SEROQUEL-GENERIC(generic name: Quetiapine ) Bibliography and References. Review.
List of selected scientific articles (abstracts). Experimental and clinical data. |
| CNS Spectr. 2005 May;10(5):356-61. Schizophrenia and obsessive-compulsive disorder (OCD) have historical,
clinical, and epidemiological links. The clinical use of atypical neuroleptics
(ie, dual serotonin-dopamine antagonists) to treat both conditions sheds
a new light on them. We report the first two cases of obsessive-compulsive
symptoms (OCS) induced by quetiapine in schizophrenia patients. A case
of successful augmentation by quetiapine in refractory OCD is also presented.
A review of the literature on OCS induced by atypical neuroleptics follows.
This paradoxically induced OCD symptomology in schizophrenia patients
administered atypical neuroleptics is discussed from new pathophysiological
and clinical perspectives. The discussion emphasizes the prognostic implications
of OCS in schizophrenia and available therapies for this comorbidity. J Clin Psychiatry. 2005 May;66(5):638-641. OBJECTIVE: To compare the long-term efficacy and tolerability of oral
quetiapine with those of intramuscular haloperidol. METHOD: Patients with
DSM-IV-diagnosed schizophrenia or schizoaffective disorder requiring long-term
antipsychotic treatment were randomly assigned to open-label oral quetiapine
or intramuscular haloperidol decanoate for 48 weeks. Clinicians were instructed
to target dosing at 500 mg/day of quetiapine or 200 mg of haloperidol
decanoate every 4 weeks. The Positive and Negative Syndrome Scale was
used to assess efficacy; the Simpson-Angus Scale and the Barnes Akathisia
Scale were used to assess safety and tolerability. For statistical analyses,
a general linear mixed-model repeated-measures analysis of covariance
was used, with change scores for dependent variables computed with the
baseline score as covariate. Data were collected from 1998 to 2001. RESULTS:
Thirty-five patients were enrolled, but 6 did not participate after being
informed of their treatment assignment; 4 of the 6 withdrawals were assigned
to haloperidol decanoate. Mean doses at week 48 were 493 mg/day of quetiapine
(N = 16) and 170 mg/28 days of haloperidol decanoate (N = 9). Survival
analysis showed no between-group differences in estimates of the number
of patients remaining exacerbation-free over time. Both drugs were efficacious,
but quetiapine was significantly better than haloperidol decanoate in
controlling negative symptoms (p < .05). The incidence of extrapyramidal
symptoms was low in both groups; patients receiving quetiapine showed
significantly greater improvement in rigidity and akathisia (p < .05).
CONCLUSION: Oral quetiapine was as efficacious as intramuscular haloperidol
in preventing symptom exacerbation over 48 weeks in patients with schizophrenia
or schizoaffective disorder, with fewer extrapyramidal symptoms, especially
rigidity and akathisia. Quetiapine was more efficacious than haloperidol
decanoate in treating negative symptoms. BMJ. 2005 Feb 18. OBJECTIVES: To determine the respective efficacy of quetiapine and rivastigmine for agitation in people with dementia in institutional care and to evaluate these treatments with respect to change in cognitive performance. DESIGN: Randomised double blind (clinician, patient, outcomes assessor) placebo controlled trial. SETTING: Care facilities in the north east of England. PARTICIPANTS: 93 patients with Alzheimer's disease, dementia, and clinically significant agitation. INTERVENTION: Atypical antipsychotic (quetiapine), cholinesterase inhibitor (rivastigmine), or placebo (double dummy). MAIN OUTCOME MEASURES: Agitation (Cohen-Mansfield agitation inventory) and cognition (severe impairment battery) at baseline and at six weeks and 26 weeks. The primary outcome was agitation inventory at six weeks. RESULTS: 31 patients were randomised to each group, and 80 (86%) started treatment (25 rivastigmine, 26 quetiapine, 29 placebo), of whom 71 (89%) tolerated the maximum protocol dose (22 rivastigmine, 23 quetiapine, 26 placebo). Compared with placebo, neither group showed significant differences in improvement on the agitation inventory either at six weeks or 26 weeks. Fifty six patients scored >10 on the severe impairment battery at baseline, 46 (82%) of whom were included in the analysis at six week follow up (14 rivastigmine, 14 quetiapine, 18 placebo). For quetiapine the change in severe impairment battery score from baseline was estimated as an average of -14.6 points (95% confidence interval -25.3 to -4.0) lower (that is, worse) than in the placebo group at six weeks (P=0.009) and -15.4 points (-27.0 to -3.8) lower at 26 weeks (P=0.01). The corresponding changes with rivastigmine were -3.5 points (-13.1 to 6.2) lower at six weeks (P=0.5) and -7.5 points (-21.0 to 6.0) lower at 26 weeks (P=0.3). CONCLUSIONS: Neither quetiapine nor rivastigmine are effective in the treatment of agitation in people with dementia in institutional care. Compared with placebo, quetiapine is associated with significantly greater cognitive decline.
