ライフサイエンスコーパス: clozapine

1 4, 'Chronic cloza ine' should read 'Chronic clozapine'.

2 psychotics regarding self-harm compared with clozapine.

3 antipsychotic drug and for combinations with clozapine.

4 may underlie some of the clinical effects of clozapine.

5 posite for rapidly measuring serum levels of clozapine.

6 mide may be a key mediator of the effects of clozapine.

7 ty, such as omega-3 fatty acids, lithium and clozapine.

8 in patients with schizophrenia treated with clozapine.

9 nt-resistant schizophrenia do not respond to clozapine.

10 schizophrenia which responds specifically to clozapine.

11 at baseline and 6-9 months after commencing clozapine.

12 1 by a QT prolonging drug: the antipsychotic clozapine.

13 in adult patients with schizophrenia taking clozapine.

14 ould enable safer and more widespread use of clozapine.

15 et for atypical antipsychotic drugs, such as clozapine.

16 enia who have not previously been exposed to clozapine.

17 mice treated for 21 days with haloperidol or clozapine.

18 , and inverse agonist and antipsychotic drug clozapine.

19 old) relative to the original pharmacophore, clozapine.

20 ance to the locomotor suppressive effects of clozapine.

21 ptor dimerization and the atypical nature of clozapine.

22 lurasidone to 1.05 mmol/L (0.41 to 1.70) for clozapine.

23 lactinemia relative to atypical APDs such as clozapine.

24 nner, similar to the atypical antipsychotic, clozapine.

25 ght underlie the unique clinical efficacy of clozapine.

26 However, clozapine administration partly antagonized the fall in

27 Herein, we sought to determine whether clozapine also utilizes betaarrestin2-mediated mechanism

28 cell count is compulsory in patients taking clozapine, although the incidence of drug-induced agranu

29 Performance at 0.1 mg/kg clozapine and 0.1 mg/kg deschloroclozapine did not diffe

30 were acquired at baseline before commencing clozapine and again after 6 months of treatment for 33 p

31 Although effects of clozapine and haloperidol alone were relatively minor, t

32 l and dilution series, were used to quantify clozapine and its major metabolite norclozapine in isola

33 e of the rs2814778 genotype for those taking clozapine and its potential as a pharmacogenetic test, d

34 and pharmacological treatments (for example, clozapine and ketamine) along with coordinated social an

35 The anti-suicidal effects of clozapine and lithium have been substantiated, but might

36 Clozapine and long-acting injectable antipsychotic medic

37 od was collected to assess concentrations of clozapine and NDMC as well as serum anticholinergic acti

38 t associations were found between individual clozapine and NDMC concentrations and working memory per

39 authors hypothesized that the ratio of serum clozapine and NDMC concentrations would be inversely ass

40 HLA-DRB1*04:01 binding clefts revealed that clozapine and olanzapine bind in a similar conformation

41 in schizophrenia, and antipsychotics such as clozapine and olanzapine have been associated with diffe

42 this mechanism to the therapeutic effects of clozapine and olanzapine, both highly effective therapeu

43 eat mood disorders and suicidality (lithium, clozapine and omega-3 fatty acids), providing a means to

44 gnitude of response in patients treated with clozapine and other antipsychotics for both treatment-re

45 ymptoms did not differ significantly between clozapine and other antipsychotics in TRS studies (VR =

46 ible by administration of the antipsychotics clozapine and risperidone suggesting that the loss of th

47 e extent to which the atypical antipsychotic clozapine and the typical antipsychotic haloperidol coul

48 f morphine, codeine, oxymorphone, oxycodone, clozapine, and buspirone and their deuterated internal s

49 Our findings suggest that clozapine, and related centrally acting drugs, might be

50 A pattern of superiority for olanzapine, clozapine, and risperidone was seen in other efficacy ou

51 chotropic drugs and contraceptives are rare, clozapine, anticonvulsants, and St.

52 tment in patients unlikely to respond to non-clozapine antipsychotics.

53 tions of typical (haloperidol) and atypical (clozapine) antipsychotics in MET mice mimicked effects i

54 We conclude that clozapine appears to affect the development and induce l

55 We sought risk alleles for clozapine-associated neutropenia in a sample of 66 cases

56 Remarkably, both haloperidol and clozapine attenuated AMP disruption of LI in Drd2-/-.

57 ng white blood cell count in patients taking clozapine, based on divergent national requirements, do

58 Our data show that clozapine binding to Kv11.1 is complex.

59 an describe the observed kinetic features of clozapine block and correctly predict the overall affini

60 n 2.5 hours while agonist DOI and antagonist clozapine bring about recycling in 7.5 hours.

