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Amisulpride

A Review of its Use in the Management of Schizophrenia

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Summary

Abstract

Amisulpride (Solian®), a substituted benzamide derivative, is a second-generation antipsychotic that preferentially binds to dopamine D2/D3 receptors in limbic rather than striatal structures. High dosages preferentially antagonise postsynaptic D2/D3 receptors, resulting in reduced dopamine transmission, and low dosages preferentially block presynaptic D2/D3 receptors, resulting in enhanced dopamine transmission.

Amisulpride (200–1200 mg/day) was at least as effective as haloperidol and as effective as risperidone or olanzapine, in studies of up to 1 year in patients with schizophrenia manifesting predominantly positive symptoms. Amisulpride (50–300 mg/day) was significantly more effective than placebo in studies of up to 6 months in patients manifesting predominantly negative symptoms. Quality of life was also improved significantly more in patients receiving amisulpride than in those receiving haloperidol in 4- and 12-month studies in patients with predominantly mixed symptoms.

Amisulpride was generally well tolerated in clinical trials. In patients with predominantly positive symptoms, amisulpride appeared to be better tolerated than haloperidol and was tolerated as well as risperidone and olanzapine. The incidence of extrapyramidal adverse effects with amisulpride was lower than with haloperidol but was generally similar to risperidone or olanzapine. Weight gain with amisulpride was less than that with risperidone or olanzapine and, unlike these agents, amisulpride does not seem to be associated with diabetogenic effects. Plasma prolactin levels are increased during amisulpride therapy and amenorrhoea occurs in about 4% of women. The incidence of adverse events with low dosages of amisulpride (≤300 mg/day) in patients with predominantly negative symptoms was similar to that observed with placebo.

In conclusion, oral amisulpride (200–1200 mg/day) is at least as effective as haloperidol, and as effective as risperidone or olanzapine, in the treatment of patients with schizophrenia manifesting predominantly positive symptoms. In the treatment of patients manifesting predominantly negative symptoms, low dosages of amisulpride (50–300 mg/day) are significantly more effective than placebo. Amisulpride appears to be better tolerated than haloperidol, causing a lower incidence of extrapyramidal adverse effects and an improved quality of life. Compared with risperidone or olanzapine, amisulpride is more likely to cause hyperprolactinaemia, but has a lower propensity to cause weight gain and does not seem to be associated with diabetogenic effects. Thus, amisulpride is an effective and well tolerated option for the first-line treatment of patients with acute schizophrenia as well as for those requiring long-term maintenance therapy.

Pharmacoloaical Properties

Amisulpride has selective affinity for human D2 and D3 receptor subtypes, no affinity for D1, D4 and D5 receptor subtypes and little affinity for the adrenergic, histaminergic, serotonergic or cholinergic receptors. Amisulpride preferentially binds to D2/D3 receptors in limbic rather than striatal structures. Low dosages (<10 mg/kg) preferentially block presynaptic D2/D3 receptors, resulting in enhanced dopamine transmission; higher dosages preferentially antagonise post-synaptic D2/D3 receptors, resulting in reduced dopamine transmission.

Unlike haloperidol, amisulpride does not appear to be associated with impaired cognitive function. Plasma prolactin concentrations are increased, particularly in the early weeks of amisulpride therapy.

Two absorption peaks are demonstrated after a single oral dose of amisulpride 50mg in healthy volunteers; peak plasma concentrations of 42 and 56 µg/L were recorded at hours 1 and 4. The absolute bioavailability is approximately 50% and the volume of distribution is 5.8 L/kg. Only minimal amounts of amisulpride are bound to plasma proteins (17%). The potential for drug interactions is low and amisulpride does not appear to affect the activity of the cytochrome P450 system.

Amisulpride undergoes minimal metabolism and is primarily excreted in the urine. The pharmacokinetics of amisulpride were unchanged after repeated administration of 200 mg/day for 7 days. Elimination is biphasic after oral administration with a plasma elimination half-life of approximately 12 hours. Renal clearance is about 20 L/h in healthy volunteers.

Clinical Efficacy

In well designed trials of 6–52 weeks’ duration in patients with schizophrenia manifesting predominantly positive symptoms, amisulpride (200–1200 mg/day) was at least as effective in the control of positive symptoms as haloperidol (5–30 mg/day), but appeared more effective than haloperidol in the control of negativesymptoms. In this patient population, amisulpride was as effective as the atypical agents risperidone (4–10 mg/day) and olanzapine (5–20 mg/day). For some parameters (e.g. percentage of patients with ≥50% improvement in Positive and Negative Syndrome Scale and Brief Psychiatric Rating Scale at 6 months), results were more favourable with amisulpride than with risperidone in a double-blind, randomised trial.

