treatment decreased expression of CD4 (p = .009), C

200 vidence for a role of 5-HT in mediating PES: SSRI administration increased PES in both genetic groups

201 Compared with placebo, SSRIs and SNRIs are more beneficial than placebo in chil

202 rmed in a subset of participants with plasma SSRI levels.

203 tiators compared to venlafaxine and possibly SSRIs, but not untreated patients.

204 d stratified subgroup analysis by predefined SSRI dose categories in order to assess the effect of SS

205 depression and took SSRIs during pregnancy (SSRI-exposed cohort) were matched to 66 children with no

206 fluoxetine (Flx), one of the most-prescribed SSRIs, acts on bone remodeling through two distinct mech

207 n on 856,493 individuals who were prescribed SSRIs, and subsequent violent crimes during 2006 through

208 nce for the actions of two widely prescribed SSRIs, fluoxetine and citalopram, in tests sensitive to

209 Offspring of mothers who purchased SSRIs at least twice during pregnancy had a significant

210 atric disorders with a history of purchasing SSRIs during pregnancy; 9537 were in the unmedicated gro

211 ic disorders without a history of purchasing SSRIs during pregnancy; and 31207 were in the unexposed

212 hiatric diagnosis or a history of purchasing SSRIs.

213 Offspring of mothers who received SSRI prescriptions during pregnancy had a lower risk for

214 otonin (5-hydroxytryptamine, 5-HT) reuptake (SSRIs) induces serotonin syndrome, which is usually mild

215 er explored mutually exclusive use of single SSRI substances.

216 e reuptake inhibitors (collectively: SSRIs), SSRIs with concomitant benzodiazepines (SSRI plus benzod

217 ected effect has a slow onset after starting SSRI treatment because of initial activation of 5-HT(1A)

218 Subchronic SSRI treatment, which does not induce antidepressant beh

219 ents with a history of depression, long-term SSRI treatment (>4 years) was significantly associated w

220 Long-term SSRI treatment may delay progression from MCI to Alzheim

221 al approach that randomly assigned long-term SSRI treatment or placebo.

222 5 years of age in association with long-term SSRI use needs to be investigated in further studies.

223 tly increased risk of cataract for long-term SSRI users (adjusted OR, 1.24; 95% CI, 1.15-1.34) compar

224 Short-term SSRI administration reversed this bias before any mood o

225 r gastrointestinal bleeding after short-term SSRI exposure by a case-crossover design.

226 roximately 3 years, compared with short-term SSRI treatment, treatment with other antidepressants, or

227 showing greater pretreatment activation than SSRI nonremitters and the SNRI group showing the opposit

228 These data suggest that SSRI administration in PD patients may result in worseni

229 The TPJ findings suggest that SSRI administration may reduce aggressive tendencies tow

230 These findings suggest that SSRI treatment, independent of depression status, downre

231 These findings indicate that SSRIs may inhibit neuroendocrine dopamine release throug

232 Here, we show that SSRIs can inhibit hypothalamic dopamine neurons that nor

233 Analysis showed that SSRIs and SNRIs were significantly more beneficial compa

234 The findings also suggest that SSRIs have the capacity to alter individual differences

235 The SSRI-exposed children were significantly more likely to

236 y and effectively elevate 5-HTExt beyond the SSRI effect and represent a novel treatment for TRD.

237 e suggests that elevating 5-HTExt beyond the SSRI effect enhances antidepressant efficacy, but previo

238 uring sustained 5-HTExt elevation beyond the SSRI effect.

239 yptophan (5-HTP) elevates 5-HTExt beyond the SSRI effect.

240 ized with SSRI to elevate 5-HTExt beyond the SSRI effect.

241 eceptor (5HT1AR, a receptor required for the SSRI response) specifically from DG GCs and found that t

242 Infants in the SSRI and SSRI plus benzodiazepine groups had lower motor

243 Infants in the SSRI plus benzodiazepine group had the least favorable s

244 risk of these disorders in offspring in the SSRI-exposed and unmedicated groups compared with offspr

245 were no differences between offspring in the SSRI-exposed group and in the unmedicated group.

246 speech/language disorders was 0.0087 in the SSRI-exposed group vs 0.0061 in the unmedicated group (h

247 ere 3 groups of offspring: 15596 were in the SSRI-exposed group, ie, had mothers diagnosed as having

248 rom DG GCs and found that the effects of the SSRI fluoxetine on behavior and the hypothalamic-pituita

249 Effects of the SSRI fluvoxamine and 5-HT(1A)R agonist 8-OH-DPAT were al

250 The suppressive effects of the SSRI on receptor expression did not differ as a function

251 of interleukin-2 with vehicle control or the SSRI (10(-6) mol/L) for 2 hours.

