geodon 40mg capsule
Ziprasidone and bupropion are medications prescribed for mood and behavior disorders. They have apparently safe cardiac safety profiles in both therapeutic and supratherapeutic doses, but recently the Federal Drug Administration has issued a caution regarding ziprasidone use in combination with other drugs that are known to prolong the QTc interval.
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Patients treated by ziprasidone more frequently belong to subgroups composed of more autonomous patients and those with mild to moderate disease severity.
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For the test and reference preparation, the pharmacokinetics parameter C(max) was 170.7-/+71.3 and 174.4-/+81.6 ng/ml, t(max) 3.73-/+1.87 and 3.69-/+1.84 h, t((1/2)) 5.57-/+1.62 and 5.61-/+1.73 h, AUC(0-t) 1273-/+252.3 and 1296-/+266.9 ng.h.ml(-1), and AUC(0-infinity)1396-/+276.9 and 1407-/+281.5 ng.h.ml(-1), respectively, with the relative bioavailability of (98.3-/+12.6)%. No significant differences were found in the main parameters of the test and reference preparations as analyzed by ANOVA and two- and one-side t-test.
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A 17-year-old male developed a widened QRS and a prolonged QTc interval following an overdose of ziprasidone and bupropion. He required hospital admission for aggressive cardiac monitoring and antidysrhythmic therapy, stabilizing to baseline by 80 hours postingestion.
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Persistence was approximately 30 days longer for patients receiving ziprasidone (n = 217; 228 days) than risperidone (n = 831; 193 days) or olanzapine (n = 762; 201 days). Compliance was significantly (P<.05) higher among patients receiving ziprasidone (87%) compared with other treatments (78%-80%). Ziprasidone patients had significantly larger decreases (- USD 6866) in mean annual psychiatric-related costs following therapy initiation than those on risperidone (- USD 3353; P = .0116) or olanzapine (- USD 4764; P = .0021). The primary driver of cost savings was reduced hospitalization after treatment initiation.
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Post hoc analysis, use of 3 SADS-C psychosis items to assess psychosis.
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To review published and nonpublished literature describing changes in weight, glucose homeostasis, and lipid milieu with antipsychotics.
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Second-generation antipsychotics (SGAs) are commonly used to treat schizophrenia. However, SGAs cause metabolic disturbances that can manifest as metabolic syndrome (MetS) in a subset of patients. The causes for these metabolic disturbances remain unclear. We performed a comprehensive metabolomic profiling of 60 schizophrenia patients undergoing treatment with SGAs that puts them at high (clozapine, olanzapine), medium (quetiapine, risperidone), or low (ziprasidone, aripiprazole) risk for developing MetS, compared to a cohort of 20 healthy controls. Multiplex immunoassays were used to measure 13 metabolic hormones and adipokines in plasma. Mass spectrometry was used to determine levels of lipids and polar metabolites in 29 patients and 10 controls. We found that levels of insulin and tumor necrosis factor alpha (TNF-α) were significantly higher (p < 0.005) in patients at medium and high risk for MetS, compared to controls. These molecules are known to be increased in individuals with high body fat content and obesity. On the other hand, adiponectin, a molecule responsible for control of food intake and body weight, was significantly decreased in patients at medium and high risk for MetS (p < 0.005). Further, levels of dyacylglycerides (DG), tryacylglycerides (TG) and cholestenone were increased, whereas α-Ketoglutarate and malate, important mediators of the tricarboxylic acid (TCA) cycle, were significantly decreased in patients compared to controls. Our studies suggest that high- and medium-risk SGAs are associated with disruption of energy metabolism pathways. These findings may shed light on the molecular underpinnings of antipsychotic-induced MetS and aid in design of novel therapeutic approaches to reduce the side effects associated with these drugs.
Recent literature documents a stronger association between nonfasting triglycerides (TG) and cardiovascular risk compared to fasting TG. Given concerns over antipsychotic effects on serum TG, this analysis explored changes in nonfasting TG in phase 1 of the CATIE Schizophrenia Trial.
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The proportion of patients who discontinued from the study was similar for lurasidone and ziprasidone (32.5% vs. 30.7%); the proportion who discontinued due to adverse events was similar (10.4% vs. 11.1%). Treatment with lurasidone and ziprasidone was associated with a small endpoint reduction in median weight (-0.65 kg vs. -0.35 kg) and median total cholesterol (-6.4 vs. -4.4 mg/dL); no endpoint change was observed in median triglycerides (0.0 vs. 0.0 mg/dL). There were no clinically significant changes in other laboratory or ECG parameters. Improvement was observed on an MMRM analysis of the PANSS total score for lurasidone and ziprasidone at Week 1 (-4.1 vs. -1.6; P=0.020), Week 2, (-6.1 vs. -3.6; P=0.074), and Week 3 (-6.3 vs. -4.5; P=0.229).
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Insufficient treatment of psychosis often manifests as violent and aggressive behaviors that are dangerous to the patient and others, and that warrant treatment strategies which are not considered first-line, evidence-based practices. Such treatment strategies include both antipsychotic polypharmacy (simultaneous use of 2 antipsychotics) and high-dose antipsychotic monotherapy. Here we discuss the hypothesized neurobiological substrates of various types of violence and aggression, as well as providing arguments for the use of antipsychotic polypharmacy and high-dose monotherapy to target dysfunctional neurocircuitry in the subpopulation of patients that is treatment-resistant, violent, and aggressive. In this review, we focus primarily on the data supporting the use of second-generation, atypical antipsychotics both at high doses and in combination with other antipsychotics.