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Two published case reports showed that addition of risperidone (1 and 2 mg/d) to a clozapine treatment resulted in a strong increase of clozapine plasma levels. As clozapine is metabolized by cytochrome P450 isozymes, a study was initiated to assess the in vivo interaction potential of risperidone on various cytochrome P450 isozymes. Eight patients were phenotyped with dextromethorphan (CYP2D6), mephenytoin (CYP2C19), and caffeine (CYP1A2) before and after the introduction of risperidone. Before risperidone, all eight patients were phenotyped as being extensive metabolizers of CYP2D6 and CYP2C19. Risperidone at dosages between 2 and 6 mg/d does not appear to significantly inhibit CYP1A2 and CYP2C19 in vivo (median plasma paraxanthine/caffeine ratios before and after risperidone: 0.65, 0.69; p = 0.89; median urinary (S)/(R) mephenytoin ratios before and after risperidone:0.11, 0.12; p = 0.75). Although dextromethorphan metabolic ratio is significantly increased by risperidone (median urinary dextromethorphan/dextrorphan ratios before and after risperidone: 0.010, 0.018; p = 0.042), risperidone can be considered a weak in vivo CYP2D6 inhibitor, as this increase is modest and none of the eight patients was changed from an extensive to a poor metabolizer. The reported increase of clozapine concentrations by risperidone can therefore not be explained by an inhibition of CYP1A2, CYP2D6, CYP2C19 or by any combination of the three.

In spite of the efficacy of the psychodynamic psychotherapies, the number of young psychiatric residents interested in psychodynamic therapies is decreasing. Our psychoanalytical group, Genden (Genève-Denver), explored the possible reasons for psychiatric residents' hesitation to get psychoanalytic training. Five psychoanalytical psychotherapists met weekly for a year in order to debate that question, focusing on personal feedbacks from all of our 100 residents in psychiatry working with us for at least 4 years. Following the residents' responses, our focus group proposed ten commonsense feedbacks for psychoanalysts regarding stimulating young psychiatric residents' interest in psychoanalytic approaches.

In this pilot study, the pharmacokinetics of citalopram (CIT) were examined in five hospitalized depressed patients after an abrupt discontinuation of a treatment with 40 mg/d of this selective serotonin reuptake inhibitor (SSRI). During the 8-day study period, clinical ratings were regularly carried out. Between days 5 and 8, the patients were treated with clomipramine (75 mg/d). The enantiomers of CIT and its metabolites, demethyl-CIT (DCIT) and CIT-propionic acid derivative (CIT-PROP), were measured repeatedly from day 0 to day 8 by a stereoselective high-performance liquid chromatography (HPLC) procedure. The following drug plasma half-lives were measured (means +/- SD): R-CIT: 66+/-11 h; S-CIT: 42+/-13 h; R-DCIT: 228+/-148 h; S-DCIT: 93+/-35 h; R-CIT-PROP: 82+/-31 h; S-CIT-PROP: 186+/-93 h.