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PubMed2005

Haloperidol-associated stealth liposomes: a potent carrier for delivering genes to human breast cancer cells.

Sigma receptors are membrane-bound proteins that are overexpressed in certain human malignancies including breast cancer. These receptors show very high affinity for various sigma ligands including neuroleptics like haloperidol. We hypothesized that in associating haloperidol-linked lipid into the cationic lipid-DNA complex, we can specifically target and deliver genes to breast cancer cells that overexpress sigma receptors. In the present study, haloperidol was chemically modified to conjugate at the distal end of the polyethylene glycollinked phospholipid, which was then incorporated into the cationic liposome known to condense and deliver genes inside cells. The resulting haloperidol-conjugated targeted lipoplex showed at least 10-fold higher (p < 0.001) reporter gene expression in MCF-7 cells than control lipoplex. The reporter gene expression of the targeted lipoplex was significantly blocked by haloperidol (p < 0.001) and by another sigma ligand, 1,3-ditolylguanidine (p < 0.001) in the majority of cationic lipid to DNA charge ratios (+/-). Spironolactone-mediated sigma receptor down-regulation enabled MCF-7 to show 10-fold lower transgene expression with targeted lipoplex compared with that obtained in spironolactone-untreated cells. The targeted lipoplex generated nonspecific gene expression in sigma receptor-nonexpressing human cancer cells such as Hela, KB, HepG2, and Chinese hamster ovary cells. Moreover, the transgene expression remained unabated in physiologically relevant serum concentrations. This is the first study to demonstrate that haloperidol-targeted gene delivery systems can mediate efficient targeting of genes to sigma receptor-overexpressing breast cancer cells, thereby becoming a novel class of therapeutics for the treatment of human cancers.

Antipsychotic Agents↗

PubMed2005

The effects of competitive displacement on haloperidol's plasma distribution in normolipidemic and hyperlipidemic plasma.

PURPOSE: To assess whether dyslipidemia affects haloperidol's overall plasma distribution when it is in the presence of another highly protein bound drug that competes for plasma protein binding sites. METHODS: We performed in vitro studies in which warfarin sodium was pre-incubated in normolipidemic and hyperlipidemic plasma samples in varying concentrations. Following the pre-incubation with warfarin, [3H]-haloperidol mixed with unlabeled haloperidol was added to the plasma samples. The plasma was separated into its lipoprotein and lipoprotein deficient fractions by density gradient ultracentrifugation and haloperidol distribution was determined. RESULTS: Our results indicate that when normolipidemic plasma was pre-incubated with various concentrations of warfarin no significant redistribution of haloperidol was noted among the various plasma lipoprotein fractions. However, in the case of the hyperlipidemic plasma, pre-incubating with warfarin did result in a significant redistribution of haloperidol from the lipoprotein-deficient fraction to the very-low-density and low-density fractions of lipoproteins. CONCLUSION: Understanding how plasma lipoproteins influence competitive displacement interactions would be valuable in helping to explain and perhaps predict pharmacokinetic parameters that may affect clinical outcome. The clinical significance of competitive displacement of drugs in patients with dyslipidemia requires further study.

Anticoagulants↗

PubMed1986

Oral haloperidol lowers human intraocular pressure.

This is a double masked, randomized, crossover design trial of orally administered haloperidol in human volunteers. There was a statistically significant drop of the intraocular pressure in non-glaucomatous volunteers at 3 and 4 hours following haloperidol administration. Glaucomatous patients on topical medications did not show a statistically significant drug effect. Non-glaucomatous volunteers showed a statistically significant decrease in pupillary diameter 3 hours following haloperidol administration while glaucomatous subjects showed no significant change in pupillary diameter. There were no significant changes in the near point of accomodation. Dopamine antagonists like haloperidol may act by blocking post-synaptic dopamine receptors in the ciliary body, resulting in vasoconstriction and subsequently decreased aqueous humor production. Pharmacologic data from human use suggests that ocular side effects of topically administered haloperidol may be less than those of pilocarpine, while systemic side effects may be less than those of timolol. Haloperidol may become a cost-effective, once daily ocular hypotensive agent. Problems with preparation of a viable topical vehicle, as well as potential long-term side effects will require a great deal of further investigation.

Administration, Oral↗

PubMed2004

Is low-dose haloperidol a useful antiemetic?: A meta-analysis of published and unpublished randomized trials.