In patients manifesting predominantly negative symptoms of schizophrenia, low dosages of amisulpride (50–300 mg/day) were significantly more effective than placebo in improving symptoms, as assessed by the Scale for the Assessment of Negative Symptoms in three double-blind studies of up to 24 weeks’ duration.

Quality-of-life measures were improved more with amisulpride than with haloperidol in patients with predominantly mixed symptoms.

Tolerability

Amisulpride is generally well tolerated at high and low dosages. In clinical trials in patients with acute exacerbations of schizophrenia manifesting predominantly positive symptoms, the incidence of adverse events was similar with amisulpride (200–1200 mg/day), haloperidol (5–30 mg/day), risperidone (4–10 mg/day) and olanzapine (5–20 mg/day), but the tolerability profiles differed. The most common adverse events associated with amisulpride therapy in a pooled analysis of 11 comparative trials were extrapyramidal disorders (15%), insomnia (11%), hyperkinesia (9%), anxiety (9%), bodyweight increase (7%) and agitation (6%). In patients with predominantly negative symptoms, the incidence of adverse events was similar with amisulpride (50–300 mg/day) or placebo.

The incidence of extrapyramidal adverse events associated with amisulpride 200–1200 mg/day was markedly lower than that with haloperidol, but was generally similar to that of atypical agents (risperidone and olanzapine). Bodyweight gain was less with amisulpride than with risperidone or olanzapine and, unlike these agents, amisulpride does not seem to be associated with diabetogenic effects.

Elevated plasma prolactin levels can occur with antipsychotic agents as a result of their D2 receptor antagonism, and hyperprolactinaemia may result in both acute (e.g. amenorrhoea, galactorrhoea, reduced libido) and chronic (predisposition to osteoporosis and cardiovascular disease) effects. Plasma prolactin levels are increased during amisulpride therapy, but the incidence of endocrine disorders is low. In a pooled analysis, amisulpride caused a higher incidence of amenorrhoea (4% of female patients) than haloperidol (0%) or risperidone (0%), although the difference was not statistically significant. Similarly, amenorrhoea was reported in 6% and 0% of women treated with amisulpride and olanzapine, respectively, in a 6-month randomised trial.

Consistent with the lack of effect on the α-adrenergic and cholinergic receptors, amisulpride does not appear to cause clinically relevant changes to the QT interval, heart rate or blood pressure.

Dosage and Administration

The recommended dosage of amisulpride for acute psychotic episodes in patients with schizophrenia is 400–800 mg/day orally. The dosage may be increased up to 1200 mg/day if necessary. Maintenance therapy should be individualised with the minimally effective dosage. For patients with predominantly negative symptoms of schizophrenia, dosages of 50–300 mg/day are recommended.

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Notes

  1. The use of trade names is for product identification purposes only and does not imply endorsement.

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    Kate McKeage & Greg L. Plosker

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Additional information

Various sections of the manuscript reviewed by: C. Feetam, Department of Psychiatric Pharmacy, Aston University, Birmingham, England; S.W. Lewis, Neuroscience and Psychiatry Unit, University of Manchester, Manchester, England; H.-J. Möller, Psychiatric Department, University of Munich, Munich, Germany; J. Peuskens, Psychiatrisch Instituut, Universitair Centrum St Jozef, Kortenberg, Belgium; S.P. Singh, Department of Mental Health, St George’s Hospital Medical School, London, England.

Data Selection

Sources: Medical literature published in any language since 1980 on amisulpride, identified using Medline and EMBASE, supplemented by AdisBase (a proprietary database of Adis International). Additional references were identified from the reference lists of published articles. Bibliographical information, including contributory unpublished data, was also requested from the company developing the drug.

Search strategy: Medline search terms were ‘amisulpride ’ and ‘schizophrenia ’ and ‘amisulpride ’ and ( ‘pharmacodynamics ’ or ‘pharmacokinetics ’). EMBASE search terms were ‘amisulpride ’ and ‘schizophrenia ’. AdisBase search terms were ‘amisulpride ’ and ‘schizophrenia ’ and ‘amisulpride ’ and ( ‘PD ’ or ‘PK ’). Searches were last updated 20 September 2004.

Selection: Studies in patients with schizophrenia who received amisulpride. Inclusion of studies was based mainly on the methods section of the trials. When available, large, well controlled trials with appropriate statistical methodology were preferred. Relevant pharmacodynamic and pharmacokinetic data are also included.

Index terms: Amisulpride, antipsychotics, schizophrenia, pharmacodynamics, pharmacokinetics, therapeutic use.

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McKeage, K., Plosker, G.L. Amisulpride. CNS Drugs 18, 933–956 (2004). https://doi.org/10.2165/00023210-200418130-00007

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