252 We first determined that the SSRI fluoxetine and the nicotinic partial agonist cytisi

253 Treatment with the SSRI at a physiologic dose decreased CD4, CCR5, and CXCR

254 y, we examined how 20-day treatment with the SSRI citalopram (CIT) alters marble-burying (MB), open f

255 ge injection of clorgyline combined with the SSRI paroxetine.

256 A combination of 11 with the SSRI sertraline increased the anorectic effect.

257 im, veterans with PTSD were treated with the SSRI, paroxetine.

258 The SSRIs produced a relatively large effect size for ADs (g

259 We further demonstrate that the SSRIs, fluoxetine and sertraline, directly suppress TIDA

260 Thus, SSRIs impair serotonin-regulation of reproductive invest

261 matched to venlafaxine initiators, 28,479 to SSRI initiators, and 22,714 to untreated patients.

262 nical observation of early adverse events to SSRI treatment in some patients with anxiety disorders.

263 ed to assess cataract risk after exposure to SSRI or to other antidepressant drugs in a large electro

264 ciated with metabolites that were related to SSRI response.

265 ounting for psychiatric diagnoses related to SSRI use.

266 signals of threat predict better response to SSRI and CBT treatment in anxious youth and that neuroim

267 Individual responsiveness to SSRI treatment may depend on a variety of factors that i

268 births) compared with 322 infants exposed to SSRIs (31.5; 95% CI, 28.3-35.2 per 10,000 births), and 7

269 Pregnancies were classified as exposed to SSRIs (N=15,729), unexposed to SSRIs but with psychiatri

270 I malformations (CIM) in children exposed to SSRIs during pregnancy.

271 limiting food conditions, females exposed to SSRIs produce more but smaller offspring, which is a mal

272 Therefore, research on in utero exposure to SSRIs can be helpful in informing patients and clinician

273 Conclusions and Relevance: Exposure to SSRIs during pregnancy was associated with an increased

274 rential responsiveness of select patients to SSRIs.

275 post-treatment among patients randomized to SSRIs, but remained stable among patients randomized to

276 is is necessary for some of the responses to SSRIs, but it is not known whether mature dentate gyrus

277 as exposed to SSRIs (N=15,729), unexposed to SSRIs but with psychiatric diagnoses (N=9,652), and unex

278 received a diagnosis of depression and took SSRIs during pregnancy (SSRI-exposed cohort) were matche

279 5-HT(1A) autoreceptor desensitization under SSRI antidepressant therapy.

280 Such effects may partly underlie SSRIs' impact in treating psychological illnesses.

281 ute and chronic actions of two commonly used SSRIs in these tests, and reinforce the utility of the S

282 gs, ultimately there may be a role for using SSRI treatment adjunctively in HIV and acquired immunode

283 Furthermore, for youths currently using SSRIs or SNRIs, the risk of type 2 diabetes increased wi

284 Clomipramine was not better than were SSRIs (-1.23 [-3.41 to 0.94]).

285 Objective: To examine whether SSRI exposure during pregnancy is associated with speech

286 Compared with SSRI treatment alone, the combined use of an SSRI and a

287 Compared with SSRI treatment alone, the concomitant use of SSRIs and s

288 uperior antidepressant effects compared with SSRI treatment alone.

289 sion between SSRI and SNRI medications, with SSRI remitters showing greater pretreatment activation t

290 with greater reduction in PTSD symptoms with SSRI treatment, irrespective of pre-treatment severity.

291 es of mice, adjunct 5-HTP SR synergized with SSRI to elevate 5-HTExt beyond the SSRI effect.

292 , COX-2 inhibitors, or low-dose aspirin with SSRIs significantly increases the risk of UGIB.

293 .9 and that for use of low-dose aspirin with SSRIs was 0.5.

294 se events are significantly more common with SSRIs and SNRIs than placebo.

295 resulted in robust advantages compared with SSRIs alone.

296 tment of maternal psychiatric disorders with SSRIs during pregnancy was related to a lower risk of pr

297 ereas that from use of COX-2 inhibitors with SSRIs was 1.9 and that for use of low-dose aspirin with

298 mall or too short to assess suicidality with SSRIs or SNRIs.

299 Combination treatment with SSRIs and CBT has been found to be more effective than e

300 uralistic cohort, concomitant treatment with SSRIs and statins resulted in robust advantages compared

301 regions may benefit most from treatment with SSRIs, which appear to augment activity in these regions