The antiemetic efficacy of haloperidol was studied using data from 15 published (1962-1988) and 8 unpublished randomized trials; 1,397 adults received haloperidol, and 1,071 were controls. Settings were postoperative nausea or vomiting (1,994 patients), gastroenterology (261), chemotherapy (189), and radiation therapy (24). The relative benefit to prevent postoperative nausea or vomiting during 24 h with 0.5-4 mg haloperidol compared with placebo was 1.26-1.51 (number needed to treat, 3.2-5.1), without evidence of dose responsiveness; 0.25 mg was not antiemetic. With 1 mg haloperidol, the relative benefit to stop postoperative nausea or vomiting during 2-4 h compared with placebo was 1.53 (95% confidence interval, 1.17-2.00; number needed to treat, 6); with 2 mg, the relative benefit was 1.73 (1.11-2.68; number needed to treat, 4). In gastroenterology, 2 mg haloperidol was more effective than 1 mg. For chemotherapy and radiation therapy, no conclusions could be drawn. With 4 mg, one patient had extrapyramidal symptoms. With 5 mg, sedation was increased, with a relative risk of 2.09 (95% confidence interval, 1.73-2.52; number needed to treat, 4.4). There were no reports on cardiac toxicity. Postoperatively and in gastroenterology, haloperidol is antiemetic, with minimal toxicity. For other clinical settings and for children, valid data are unavailable.

Antiemetics↗

PubMed1986

Differential alterations in striatal acetylcholine function in rats during 12 months' continuous administration of haloperidol, sulpiride, or clozapine.

Rats were treated continuously for 12 months with therapeutically equivalent doses of either haloperidol (1.4-1.6 mg/kg/day), sulpiride (102-109 mg/kg/day), or clozapine (24-27 mg/kg/day). After treatment for 3 and 12 months with haloperidol or clozapine but not sulpiride, striatal acetylcholine levels were increased. Striatal choline acetyltransferase activity was not altered by any drug treatment. Vmax for striatal acetylcholinesterase activity during the course of 12 months' treatment with haloperidol or clozapine, but not with sulpiride, tended to increase; Km was not altered by any drug treatment. Bmax for specific striatal [3H]quinuclidinyl benzilate binding was not altered by haloperidol or sulpiride treatment but was transiently elevated after 6 months of clozapine treatment, thereafter returning to control levels. Kd was not altered by any drug treatment. These findings indicate that alterations in striatal acetylcholine content caused by chronic treatment with some but not all neuroleptics are due to changes in cholinergic neuronal activity rather than neurotransmitter synthesis or destruction. The effects of haloperidol but not those of clozapine may be related to the emergence of functional striatal dopamine receptor supersensitivity. Since haloperidol (which is associated with a high prevalence of tardive dyskinesias) but not clozapine (which is not) had similar effects on striatal cholinergic function, the latter may not be related to the emergence of tardive dyskinesias during chronic therapy.

Acetylcholine↗

PubMed2001

In vivo measurement of haloperidol affinity to dopamine D2/D3 receptors by [123I]IBZM and single photon emission computed tomography.

This study examines the feasibility of a steady-state bolus-integration method with the dopamine D2/D3 receptor single photon emission computer tomography (SPECT) tracer, [123I]IBZM, for determination of in vivo affinity of haloperidol. The nonspecific binding of [123I]IBZM was examined in the rat brain by infusion of haloperidol to plasma levels approximately 100 times the Kd level in man. In humans, Kd for haloperidol binding was measured in four healthy volunteers that were examined twice: once with partial dopamine D2/D3 receptor blockade obtained by a scheduled infusion of unlabeled haloperidol (0.7 mg total dosage), and once in an unblocked state. Blood sampling and SPECT were performed intermittently during 6 hours after intravenous [123I]IBZM bolus injection. Plasma [123I]IBZM was determined by octane extraction. Plasma haloperidol was determined by a radioimmunoassay, and plasma protein binding was determined by equilibrium dialysis. In humans, the striatal D2/D3 receptor occupancy was 0.27+/-0.085 and the in vivo Kd for haloperidol was 0.25+/-0.1 nmol/L, which is comparable to Kd values as obtained from in vitro studies. The authors conclude that steady-state [123I]IBZM SPECT studies allow for determination of dopamine D2/D3 receptor occupancy in striatum and in vivo measurement of drug affinity to striatal dopamine D2 and D3 receptors.

