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Twenty-eight patients meeting the criteria for a diagnosis of schizophrenic disorder according to ICD-10 were assigned to monotherapy with olanzapine, clozapine, quetiapine, amisulpride, ziprasidone or risperidone. The levels of glucose and lipid metabolism were assessed before and after 28 days of treatment.
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This study shows the efficacy of ziprasidone in controlling agitation during the PTA period. Despite the small size of our sample, ziprasidone reduced symptoms of agitation quickly and with good tolerability, safety and no side effects.
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This observational cohort study examined Medicaid administrative claims data for patients aged 20 to 64 years with a new prescription for an atypical antipsychotic medication (clozapine, olanzapine, quetiapine, risperidone, ziprasidone) between January 1, 2004, and December 31, 2004. Patient diagnostic information was identified using the International Classification of Diseases, Ninth Revision, Clinical Modification codes on submitted medical claims. Patient characteristics, prescribing provider characteristics, length of therapy, and dosing were examined. A logistic regression assessed the probability of subtherapeutic dosing.
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Ziprasidone appears to independently lead to a lowering of serum lipid levels.
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Somnolence is a common side effect of antipsychotics. To assess the incidence of this side effect, we performed a MEDLINE search for randomized, double-blinded, placebo- or active-controlled studies of adult patients treated with antipsychotics for schizophrenia, mania, bipolar depression, or bipolar disorder. We extracted rates of somnolence from original publications and pooled them based on the dose of each antipsychotic in the same psychiatric condition, then estimated the absolute risk increase (ARI) and the number needed to harm (NNH) of an antipsychotic relative to placebo or an active comparator in the same psychiatric condition. According to the ARI in acute schizophrenia, bipolar mania, and bipolar depression, antipsychotics can be classified as high somnolence (clozapine), moderate somnolence (olanzapine, perphenazine, quetiapine, risperidone, ziprasidone), and low somnolence (aripiprazole, asenapine, haloperidol, lurasidone, paliperidone, cariprazine). The risk of somnolence with blonanserin, brexpiprazole, chlorpromazine, iloperidone, sertindole, and zotepine needs further investigation. The rates of somnolence were positively correlated to dose and duration for some antipsychotics, but not for others. Many factors, including antipsychotic per se, the method used to measure somnolence, patient population, study design, and dosing schedule, might affect the incidence of antipsychotic-induced somnolence. The mechanisms of antipsychotic-induced somnolence are likely multifactorial, although the blockade of histamine 1 receptors and α1 receptors may play a major role. The management of antipsychotic-induced somnolence should include sleep hygiene education, choosing an antipsychotic with a lower risk for somnolence, starting at a lower dose with a slower titration based on psychiatric diagnoses, adjusting doses when necessary, and minimizing concurrent somnolence-prone agents. Since most cases of somnolence were mild to moderate, allowing tolerance to develop over at least 4 weeks is reasonable before discontinuing an antipsychotic.
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Atypical antipsychotics and selective serotonin reuptake inhibitors (SSRIs) have been prescribed extensively, often in combination with each other. When toxic encephalopathy develops with neuromuscular and autonomic symptoms in a patient taking medication including atypical antipsychotics, it has tended to be diagnosed as neuroleptic malignant syndrome (NMS). However, there have recently been several case reports where the diagnosis of serotonin syndrome is given or raised as a likely differential diagnosis to such cases. In the present review, the author addressed himself to the issues surrounding the neurotoxic reaction to the treatment regimen containing atypical antipsychotics, focusing on the "atypical" forms of NMS and pathophysiological as well as clinical features of serotonin toxicity. Although NMS is idiosyncratic in nature, it appears practically useful to comprehend this syndrome as a spectrum-based concept. Likewise, serotonin toxicity is a broad spectrum of clinical syndromes in close connection with serotomimetic drug use, including varied severity. Some of atypical antipsychotics, i.e., perospirone, aripiprazole, ziprasidone, clozapine, and quetiapine, have been shown to behave as partial agonists at 5-HT1A receptors, providing direct evidence that these atypical antipsychotics are serotomimetic per se. The reciprocal interaction between the dopaminergic and serotonergic systems disturbed by either dopaminergic blockers or serotonergic enhancers leads to the disruption of homeostasis, with typical forms of NMS and serotonin syndrome representing the ends of the common pathophysiological background. The practical and flexible way to consider and manage such cases with updated knowledge derived from basic research should be warranted to be beneficial to our patients.
