J A Arnaiz1,2, C Rodrigues-Silva3, G Mezquida2,4,5,6, S Amoretti4,5,6, M J Cuesta7, D Fraguas8, A Lobo5,9, A González-Pinto5,10, M C Díaz-Caneja11, I Corripio5,12, E Vieta13, I Baeza14, A Mané5,15,16, C García-Rizo5,6,17,18, M Bioque5,6,17,18, J Saiz5,19, M Bernardo5,6,17,18, S Mas20,21,22. 1. Phase I Unit, Clinical Pharmacology Department, Hospital Clinic de Barcelona (HCB), Barcelona, Spain. 2. Department of Basic Clinical Practice, University of Barcelona (UB), Casanova 143, E-08036, Barcelona, Spain. 3. Department of Pharmacology, Institute of Biological Sciences, Federal University of Goiás, Goiânia, GO, Brazil. 4. Barcelona Clínic Schizophrenia Unit, Neuroscience Institute, HCB, Barcelona, Catalunya, Spain. 5. Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Madrid, Spain. 6. Institut d'investigacions Biomèdiques August Pi i Sunyer (IDIBAPs), Barcelona, Spain. 7. Departmentof Psychiatry, Complejo Hospitalario de Navarra, Instituto de Investigaciones Sanitarias de Navarra (IdiSNa), Pamplona, Spain. 8. Institute of Psychiatry and Mental Health, Hospital Clínico San Carlos, IdISSC, CIBERSAM, School of Medicine, Universidad Complutense, Madrid, Spain. 9. Department of Medicine and Psychiatry, Zaragoza University, Instituto de Investigación Sanitaria Aragón (IIS Aragón), Zaragoza, Spain. 10. Hospital Universitario Araba, Servicio de Psiquiatria, UPV/EHU, Bioaraba, Spain. 11. Department of Child and Adolescent Psychiatry, Institute of Psychiatry and Mental Health, Hospital General Universitario Gregorio Marañon, CIBERSAM, IiSGM, School of Medicine, Universidad Complutense, Madrid, Spain. 12. Psychiatry Department, Institut d'Investigació Biomèdica-Sant Pau (IIB-SANT PAU), Hospital de la Santa Creu i Sant Pau; Universitat Autònoma de Barcelona (UAB), Barcelona, Spain. 13. Hospital Clinic, Institute of Neuroscience, University of Barcelona, IDIBAPS, CIBERSAM, Barcelona, Catalonia, Spain. 14. Department of Child and Adolescent Psychiatry and Psychology, Clínic Institute of Neurosciences, Hospital Clínic de Barcelona, 2017SGR881, University of Barcelona, CIBERSAM, IDIBAPS, Barcelona, Spain. 15. Hospital del Mar Medical Research Institute (IMIM), Barcelona, Spain. 16. Autonomous university of Barcelona (UAB), Barcelona, Spain. 17. Barcelona Clínic Schizophrenia Unit, Neuroscience Institute, Hospital Clínic of Barcelona, Barcelona, Spain. 18. Department of Medicine, Barcelona, UB, Spain. 19. Department of Psychiatry, Hospital Universitario Ramón y Cajal, IRYCIS, Universidad de Alcalá, Madrid, Spain. 20. Department of Basic Clinical Practice, University of Barcelona (UB), Casanova 143, E-08036, Barcelona, Spain. sergimash@ub.edu. 21. Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Madrid, Spain. sergimash@ub.edu. 22. Institut d'investigacions Biomèdiques August Pi i Sunyer (IDIBAPs), Barcelona, Spain. sergimash@ub.edu.
Abstract
INTRODUCTION: The role of Olanzapine therapeutic drug monitoring is controversial. The present study explores the associations of Olanzapine plasma concentrations with clinical response and metabolic side effects in first episode psychosis (FEP) after 2 months of treatment. METHODS: Forty-seven patients were included. Improvement in clinical symptomatology was assessed using the PANSS. Metabolic assessment included weight, blood pressure, waist circumference, blood glucose, total cholesterol, high-density lipoprotein, low-density lipoprotein, and triglycerides. RESULTS: The Olanzapine plasma concentrations after 2 months of treatment were positively correlated with weight gain (r = 0.49, p = 0.003), and a concentration > 23.28 ng/mL was identified as a positive predictor of weight gain (≥ 7%). The Olanzapine concentration to dose (C/D) ratio was positively correlated with the percentage of improvement in the total PANSS (r = 0.46, p = 0.004), and a C/D ratio > 2.12 was identified as a positive predictor of a good response (percentage of improvement > 30%) after 2 months of treatment. We also identified several factors that could alter Olanzapine pharmacokinetics: gender (p = 0.03), diagnosis (p = 0.05), smoking habit (p = 0.05), and co-medications such as valproic acid (p = 0.05) and anxiolytics (p = 0.01). DISCUSSION: In conclusion, our results suggest that therapeutic drug monitoring of Olanzapine could be helpful to evaluate therapeutic efficacy and metabolic dysfunction in FEP patients treated with Olanzapine.
INTRODUCTION: The role of Olanzapine therapeutic drug monitoring is controversial. The present study explores the associations of Olanzapine plasma concentrations with clinical response and metabolic side effects in first episode psychosis (FEP) after 2 months of treatment. METHODS: Forty-seven patients were included. Improvement in clinical symptomatology was assessed using the PANSS. Metabolic assessment included weight, blood pressure, waist circumference, blood glucose, total cholesterol, high-density lipoprotein, low-density lipoprotein, and triglycerides. RESULTS: The Olanzapine plasma concentrations after 2 months of treatment were positively correlated with weight gain (r = 0.49, p = 0.003), and a concentration > 23.28 ng/mL was identified as a positive predictor of weight gain (≥ 7%). The Olanzapine concentration to dose (C/D) ratio was positively correlated with the percentage of improvement in the total PANSS (r = 0.46, p = 0.004), and a C/D ratio > 2.12 was identified as a positive predictor of a good response (percentage of improvement > 30%) after 2 months of treatment. We also identified several factors that could alter Olanzapine pharmacokinetics: gender (p = 0.03), diagnosis (p = 0.05), smoking habit (p = 0.05), and co-medications such as valproic acid (p = 0.05) and anxiolytics (p = 0.01). DISCUSSION: In conclusion, our results suggest that therapeutic drug monitoring of Olanzapine could be helpful to evaluate therapeutic efficacy and metabolic dysfunction in FEP patients treated with Olanzapine.
Entities:
Keywords:
Drug level; Efficacy; First-episode psychosis; Olanzapine; Pharmacokinetics; Therapeutic drug monitoring; Weight gain
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