Adult↗

PubMed2001

Risperidone versus haloperidol in the treatment of acute exacerbations of chronic inpatients with schizophrenia: a randomized double-blind study.

The purpose of this study was to compare the efficacy and safety of risperidone and haloperidol in treatment-resistant chronic schizophrenic patients. Subjects (n = 78) who met DSM-III criteria for schizophrenia were randomly assigned to receive 6 mg/day of risperidone or 20 mg/day of haloperidol for 12 weeks. Clinical efficacy was determined using the Positive and Negative Syndrome Scale (PANSS), and side-effects with the Treatment Emergent Symptom Scale (TESS). Risperidone produced a mean 39.8 +/- 24.1% reduction in total PANSS score compared to a mean 28.3 + 19.4% reduction in the haloperidol group (P < 0.05). Analysis of changes for the three subscores of the PANSS revealed that the general psychopathology and negative subscores were significantly improved in the risperidone group compared to the haloperidol group. As for the side-effects, the risperidone group showed a significantly lower TESS total score, as well as nervous system symptoms subscore and cardiovascular symptoms subscore, compared to the haloperidol group. Risperidone appears to be a more effective and better tolerated antipsychotic drug in treatment-refractory Chinese schizophrenia than haloperidol.

Adult↗

PubMed2002

Olanzapine versus haloperidol in the treatment of acute mania: clinical outcomes, health-related quality of life and work status.

We aimed to compare clinical outcomes, health-related quality of life (HRQOL) and work status associated with olanzapine and haloperidol treatment in patients with bipolar disorder. This double-blind, randomized controlled trial, comparing flexible dosing of olanzapine (5-20 mg/day, n = 234) to haloperidol (3-15 mg/day, n = 219), consisted of a 6-week acute phase, followed by a 6-week continuation phase. Symptomatic remission rates were similar for olanzapine- and haloperidol-treated patients at weeks 6 and 12. At week 6, significant changes in five dimensions of the Medical Outcomes Study 36-Item Short Form Health Survey (SF-36) [general health (P = 0.010), physical functioning (P < 0.001), role limitations due to physical problems (P < 0.001), social functioning (P < 0.05) and vitality (P < 0.01)] and the SF-36 physical components summary score were found in favour of olanzapine compared to haloperidol. At week 12, olanzapine treatment maintained the significantly favourable HRQOL changes. At the end of week 12, patients on olanzapine showed significantly greater improvement than haloperidol in work activities impairment and household activities impairment scores on the Streamlined Longitudinal Interview Clinical Evaluation from the Longitudinal Interval Follow-up Evaluation (SLICE/LIFE) activities impairment scores. Subgroup analyses revealed that olanzapine treatment significantly increased a proportion of employed patients and their weekly paid working hours. In conclusion, compared to haloperidol, olanzapine treatment was comparably effective in the remission of bipolar mania and significantly improved HRQOL and work status in patients with bipolar I disorder.

Acute Disease↗

PubMed1989

Human scalp hair as evidence of individual dosage history of haloperidol: prospective study.

The concentration of haloperidol in hair was measured by radioimmunoassay after hairs were dissolved in 2.5 N NaOH solution and the drug was extracted. In patients to whom haloperidol had been administered at fixed daily doses for more than 1 month, and in whom therapy had been just discontinued (group A, n = 5) or the doses cut to half (group B, n = 3), hairs were collected when the dose was changed and at 1 and 2 or 3 months thereafter. A few strands of hair collected on each occasion were cut into 1-cm-long portions from the roots, and the haloperidol concentration was measured in each portion. When hairs were assumed to grow at a rate of 1-1.5 cm/month, the portion of hair that reflected the change of dose was observed to move upward along the hair length in all patients of group A. However, these phenomena were less obvious in group B. These results indicate that at the least, hair could serve as an indicator of individual exposure or nonexposure to haloperidol and could yield retrospective information. In rats whose hairs had been removed by plucking from an area on the back, either saline or 1 mg/kg of haloperidol (i.p., b.i.d.) was administered for 2 weeks (first period), followed by 0, 0.5, 1, or 2 mg/kg b.i.d. for the subsequent 2 weeks (second period). At the end of each period, hairs that had grown in the plucked area were collected. Within-groups, haloperidol levels in hairs collected at the end of each period corresponded to the doses given.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1998

Effects of single oral administrations of haloperidol and d-amphetamine on prepulse inhibition of the acoustic startle reflex in healthy male volunteers.