We report a case of myoclonus induced by quetiapine. A 64-year-old man with schizophrenia developed myoclonic jerks when given higher doses of quetiapine. These movements were dose-related and completely abated on reducing the dose. To our knowledge, these movements have not been reported previously as an adverse effect of quetiapine.
The topic of antipsychotic-induced weight-gain and its relationship to
glucose metabolism is under-studied. We evaluated the long-term effects
of a new-generation antipsychotic, quetiapine and a conventional antipsychotic,
haloperidol on body mass index (BMI) and glycaemic control in patients
with schizophrenia previously treated with conventional antipsychotics.
Forty-five clinically stable patients with schizophrenia participated
in this randomized, investigator-blinded, parallel-group comparison of
flexible doses of quetiapine and haloperidol treatment over 52 wk. Primary
outcome measures were change from baseline in BMI and glycosylated haemoglobin
(HBA1c) levels. There were no between-group differences at any of the
time-points for BMI (F=1.90, p=0.1) and HBA1c (F=1.17, p=0.3) values,
and there were no significant changes in BMI from baseline for either
group. HBA1c levels decreased significantly at end-point for the haloperidol
group (-1.5%, p=0.04), but not for the quetiapine group (-0.3%, p=0.5).
Although the sample was not generally obese (mean baseline BMI 25.5+/-6.3
kg/m2), a large proportion exhibited evidence of abnormal glycaemic control
prior to randomization (mean HBA1c 6.7+/-1.9%), with 48% having values
that were at least mildly elevated (HBA1c >6.1%) and 19% markedly elevated
(HBA1c >7%). The number of subjects with elevated HBA1c values decreased
from baseline in both the haloperidol and quetiapine treatment groups.
These findings suggest that switching treatment from a conventional antipsychotic
to quetiapine is not associated with weight gain or worsening of glycaemic
control, even in the long term. The study also highlights the high incidence
of unrecognized glucose dysregulation in patients with schizophrenia receiving
conventional antipsychotic treatment. Pharmacopsychiatry. 2005 Jan;38(1):17-9. INTRODUCTION: Conventional antipsychotic medications are associated with
elevated prolactin levels, resulting in hyperprolactinemia and a number
of unwanted side effects. Several atypical antipsychotics, on the other
hand, are less likely to evoke hyperprolactinemia. The aim of this study
was to investigate the prevalence of hyperprolactinemia induced by conventional
antipsychotic drugs, examine changes in serum prolactin levels and psychiatric
symptoms after switching to quetiapine, and identify the relevant characteristics
of patients who may be suitable to switch to quetiapine. METHOD: Sixty-nine
of 74 consecutive female patients who had received conventional antipsychotic
drugs were initially included in the study. Of these, 49 (71 %) patients
suffered from hyperprolactinemia, of which a further 25 were subsequently
switched to quetiapine. Psychiatric symptoms were assessed by the Positive
and Negative Syndrome Scale (PANSS), and serum prolactin levels were measured
just before and at 4 and 8 weeks after switching. RESULTS: Eight of the
25 (32 %) "switch" patients dropped out due to psychotic exacerbation
during the 8 weeks. In the remaining 17 (68 %) patients, serum prolactin
levels were significantly decreased without any significant change in
PANSS scores after switching. The 17 patients who completed the switch
had previously demonstrated significantly lower positive symptom scores
compared to the 8 dropout patients. CONCLUSION: The present findings suggest
that 71 % of female patients receiving conventional antipsychotic drugs
may suffer from hyperprolactinemia and that approximately two-thirds of
patients can be switched to quetiapine, resulting in an improvement in
hyperprolactinemia. The main characteristic of the switched patients may
be fewer positive symptoms.
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