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Atypical antipsychotic treatment has been associated with serious metabolic adverse events, such as glucose dysregulation and development of type 2 diabetes. As part of our studies on possible underlying mechanisms, we investigated the acute effects of various typical and atypical antipsychotics on plasma glucose and insulin in FVB/N mice, a strain that showed a more pronounced hyperglycemic response to clozapine than C57BL/6 and CD-1 mice. Acute administration of high doses of clozapine, olanzapine, quetiapine, perphenazine, or chlorpromazine significantly increased plasma glucose by 100%-140% above basal levels without significant effects on insulin levels. In contrast, risperidone reduced plasma glucose (-30%) and markedly enhanced plasma insulin levels. Doses of ziprasidone that gave 50-fold higher free plasma concentrations than therapeutic plasma levels, as well as high doses of aripiprazole and haloperidol, did not significantly alter either glucose or insulin levels. Clozapine- and olanzapine-induced hyperglycemia occurred at free plasma concentrations that were within, or one order of magnitude above, the range of therapeutic plasma levels. Pretreatment with either the ganglionic blocker hexamethonium, or the alpha(2) adrenergic receptor antagonist yohimbine, blocked the clozapine- and chlorpromazine-induced increase in glucose levels. Taken together, these results suggest that typical and atypical antipsychotics with known metabolic liability produce acute hyperglycemia in mice and that this effect is likely driven by activation of the sympathetic autonomic nervous system via a central mechanism.
Ziprasidone was associated with a dose- and level-independent, significant prolongation of QTc duration in one-quarter of youth. However, prolongation of QTc dispersion was nonsignificant, and no patient experienced concomitant abnormal prolongation of both QTc duration and QTc dispersion. The dissociation between prolonged QTc duration and dispersion suggests low arrhythmogenic potential in youth with normal baseline ECGs.
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The effect of study design on findings regarding diabetes risk associated with antipsychotics was studied.
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Fourteen randomised clinical trials (6221 patients) of lurasidone, quetiapine (extended release and immediate release), aripiprazole, olanzapine, and ziprasidone for bipolar depression were included. Efficacy assessments included change in the Montgomery-Åsberg Depression Rating Scale (MADRS), rates of response (≥50% improvement in MADRS) and remission (MADRS ≤12 at study endpoint), and change in the Clinical Global Impressions-Bipolar Disorder-Severity (CGI-BP-S) scale. Tolerability outcomes included weight, somnolence, extrapyramidal symptoms (EPS), and all-cause discontinuation. Changes from baseline or odds ratios (OR) with 95% credible intervals (CrI) were evaluated.
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Despite intraclass differences and the complexities of antipsychotic choice, the second-generation antipsychotics are important contributions not only to the acute phase but, more importantly, to the maintenance treatment of schizophrenia.
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A MEDLINE search (1990-March 2003) was conducted.
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This overview of antipsychotic-induced hyperprolactinemia provides a summary of the current literature in relation to conventional antipsychotic agents and the five atypical antipsychotics currently available in the United States--clozapine, risperidone, olanzapine, quetiapine, and ziprasidone. Dopaminergic antagonism within the tuberoinfundibular system causes elevation in plasma prolactin levels. Conventional antipsychotic medications and the atypical agent risperidone cause significant elevations in prolactin. Clozapine, olanzapine, quetiapine, and ziprasidone cause minimal effects on prolactin levels in adults, which may be due to a higher 5-HT2A:D2 binding ratio and differential effects on dopamine neurotransmission, with less interference in the tuberoinfundibular pathway. Antipsychotic-induced hyperprolactinemia presumably causes clinical side effects similar to those caused by other forms of hyperprolactinemia. Clinical and endocrinologic changes of hypogonadism also likely occur during chronic antipsychotic-induced hyperprolactinemia. Because hyperprolactinemia may cause clinically significant side effects in patients treated with antipsychotic medications, clinicians should be familiar with the evaluation and treatment of antipsychotic-induced hyperprolactinemia.