The effects of acute administration of an indirect dopamine-agonist, d-amphetamine, and a non-selective dopamine receptor antagonist, haloperidol, were investigated in normal male volunteers on habituation and prepulse inhibition (PPI) of the acoustic startle reflex in two experiments. In Experiment 1, 40 male non-smoker volunteers were tested for habituation and PPI (defined as percentage reduction of the pulse-alone amplitude; prepulses 9 dB above background) before and after double-blind administration of either 2 mg haloperidol or placebo. No influence of haloperidol was observed on either habituation or PPI of the startle reflex in this experiment. In Experiment 2, 60 male volunteers underwent startle testing before and after double-blind administration of a single oral dose of 5 mg haloperidol, 5 mg d-amphetamine or placebo. Habituation and PPI (prepulses 15 dB above background) for the placebo group did not differ significantly from that observed for the d-amphetamine or for the haloperidol group. However, in a subgroup of smoking subjects, both d-amphetamine and haloperidol reduced PPI as compared to that observed prior to drug administration. The implications of these findings in relation to animal pharmacological studies and observed sensorimotor gating deficits in schizophrenia are discussed.

Acoustic Stimulation↗

PubMedDate not supplied

The use of haloperidol and associated complications in the agitated, acutely ill pediatric burn patient.

The use of haloperidol to induce sedation and control agitation in the acutely ill adult patient has been well documented. There are few reports, however, of the use of this neuroleptic agent to control the severe delirium and agitation that may occur in critically ill pediatric patients or acute pediatric patients suffering from burn wounds. We assessed the effectiveness and safety of the use of haloperidol by completing a retrospective chart review of 855 acutely ill children treated consecutively during the period from April 1999 to May 2002, during which time 26 children received haloperidol. The safe use of haloperidol was assessed by documenting any adverse effects or reactions observed after the administration of the drug. Of patients given haloperidol, 23% had adverse effects. This result suggests that the use of haloperidol to treat the acutely agitated and delirious pediatric burn patients is fraught with a number of difficulties and is not completely safe and effective.

Adolescent↗

PubMedDate not supplied

A novel brain-targeted antioxidant (AD4) attenuates haloperidol-induced abnormal movement in rats: implications for tardive dyskinesia.

BACKGROUND: Tardive dyskinesia (TD), characterized by abnormal movements, is the major late-onset chronic side effect of antipsychotic treatment found in about 30% of those patients. The association of oxidative stress and the release of free radicals is one of the hallmarks of dopaminergic malfunctions and is one of the leading theories suggested for the pathophysiology of TD. To this day, no brain-targeted antioxidant has been tested as a potential treatment of TD. In light of this assumption, the authors chose a novel, low-molecular weight thiol antioxidant, N-acetyl cysteine amide (AD4), that crosses the blood-brain barrier as a possible treatment of TD. OBJECTIVE: To examine the protective effects of the novel brain-penetrating antioxidant AD4 on TD experimental models. METHODS: The typical vacuous chewing movement occurs in rats following chronic haloperidol injections (1.5 mg/kg/day intraperitoneally for 21 days). This purposeless mouth opening in the vertical plane is similar to TD symptoms in humans. The authors tested rats treated with haloperidol without or with AD4 in the drinking water (1 g/kg orally). Thiobarbituric acid reactive substances and anticarbonyl antibodies were used to measure oxidation of membranes and proteins. RESULTS: Haloperidol increased the vacuous chewing movements to 66.5 +/- 7.6 movements/5 minutes compared with 16.4 +/- 2.4 movements/5 minutes in untreated rats (P < 0.01). Coadministration of haloperidol and AD4 decreased the vacuous chewing movements level to 42.1 +/- 6.7 movements/5 minutes (P < 0.05). Haloperidol also increased the level of lipid peroxidation and protein oxidation in the rat brain, whereas coadministration with AD4 preserved their normal levels. CONCLUSION: Haloperidol causes behavioral abnormalities associated with oxidative stress in rats, similar to TD. AD4, the brain-targeted potent antioxidant, reduces the cellular oxidation markers and improves the typical clinical behavior. Hence, AD4 is a potential new treatment of antipsychotic-induced TD.

