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Guía de Actuación Farmacéutica en pacientes con esquizofrenia.

DOI: 10.13140/2.1.5062.1445 Edition: 1, Publisher: Grupo de Investigación en Atención Farmacéutica, Universidad de Granada. Promoción y Prevención Farmacéutica Universidad de Antioquia. Medellín-Colombia, ISBN: 978-858-99075-0-4
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    ABSTRACT: The study concerned 7 patients suffering from schizophrenic disorder according to the DSM III R criteria, treated with a stable dose of haloperidol decanoate (Haldol décanoas) added with fluoxetine (Prozac) from 20 mg to 40 mg/day because of major depression. Patients were assessed at baseline and weekly during the first cycle, and then once a month before each haloperidol decanoate injection, using the brief psychiatric rating scale (BPRS), the general clinical impression scale (CGI) and the Montgomery and Asberg depression rating scale (MADRS). Extrapyramidal and anticholinergic side-effects, blood pressure and pulse were noted. Determinations of plasma and red blood cells concentrations of haloperidol and reduced haloperidol, and of fluoxetine and norfluoxetine, were conducted at the same time than clinical evaluations. For all patients, we observed an improvement by the end of the first week, which became significant at the end of the second week, and continued in subsequent weeks (more than 30 per cent). Two weeks after the addition of fluoxetine, a very significant increase in haloperidol concentrations (more than 100 per cent) was noted; fluoxetine seems to have pharmacokinetic interactions with haloperidol, either by inhibiting its hepatic metabolism (inhibition of cytochrome P450 isoenzyme) or/and by displacing it from protein binding sites.
    Thérapie 01/1996; 51(1):19-25. · 0.37 Impact Factor
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    ABSTRACT: A reduction in haloperidol concentration induced by carbamazepine coadministration has been consistently reported. However, the degree of this reduction is very different among individuals treated with various doses of carbamazepine. Thus, we investigated dose effect of carbamazepine on the steady-state plasma concentration of haloperidol. Eleven excited schizophrenic inpatients, despite receiving haloperidol 12 mg/d, were treated with incremental doses of carbamazepine for 6 weeks (100, 300, 600 mg/d for 2 weeks each). Plasma drug concentrations were monitored together with clinical assessments before and after each phase of the 3 carbamazepine doses. Mean haloperidol concentrations during coadministration of carbamazepine 100, 300, and 600 mg/d were 75%, 39%, and 15%, respectively, of corresponding variables before carbamazepine coadministration. Negative linear correlations were observed between dose or plasma concentration of carbamazepine and the degree of reduction in haloperidol concentration. Mean carbamazepine dose and plasma carbamazepine concentrations at 50% reduction of haloperidol concentration were 240 mg/d and 3.5 microg/mL, respectively. Scores in total and excitement symptoms were significantly reduced after carbamazepine coadministration, whereas no changes were observed in other clinical symptoms or any of the subgroup side effects. Therefore, this study indicates that carbamazepine decreases plasma haloperidol concentration in a dose-dependent or concentration-dependent manner, and that reduction in haloperidol concentration is apparent even at subtherapeutic dose of carbamazepine.
    Journal of Clinical Psychopharmacology 11/2003; 23(5):435-40. · 3.51 Impact Factor
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    ABSTRACT: This paper emphasises that besides the direct action of psychotropic drugs on cytochrome P450 (CYP) (i.e., the binding of the parent drug to the enzyme) indirect mechanisms of CYP-psychotropic interactions, namely the formation of CYP-reactive metabolite complexes and their influence on enzyme regulation, are also very important. The described interactions that are time-, drug- and CYP isoform-dependent may overlap during long-term treatment. The final result of the overlapping depends on the dosage and time interval after the last administration of a drug, which determines the concentration of the parent drug and its metabolites in the environment of the enzyme. These interactions may occur not only in the liver, but also in the brain, and may change the activity of CYP towards the metabolism of drugs, sex steroids, neurosteroids and amine neurotransmitters. The role of the CNS in the regulation of CYP by psychotropics and the significance of CYP-psychotropic interactions for pharmacological and clinical profiling of these drugs is discussed. In addition, different experimental approaches for studying CNS-acting drugs are compared.
    Expert Opinion on Drug Metabolism &amp Toxicology 09/2005; 1(2):203-17. · 2.94 Impact Factor

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