61 Only four ligands (5-HT, DA, DOI, and clozapine) bring about receptor endocytosis.

62 Such hyperactivity was ameliorated by clozapine but not haloperidol or ziprasidone.

63 ight pharmacological 5-HT(2A)R blockade with clozapine, but not with M100907, decreased mGluR2 densit

64 Unfortunately, clozapine can cause severe side effects independent of i

65 We further observed that clozapine clears protein aggregates, such as alpha-synuc

66 nical diagnosis of schizophrenia attending a clozapine clinic (CLOZUK), 2504 cases with a research di

67 To establish whether clozapine (CLO) produces its behavioral and molecular ac

68 k) typical (haloperidol (HAL)) and atypical (clozapine (CLZ)) APDs on the neuroanatomy of wild-type (

69 P), haloperidol (HAL), risperidone (RIS) and clozapine (CLZ), at concentrations typical of high thera

70 e for interactions between the metabolism of clozapine, coffee, and tobacco.

71 dequately informed patients, the Netherlands Clozapine Collaboration Group now permits quarterly moni

72 ent-resistant schizophrenia not treated with clozapine compared with clozapine-treated individuals.

73 evidence of treatment resistance, initiating clozapine compared with initiating a standard antipsycho

74 rovide little evidence of the superiority of clozapine compared with other second-generation antipsyc

75 duced sensitivity to the sedating effects of clozapine compared with wild-type (WT) littermates, para

76 c activity was significantly associated with clozapine concentration, but not with working memory per

77 97, which was associated with a reduction in clozapine concentrations roughly equivalent to a decreas

78 sub-chronic administration of haloperidol or clozapine counteracted the reduction of striatal A(2A)R-

79 We also demonstrate that clozapine decreases locomotor activity in a 5-HT(2A)-dep

80 bcortical volume deficits after switching to clozapine despite experiencing symptomatic improvement.

81 hotic drug treatment, including the atypical clozapine, did not affect Hdac1 levels in PFC but induce

82 ess mortality was observed in the year after clozapine discontinuation (hazard ratio: 2.65, 95% CI: 1

83 t extent the observed excess mortality after clozapine discontinuation is confounded by nonadherence

84 in physical or mental health precipitated by clozapine discontinuation.

85 hly equivalent to a decrease of 50 mg/day in clozapine dosage.

86 Clozapine dosages remained constant.

87 A low clozapine dose (1 mg/kg intravenous) significantly count

88 Clozapine dose-dependently attenuated the absolute S-(+)

89 alantamine, modafinil, levodopa, rotigotine, clozapine, duloxetine, clonazepam, ramelteon, gabapentin

90 ine group) or a course of bilateral ECT plus clozapine (ECT plus clozapine group).

91 granulocytosis is rare during treatment with clozapine, especially in monotherapy.

92 - and second-generation APDs that we tested, clozapine exhibited the lowest efficacy for translocatin

93 metabolic side-effects, with olanzapine and clozapine exhibiting the worst profiles and aripiprazole

94 tion/slow dissociation at the D(2)R, whereas clozapine exhibits relatively slow association/fast diss

95 ssociated with symptomatic improvement after clozapine exposure may reflect an adaptive response rela

96 t is mediated by adverse effects from recent clozapine exposure or deterioration in physical or menta

97 xamined the use of ECT as an augmentation to clozapine for treatment-refractory schizophrenia.

98 or haloperidol to 3.01 kg (1.78 to 4.24) for clozapine; for BMI from -0.25 kg/m(2) (-0.68 to 0.17) fo

99 xpiprazole to 0.98 mmol/L (0.48 to 1.49) for clozapine; for glucose from -0.29 mmol/L (-0.55 to -0.03

100 r cariprazine to 0.56 mmol/L (0.26-0.86) for clozapine; for LDL cholesterol from -0.13 mmol/L (-0.21

101 None of the patients in the clozapine group met the criterion.

102 Nonresponders from the clozapine group received an 8-week open trial of ECT (cr

103 All 19 patients from the clozapine group received ECT in the crossover phase.

104 phrenia were assigned to treatment as usual (clozapine group) or a course of bilateral ECT plus cloza

105 se of bilateral ECT plus clozapine (ECT plus clozapine group).

