A Review of Meta-analysis Studies with Amisulpride / 대한정신약물학회지

ABSTRACT

Amisulpride, a substituted benzamide derivative, is a newer atypical antipsychotics. It mainly blocks presynaptic dopamine D2/D3 autoreceptors which is preferentially located in prefrontal area and blocks postsynaptic dopamine D2/D3 receptors in the limbic system. By these mechanism, amisulpride can improve both negative and positive symptoms. In addition to these action, its property of fast dissociation (Koff) and selectivity to D2/D3 receptors can explain more favorable side effects profiles. A lot of studies showed that amisulpride has equivalent or better efficacy and safety to other atypical antipsychotics. Meta-analysis studies is very informative because it contains many cases of previous studies. So we reviewed some meta-analysis studies which compared amisulpride with placebo or other antipsychotics. On positive symptoms of acute schizophrenia, the most pooled analyses of amisulpride have shown to be equally effective with conventional antispychotics. One meta-analysis study have shown that amisulpride is more effective than conventional drugs. On primary negative symptoms, amisulpride is only agents which is investigated for the efficacy in patients with predominantly negative symptoms. as a results of meta-analysis, amisulpride was shown to be more effective than placebo in primary negative symptoms and have a trend of superiority to conventional agents. The safety and tolerability of amisulpride was equal to or better than other atypical drugs on pooled analysis. The drop out rate was also more favorable than conventional antipsychotics. In Summary, amisulpride showed efficacy similar to that of other atypical antipsychotics in reducing positive symptoms. Moreover, its better properties for negative and affective symptoms, and favorable side effects profiles provides another alternative for treatment of schizophrenia. These results show that amisulpride is a favorable `atypical' antipsychotics, and that 5-HT2/D2 antagonism is not only mechanism of `atypicality'.