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IntroductionClozapine is the only drug approved for resistant schizophrenia, but remains underused because of its side effects. Sedation is common, but its management is unclear.ObjectivesTo analyze factors associated with clozapine-induced sedation and the efficacy of common treatment strategies.AimsTo determine clozapine-induced sedation factors and possible therapeutic strategies.MethodsUsing two years’ electronic records of a community cohort of resistant schizophrenia spectrum disorder cases on clozapine, we performed three analyses: a cross-sectional analysis of which factors were associated with number of hours slept (objective proxy of sedation), and two prospective analyses: which factors were associated with changes in hours slept, and the efficacy of the main pharmacological strategies for improving sedation.ResultsOne hundred and thirty-three patients were included; 64.7% slept at least 9 hours/daily. Among monotherapy patients (n = 30), only norclozapine levels (r = .367, P = .033) correlated with sleeping hours. Multiple regression analyses confirmed the findings (r = .865, P < .00001). Using the cohort prospectively assessed (n = 107), 42 patients decreased the number of hours slept between two consecutive appointments. Decreasing clozapine (40%) or augmenting with aripiprazole (36%) were the most common factors. In the efficacy analysis, these two strategies were recommended to 22 (20.6%) and 23 (21.5%) subjects, respectively. The majority (81.8% and 73.9%) did not report differences in the hours slept.ConclusionsSedationis common and involves pharmacological and non-pharmacological factors. The only correlation was a weak correlation between norclozapine plasma levels and total sleeping hours. Reducing clozapine and aripiprazole augmentation were the most successful strategies to ameliorate sedation, although both strategies were effective only in a limited numbers of subjects.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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IntroductionFor resistant schizophrenia, the only approved treatment is clozapine. However, clozapine is underused, mainly due to its wide range of side-effects. Secondary effects differ amongst antipsychotics (Leucht et al., 2009). Despite that there is no good evidence that combined antipsychotics offer any advantage over the use of a single antipsychotic, combination increases the frequency of adverse events (Maudsley guidelines).ObjectivesTo compare the side-effect profile between clozapine and non-clozapinepatients.AimsTo provide evidence that clozapine patients do not show a worse side-effects profile.MethodsWe cross-sectionally analysed all patients from a Spanish long-term mental care facility (n = 139). Schizophrenic/schizoaffective patients were selected (n = 118) and their treatment was assessed, 31 patients used clozapine. We paired clozapine and non-clozapine patients by sex and age and assessed antipsychotic side effects and possible confounder variables.ResultsOur sample was 27 clozapine patients and 29 non-clozapine patients. 67,9% were male with a mean age of 51.3 (SD 9.6) years. For continuous variables: age, BMI, waist/hip, cholesterol, TG, glucose, prolactin, heart-rate, blood pressure, sleeping hours, the only statistical differences found were lower heart-rate (P = 0.001) in clozapine group and higher salivation subscale of SAS (P = 0.002) in clozapine group. For discrete variables: monotherapy, obesity, overweight, metabolic syndrome or possible confounders as propranolol, laxative, diet, antiglycemiant or insulin, fibrates or statins, antihypertensive or anticholinergic, no statistical differences were found.ConclusionsWe did not find differences in cardiometabolic parameters, which are the main barrier to prescribing clozapine, probably due to the concomitant use of other drugs in both groups.Disclosure of interestThe authors have not supplied their declaration of competing interest.

IntroductionSchizophrenia is a developmental disorder that includes non-psychiatric abnormalities [2]. Metabolic abnormalities prior to antipsychotic treatment exist. The clozapine metabolic profile causes clozapine underuse in resistant schizophrenia [1].ObjectivesTo correlate metabolic profile with psychiatric severity and compare the correlations between clozapine/non-clozapine patients.AimsTo determine possible contributory factors to metabolic abnormalities in schizophrenia.MethodsWe cross-sectionally analyzed all patients from a Spanish long-term mental care facility (n = 139). Schizophrenic/schizoaffective patients were selected (n = 118). N = 31 used clozapine. We paired clozapine and non-clozapine patients by sex and age and assessed metabolic and psychopathologic variables.We compared psychopathologic variables between patients with/without cardiometabolic treatment and the differences between clozapine/non-clozapine groups.ResultsWe analyzed: 27 clozapine/29 non-clozapine patients. A total of 67,9% males with a mean age of 51.3 (SD 9.6) years. In the whole sample TG negatively correlated with Negative-CGI (r: −0,470, P: 0.049) and HDL-cholesterol correlates with Global-CGI(r: 0,505, P: 0.046). Prolactin correlated with the number of antipsychotics (r: 0.581, P: 0.023) and IMC (r: 0.575, P: 0.025). Clozapine group took less antipsychotics [Fisher (P: 0.045)] and had higher scores in total BRPS scale [t-Student (P: 0.036)]. They did not use more cardiometabolic treatment. There were no psychopathological differences between cardiometabolic treated/non-treated patients. In the non-cardiometabolic treated group (n = 35/62,5%), IMC negatively correlated with positive and total BPRS, positive, cognitive and global-CGI. We found negative correlations between metabolic parameters and psychopathology in clozapine (40%) and non-clozapine subgroups (60%). In the cardiometabolic treated group (n = 21/37,5%), we did not find these correlations in either of clozapine (61.9%) or non-clozapine (38.1%) subgroups.ConclusionsSeverity [2], prolactine [3] and treatment [1] could play a role in metabolic parameters. In our sample we found negative correlations between psychopathological and metabolic parameters.References not available.Disclosure of interestThe authors have not supplied their declaration of competing interest.