106 articipants (ECT plus clozapine group, N=20; clozapine group, N=19).

107 at sample included 39 participants (ECT plus clozapine group, N=20; clozapine group, N=19).

108 were available for antipsychotics other than clozapine, haloperidol, olanzapine, and risperidone.

109 Pharmacological augmentation to clozapine has been studied with unimpressive results.

110 her for nonclozapine antipsychotics than for clozapine (hazard ratio: 1.36, 95% CI: 1.04-1.78).

111 not receiving clozapine than for those given clozapine (hazard ratio: 1.88, 95% confidence interval [

112 uclopenthixol (HR, 0.53; 95% CI, 0.48-0.57), clozapine (HR, 0.53; 95% CI, 0.48-0.58), long-acting inj

113 Clozapine (HR, 0.58; 95% CI, 0.53-0.63) and all long-act

114 0.2 mg/kg clozapine impaired working memory function in three of t

115 hanges 6 months after switching treatment to clozapine in patients with treatment-resistant schizophr

116 the distinct therapeutic characteristics of clozapine in schizophrenia.

117 nd labetalol, and the atypical antipsychotic clozapine, in reversing MDMA-induced brain and body hype

118 ent-resistant patients with schizophrenia to clozapine indicated a potential healthcare cost saving o

119 In contrast, clozapine induced a marked and immediate reversal of MDM

120 riants in a meta-analysis with data from the Clozapine-Induced Agranulocytosis Consortium (up to 163

121 ealthy donors and patients with a history of clozapine-induced agranulocytosis.

122 tion but its use is curtailed by the risk of clozapine-induced agranulocytosis/granulocytopenia (CIAG

123 s genome-wide RNAi screen for suppressors of clozapine-induced developmental delay and lethality reve

124 ay explain the role of the gene in mediating clozapine-induced developmental delay/lethality.

125 xamined pharyngeal pumping and observed that clozapine-induced inhibition of pharyngeal pumping requi

126 ophrenia was the earliest instance of either clozapine initiation or hospital admission for schizophr

127 essed DREADDs, whereas systemic subthreshold clozapine injections induce preferential DREADD-mediated

128 iments; activation of TCC required APC, with clozapine interacting directly at therapeutic concentrat

129 Collectively, these data show that clozapine interacts at therapeutic concentrations with H

130 Clozapine is a particularly effective antipsychotic medi

131 Use of the atypical antipsychotic clozapine is associated with life-threatening agranulocy

132 t with available medication data showed that clozapine is associated with male-specific decelerations

133 In treatment-resistant schizophrenia, clozapine is considered the standard treatment.

134 ipsychotics, and whether greater efficacy of clozapine is dependent on the degree of treatment-resist

135 ism are effective for motor fluctuations and clozapine is effective for hallucinations.

136 Although clozapine is known to inhibit 5-HT2AR signaling through

137 (APD), clozapine, is of great importance, as clozapine is more effective and has therapeutic benefits

138 Clozapine is more effective than other antipsychotics ir

139 Clozapine is one of the most promising medications for m

140 Clozapine is the only effective medication for treatment

141 Clozapine is unique among the atypical APDs in its effic

142 The antipsychotic clozapine is uniquely effective in the management of sch

143 Increasing the judicious use of clozapine is warranted together with vigilance to preven

144 s of action of the antipsychotic drug (APD), clozapine, is of great importance, as clozapine is more

145 Chronic treatment with the antipsychotic clozapine led to a decrease in mouse frontal cortex mGlu

146 ver time was associated with increased serum clozapine level at follow-up (r = -0.44; p = 0.010).

147 Timely measurement of serum clozapine levels has been identified as a barrier to the

148 c rate constants, affording compounds with a clozapine-like kinetic profile.

149 xide (CNO) lacks brain entry and converts to clozapine, making it difficult to apply in basic and tra

150 implicate biological pathways through which clozapine may act to cause this serious adverse effect.