Acetylcysteine↗

PubMed1988

Investigations of some physiochemical properties of haloperidol which may affect its activity.

Since the clinical response to haloperidol varies from individual to individual, an investigation was carried out to investigate some of the physiochemical properties of haloperidol which may affect its pharmacological activity. The stability of haloperidol in aqueous solutions containing 1% lactic acid, with or without 0.1% methyl paraben, was investigated. A colorimetric method based on a reaction between methyl orange and haloperidol was used. The samples (0.5 mg/ml) were stored in glass and plastic containers at 25, 37, 50, 80 and 110 degrees C for 9 months. The resulting data were analysed using principles of chemical kinetics. The shelf-life of haloperidol solutions was estimated to be at least 4 years. Other physiochemical factors which can affect the pharmacological activity of haloperidol were investigated, namely its solubility and complex-forming properties.

Beverages↗

PubMed1996

Risperidone versus haloperidol in the treatment of schizophrenia: a meta-analysis comparing their efficacy and safety.

The aim of this study was to compare the short-term clinical efficacy and safety of risperidone with haloperidol and placebo. A meta-analysis of seven published randomized double-blind controlled trials was carried out. Study quality was assessed. The proportion of patients failing to reach at least 20% improvement on the positive and negative syndrome scale (PANSS) or brief psychiatric rating scale (BPRS), the proportion of patients discontinuing treatment because of adverse effects and the number of patients who needed antiparkinsonian medication were abstracted for use as outcome measures. Treatment failure was present in 50% of risperidone-treated patients compared to 66% in those treated with haloperidol and 83% in those treated with placebo. It would be necessary to treat 11 patients with risperidone to prevent one treatment failure in those patients treated with haloperidol (Odds ratio (OR) = 0.74, 95% CI of 0.58-0.94, P = 0.02). Pooling of the three multicentre trials which included placebo as a treatment arm, showed that one in three patients treated with risperidone 4-16 mg/day (OR = 0.22, 95% CI of 0.13-0.39, P < 0.00001) and one in six treated with haloperidol 10-20 mg/day. (OR = 0.44, 95% CI of 0.22-0.84, P = 0.02) would derive significant benefit. Moreover, there was a highly significant greater need for anticholinergic medication due to extrapyramidal symptoms (EPS) in the haloperidol-treated patients compared to risperidone (OR = 0.54, 95% CI of 0.42-0.70, P < 0.00001). In conclusion, risperidone seems to be more effective and causes less EPS than haloperidol, as suggested by the significantly lower requirement for antiparkinsonian medication.

Antiparkinson Agents↗

PubMed1996

7-OH-DPAT differentially reverses clozapine- and haloperidol-induced increases in Fos-like immunoreactivity in the rodent forebrain.

The pattern of neurons which display haloperidol-induced Fos-like immunoreactivity closely matches the distribution of striatal D2 dopamine receptors, whereas clozapine-induced Fos-like immunoreactivity occurs primarily in regions that contain high levels of the D3 dopamine receptor. These neuroanatomical correlations suggest that haloperidol and clozapine may elevate Fos-like immunoreactivity by blocking D2 and D3 receptors respectively. In order to test this hypothesis, the abilities of prior administration of the D3 receptor-preferring agonist 7-hydroxy-N,N'-di-n-propyl-2-aminotetraline (7-OH-DPAT) to competitively reverse haloperidol- and clozapine-induced increases in Fos-like immunoreactivity were compared. Administration of 7-OH-DPAT (0.05 mg/kg, s.c.) 30 min before clozapine (20 mg/kg, s.c.) produced a 60% reduction in the number of neurons that displayed clozapine-induced Fos-like immunoreactivity in the major island of Calleja, nucleus accumbens and medial aspect of the striatum, while prior administration of 0.5 mg/kg (s.c.) of 7-OH-DPAT completely reversed these increases in Fos-like immunoreactivity. In contrast, the increases in Fos-like immunoreactivity in the major island of Calleja, nucleus accumbens and striatum (medial and dorsal aspects) induced by haloperidol (0.1 mg/kg, s.c.) were only reduced by the high dose of 7-OH-DPAT (0.5 mg/kg, s.c.). Hence, clozapine-induced increases in Fos-like immunoreactivity were more readily reversed by 7-OH-DPAT than elevations in Fos-like immunoreactivity produced by haloperidol. These results suggest that D3 receptor blockade plays a larger role in mediating clozapine- than haloperidol-induced increases in Fos-like immunoreactivity.