151 In this regard, clozapine may also be considered a functionally selectiv

152 Despite evidence that clozapine may be neuroprotective, there are few longitud

153 and rapid electrochemical approach for serum clozapine measurements should provide clinicians with th

154 We demonstrate that unlike serotonin, clozapine-mediated 5-HT2AR internalization and Akt phosp

155 ed receptor endocytosis, but DA-mediated and clozapine-mediated internalization is not affected if PK

156 Moreover, clozapine-mediated suppression of MK-801 and phencyclidi

157 ommon genetic variants with large effects on clozapine metabolism exist and can be found via genome-w

158 the discovery of pharmacogenomic variants of clozapine metabolism may improve clinical management, no

159 d for demographic factors known to influence clozapine metabolism, although it was not possible to ad

160 sion to combine data from multiple assays of clozapine metabolite plasma concentrations from a clozap

161 T cell activation and cross-reactivity with clozapine metabolites and olanzapine.

162 ectrochemical measurement approach for serum clozapine monitoring are: (i) rapid measurement ( approx

163 pine metabolite plasma concentrations from a clozapine monitoring service and carried out a genome-wi

164 schizoaffective disorder who were receiving clozapine monotherapy at bedtime completed the MATRICS C

165 is that emerged after 19 years of continuous clozapine monotherapy.

166 Among multiple actions of clozapine, muscarinic acetylcholine (ACh) activation mar

167 While clozapine N-oxide (CNO) activation of interneurons suppr

168 g intracranial or systemic administration of clozapine N-oxide (CNO) and tested the ability of system

169 The prototypical DREADD agonist clozapine N-oxide (CNO) lacks brain entry and converts t

170 Males received clozapine N-oxide (CNO) or vehicle injections before eac

171 mporally by the administration of the ligand clozapine N-oxide (CNO).

172 exclusively activated by the "designer drug" clozapine N-oxide (CNO).

173 Chemogenetic activation with clozapine N-oxide resulted in delayed estrous cycles and

174 NAcC-projecting BLA neurons, treatment with clozapine N-oxide, but not vehicle, selectively prevente

175 o the P4-P6 peptide binding pockets, whereas clozapine N-oxide, which did not activate the TCC, bound

176 , as it was reversible, and it was absent in clozapine N-oxide-treated rats expressing an empty contr

177 a concurrent gain in potency for the ligand clozapine N-oxide.

178 althy controls (n=12), patients treated with clozapine (n=12) who had not responded to first-line ant

179 dence of treatment resistance that initiated clozapine (N=3,123) and in a propensity score-matched co

180 Administering clozapine-N-oxide (CNO) enabled precise DREADD-dependent

181 coupled receptor with the synthetic compound clozapine-N-oxide (CNO) evoked a short and transient Ca(

182 combination of muscarinic-based DREADDs with clozapine-N-oxide (CNO) has been widely used, sluggish k

183 d and subsequently activated by their ligand Clozapine-N-oxide (CNO) in conjunction with fear extinct

184 adora2A-rM3Ds mouse, activation of rM3Ds by clozapine-N-oxide (CNO) induces DARPP-32 phosphorylation

185 We confirmed that clozapine-N-oxide (CNO) itself did not alter the CD resp

186 nd after administration of the DREADD ligand clozapine-N-oxide (CNO) or vehicle (saline).

187 ce expressing Gi-DREADD were normal, 1 mg/kg clozapine-N-oxide (CNO) produced a significant 3 h incre

188 er injection of saline or the hM3/hM4 ligand clozapine-N-oxide (CNO) under baseline conditions and un

189 livered after 4-weeks of alcohol intake, and clozapine-N-oxide (CNO) was administered to selectively

190 Chemogenetic [clozapine-N-oxide (CNO)-hM4Di] perturbation of Tac1-Pet1

191 ated by an otherwise inert synthetic ligand, clozapine-N-oxide (CNO).

192 idal neurons and activated the receptor with clozapine-N-oxide (CNO).

193 tion to a bioinert drug-like small molecule, clozapine-N-oxide (CNO).

194 ons could be dose-dependently inactivated by clozapine-n-oxide (CNO).

195 lencer in the presence of its cognate ligand clozapine-N-oxide (CNO).

196 lly inactive and orally bioavailable agonist clozapine-N-oxide (CNO).

197 ated by an otherwise inert synthetic ligand, clozapine-N-oxide (CNO).

198 d AAV-hSYN-eYFP vector that was treated with clozapine-N-oxide (CNO; 3 mg/kg, i.p.) before stage II s

199 Activation of the transfected Gi-DREADD with clozapine-N-oxide administered into the ventral pallidum

200 with intra-VTA microinfusions of the agonist clozapine-n-oxide to bidirectionally modulate dopamine n

201 was later activated by systemic injection of clozapine-N-oxide, neural activity in RSC was transientl

202 M3D-arr using the otherwise inert compound, clozapine-N-oxide, we found that M3D-arr activation incr

203 Likewise, clozapine-N-oxide-induced inhibition of PV interneurons

204 us administration of the inert DREADD ligand clozapine-N-oxide.

205 cologically inert, but bioavailable, ligand (clozapine-N-oxide; CNO), while being non-responsive to e

206 This finding suggests that manipulating the clozapine/NDMC ratio could enhance cognition in patients

207 This hypothesis-driven study confirms that clozapine/NDMC ratio is a strong predictor of working me

208 The clozapine/NDMC ratio was significantly and negatively as

209 ce and carried out a genome-wide analysis of clozapine, norclozapine, and their ratio on 10,353 assay

210 after injections of three DREADD actuators, clozapine, olanzapine, and deschloroclozapine, in four m

211 Some second-generation antipsychotics (eg, clozapine, olanzapine, quetiapine, and risperidone) are

212 The dissociable effects of haloperidol and clozapine on ketamine-induced hyperoxygenation and mPFC-

213 dditionally, studies examining the effect of clozapine on the brain can help to identify aspects of c

214 Drug effects (PCP followed by clozapine) on the activity of RtN (single unit and local

215 tiveness of initiating treatment with either clozapine or a standard antipsychotic among adults with

216 Interventions were new initiation of clozapine or a standard antipsychotic medication, define

217 common variants affecting the metabolism of clozapine or its metabolites.

218 tide-1 receptor agonist liraglutide added to clozapine or olanzapine treatment of schizophrenia spect

219 Participants received stable treatment with clozapine or olanzapine, were overweight or obese, and h

220 chizophrenia spectrum disorders treated with clozapine or olanzapine.

221 No combination strategies with clozapine outperformed controls.

222 Fifty percent of the ECT plus clozapine patients met the response criterion.

223 hways and compounds that might interact with clozapine pharmacokinetics.

224 udies (GWASs) to discover genetic markers of clozapine plasma concentrations in a large sample of pat

225 mining clinical and functional outcomes with clozapine positioned as a second-line treatment.

226 en studies showed the atypical antipsychotic clozapine possessed higher affinity for D4, relative to

227 f rare variants to treatment response, using clozapine prescription as a proxy for treatment resistan

228 olicy makers in the revision of guidance for clozapine prescription.

229 Acute administration of clozapine rapidly increased extracellular dopamine level

230 Upon systemic CNO injections, converted clozapine readily enters the brain and occupies central

231 schizophrenia which responds differently to clozapine relative to other antipsychotics, and whether

232 zed single-blind 8-week study, patients with clozapine-resistant schizophrenia were assigned to treat

233 previous suggestive evidence of an impact on clozapine response in patients with schizophrenia, we co

234 Six well-growing clozapine-responsive CD4(+) and CD8(+) TCC were used for

235 However, clozapine reversal of PCP effects is not driven by resto

236 Although betaarrestin2 has no effect on clozapine's actions in vivo, Akt phosphorylation is requ

237 in vivo, Akt phosphorylation is required for clozapine's efficacy in blocking MK-801- and PCP-induced

238 Clozapine's potent antagonism of muscarinic M1 receptors

239 rate to second-line treatments, coupled with clozapine's substantial response rate in refractory schi

240 We found that patients treated with clozapine show lower dopamine synthesis capacity than pa

241 The objective of this study was to generate clozapine-specific T cell clones (TCC) and characterize

242 Future clozapine studies with high doses and patients with extr

243 national registries of patients treated with clozapine, study cohorts, and a pharmacovigilance databa

244 tipsychotic effects of either haloperidol or clozapine, suggesting that these compounds mediate their

245 ry drugs (haloperidol, bufuralol, midazolam, clozapine, terfenadine, erlotinib, olanzapine, and moxif

246 tality was higher for patients not receiving clozapine than for those given clozapine (hazard ratio:

247 on the brain can help to identify aspects of clozapine that make it uniquely effective in patients wi

248 The antipsychotic clozapine, the only licensed medication for treatment-re

249 Clozapine, the treatment of choice in refractory schizop

250 ging from -0.89 (95% CrI -1.08 to -0.71) for clozapine to -0.03 (-0.59 to 0.52) for levomepromazine (

251 15 participants) from -0.62 (-0.84 to -0.39; clozapine) to -0.10 (-0.45 to 0.25; flupentixol), for de

252 pants) from -77.05 ng/mL (-120.23 to -33.54; clozapine) to 48.51 ng/mL (43.52 to 53.51; paliperidone)

253 4 911 participants) from 0.46 (0.19 to 0.88; clozapine) to 6.14 (4.81 to 6.55; pimozide).