Animals↗

PubMed2004

Regulation of striatal tyrosine hydroxylase phosphorylation by acute and chronic haloperidol.

The typical neuroleptic haloperidol increases the state of phosphorylation and activity of tyrosine hydroxylase (TH), the rate-limiting enzyme in the synthesis of catecholamines. Here we show that the increases in TH phosphorylation produced by haloperidol at Ser31 and Ser40, two sites critically involved in the regulation of enzymatic activity, are abolished in dopamine D2 receptor-null mice and mimicked by the selective dopamine D2 receptor antagonist, eticlopride. Moreover, the ability of haloperidol and eticlopride to stimulate phosphorylation at both seryl residues is prevented by treatment with SL327, a compound that blocks activation of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2). We also show that chronic administration of haloperidol reduces the basal levels of phosphoSer31-TH and decreases the ability of the drug to stimulate Ser40 phosphorylation. These results provide a model accounting for the stimulation exerted by haloperidol on dopamine synthesis. According to this model, haloperidol increases TH activity via blockade of dopamine D2 receptors, disinhibition of dopaminergic projection neurons and ERK1/2-dependent phosphorylation of TH at Ser31 and Ser40. These studies also show that lower levels of phosphorylated TH are associated with chronic neuroleptic treatment and may be related to depressed dopaminergic transmission in nigrostriatal neurons.

Animals↗

PubMed1990

Development of haloperidol-induced dopamine release in the rat striatum using intracerebral dialysis.

Haloperidol-induced dopamine (DA) release and metabolism were studied in the rat striatum at 10-11, 21-22, and 35-36 days of age using intracerebral dialysis and HPLC with electrochemical detection. There was an age-related increase in basal DA release and extracellular levels of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), with the greatest increases occurring between 10-11 and 21-22 days of age. Haloperidol (0.1 mg/kg, i.p.) significantly increased DA release at each age compared to control. Also, haloperidol produced a significantly greater increase in DA release at 10-11 days than at 21-22 or 35-36 days of age when expressed as percentage of predrug release. Haloperidol increased DA release over 60 min to 235%, 138%, and 158% above baseline at 10-11, 21-22, and 35-36 days of age, respectively, after which time the levels remained relatively constant. Haloperidol significantly increased extracellular DOPAC and HVA levels at each age compared to controls, but there were no significant differences in DOPAC or HVA levels between ages in response to haloperidol. The results indicate that, at 10 days of age, DA release in the striatum is physiologically functional and that the regulatory feedback control of DA release and metabolism in the striatum develops prior to 10 days of age.

3,4-Dihydroxyphenylacetic Acid↗

PubMedDate not supplied

The impact of olanzapine, risperidone, or haloperidol on the cost of schizophrenia care in a medicaid population.

OBJECTIVE: The objective of this study was to assess the impact of medication treatment on Medicaid costs for persons with schizophrenia. METHODS: Michigan Medicaid claims from January 1995 through September 1998 were analyzed for persons with schizophrenia diagnoses who initiated olanzapine (n = 458), risperidone (n = 481), or haloperidol (n = 252) treatment between January 1996 and September 1997. Total and component Medicaid payments were compared for the year after treatment initiation, with simultaneous adjustment for patient demographics, comorbid conditions, prior medication use, prior service use, and prior year costs. RESULTS: Significant baseline differences existed between the groups in prior medication and service use. Adherence to index medication varied between the groups (O = 60%; R = 54%; H = 37%; P < =.01 for each pairwise comparison). Average postperiod costs were US dollars 14512 per subject. After baseline adjustment, there were no significant differences in mean total cost. Excluding index medication costs, the olanzapine group's average cost was significantly lower than risperidone (-US dollars 1791, P =.002) and haloperidol (-US dollars 2080, P =.003), whereas the risperidone and haloperidol groups were not significantly different. The differences were driven by significantly lower cost for inpatient services for other medications among the olanzapine group. CONCLUSION: Total costs of schizophrenia care associated with olanzapine, risperidone, or haloperidol were similar, but component costs differed. Relative to risperidone or haloperidol, olanzapine may have a higher acquisition cost, but may decrease inpatient costs and be associated with more optimal medication use patterns. Use of risperidone may also increase pharmacy costs and be associated with greater persistence, relative to haloperidol.

Adult↗