254 Clozapine, to which CNO rapidly converts in vivo, shows

255 chemical measurements in clinical serum from clozapine-treated and clozapine-untreated schizophrenia

256 neutropenia in a sample of 66 cases and 5583 clozapine-treated controls, through a genome-wide associ

257 nia not treated with clozapine compared with clozapine-treated individuals.

258 kely to develop neutropenia and have to stop clozapine treatment (OR = 20.4, P = 3.44 x 10(-7)).

259 Chronic clozapine treatment blunted the antipsychotic-related be

260 We found that chronic clozapine treatment decreased via HDAC2 the capabilities

261 lored an association between commencement of clozapine treatment for schizophrenia and changes in reg

262 mortality and self-harm in association with clozapine treatment in individuals with treatment-resist

263 clinical benefit in minimising the delay to clozapine treatment in patients unlikely to respond to n

264 Clozapine treatment led to reductions in caudate nucleus

265 otein expression profiles were observed when clozapine treatment was compared with olanzapine and the

266 ssociation study of neutrophil levels during clozapine treatment, in 552 individuals with treatment-r

267 rrently showed low symptom severity with the clozapine treatment.

268 ts or longitudinally assessed the effects of clozapine treatment.

269 or that it is contributed to by switching to clozapine treatment.

270 ients with schizophrenia who are switched to clozapine treatment.

271 terly monitoring after the first 6 months of clozapine treatment.

272 blood cell counts that are now required for clozapine treatment.

273 in the initiation and on-going management of clozapine treatment.

274 eviously been investigated in the context of clozapine treatment.

275 associated with low neutrophil counts during clozapine treatment.

276 in clinical serum from clozapine-treated and clozapine-untreated schizophrenia groups are well correl

277 However, clozapine use has restrictions owing to its many adverse

278 Practical issues related to clozapine use, in combination with the robust response r

279 ogically oppositional ligands, serotonin and clozapine, utilize differential mechanisms to achieve th

280 -1.78), and intestinal obstruction (0.9% for clozapine vs. 0.3% for standard antipsychotic; hazard ra

281 sed incidence of diabetes mellitus (2.8% for clozapine vs. 1.4% for standard antipsychotic; hazard ra

282 95% CI=0.98-2.70), hyperlipidemia (12.9% for clozapine vs. 8.5% for standard antipsychotic; hazard ra

283 Initiation of clozapine was associated with a significantly decreased

284 Clozapine was associated with significantly increased in

285 A sample from rat liver perfused with clozapine was distributed to three sites for analysis by

286 Clozapine was localized and quantified in individual bra

287 13), and sertindole (-0.46; -0.80 to -0.06); clozapine was more effective than haloperidol (-0.22; -0

288 The most surprising finding was that clozapine was not significantly better than most other d

289 Furthermore, clozapine was superior in improving positive symptoms in

290 Clozapine was superior to other antipsychotics in improv

291 ychotic drug and 5 strategies that augmented clozapine were examined.

292 r the readily detected uric acid and for the clozapine which is present at 100-fold lower concentrati

293 dentified as a barrier to the broader use of clozapine, which is however challenging due to the compl

294 The augmentation of clozapine with ECT is a safe and effective treatment opt

295 d apparent nonstate-dependent interaction of clozapine with Kv11.1.

296 blind randomised controlled trials comparing clozapine with other antipsychotics in patients with sch

297 be a case of serotonin syndrome secondary to clozapine withdrawal and concomitant use of citalopram h

298 s of serotonin syndrome attributed to abrupt clozapine withdrawal with concomitant use of citalopram.

299 ainly call into question the likelihood that clozapine would be chosen if it were an option at this s

300 This raises the question of whether clozapine would be more effectively positioned as a firs