A Successful Switching to Oral Ziprasidone in Patient with Metabolic Side Effects

2015 ◽  
Vol 30 ◽  
pp. 1587
Author(s):  
B. Batinic ◽  
D. Duisin
2021 ◽  
Vol 35 (3) ◽  
pp. 284-302
Author(s):  
Ilijana Babic ◽  
Dominic Sellers ◽  
Paul L Else ◽  
Jessica Nealon ◽  
Ashleigh L Osborne ◽  
...  

Background: Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist that prevents metabolic side effects of the antipsychotic drugs (APDs) olanzapine and clozapine through unknown mechanisms. Aim: This study aimed to investigate the effect of chronic APD and liraglutide co-treatment on key neural and peripheral metabolic signals, and acute liraglutide co-treatment on clozapine-induced hyperglycaemia. Methods: In study 1, rats were administered olanzapine (2 mg/kg), clozapine (12 mg/kg), liraglutide (0.2 mg/kg), olanzapine + liraglutide co-treatment, clozapine + liraglutide co-treatment or vehicle for six weeks. Feeding efficiency was examined weekly. Examination of brain tissue (dorsal vagal complex (DVC) and mediobasal hypothalamus (MBH)), plasma metabolic hormones and peripheral (liver and kidney) cellular metabolism and oxidative stress was conducted. In study 2, rats were administered a single dose of clozapine (12 mg/kg), liraglutide (0.4 mg/kg), clozapine + liraglutide co-treatment or vehicle. Glucose tolerance and plasma hormone levels were assessed. Results: Liraglutide co-treatment prevented the time-dependent increase in feeding efficiency caused by olanzapine, which plateaued by six weeks. There was no effect of chronic treatment on melanocortinergic, GABAergic, glutamatergic or endocannabionoid markers in the MBH or DVC. Peripheral hormones and cellular metabolic markers were unaltered by chronic APD treatment. Acute liraglutide co-treatment was unable to prevent clozapine-induced hyperglycaemia, but it did alter catecholamine levels. Conclusion: The unexpected lack of change to central and peripheral markers following chronic treatment, despite the presence of weight gain, may reflect adaptive mechanisms. Further studies examining alterations across different time points are required to continue to elucidate the mechanisms underlying the benefits of liraglutide on APD-induced metabolic side effects.


2011 ◽  
Vol 62 (10) ◽  
pp. 1235-1236
Author(s):  
Christina Mangurian ◽  
Susan M. Essock ◽  
Lloyd I. Sederer

Author(s):  
Jonathan M. Meyer ◽  
Donald C. Goff ◽  
Joseph P. McEvoy

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Aurélie Delacrétaz ◽  
Anaïs Glatard ◽  
Céline Dubath ◽  
Mehdi Gholam-Rezaee ◽  
Jose Vicente Sanchez-Mut ◽  
...  

Abstract Background Metabolic side effects induced by psychotropic drugs represent a major health issue in psychiatry. CREB-regulated transcription coactivator 1 (CRTC1) gene plays a major role in the regulation of energy homeostasis and epigenetic mechanisms may explain its association with obesity features previously described in psychiatric patients. This prospective study included 78 patients receiving psychotropic drugs that induce metabolic disturbances, with weight and other metabolic parameters monitored regularly. Methylation levels in 76 CRTC1 probes were assessed before and after 1 month of psychotropic treatment in blood samples. Results Significant methylation changes were observed in three CRTC1 CpG sites (i.e., cg07015183, cg12034943, and cg 17006757) in patients with early and important weight gain (i.e., equal or higher than 5% after 1 month; FDR p value = 0.02). Multivariable models showed that methylation decrease in cg12034943 was more important in patients with early weight gain (≥ 5%) than in those who did not gain weight (p = 0.01). Further analyses combining genetic and methylation data showed that cg12034943 was significantly associated with early weight gain in patients carrying the G allele of rs4808844A>G (p = 0.03), a SNP associated with this methylation site (p = 0.03). Conclusions These findings give new insights on psychotropic-induced weight gain and underline the need of future larger prospective epigenetic studies to better understand the complex pathways involved in psychotropic-induced metabolic side effects.


2011 ◽  
Vol 62 (10) ◽  
pp. 1235-1235
Author(s):  
Edward L. Knight ◽  
Alex Young

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e98684 ◽  
Author(s):  
Erik J. M. Toonen ◽  
Anke J. Laskewitz ◽  
Theo H. van Dijk ◽  
Aycha Bleeker ◽  
Aldo Grefhorst ◽  
...  

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S321-S321
Author(s):  
Araba Chintoh ◽  
Mahavir Agarwal ◽  
Nicole Mackenzie ◽  
Gary Remington ◽  
Margaret Hahn

Abstract Background This observational, exploratory pilot study aims to understand changes in clinical presentation and quality of life (QoL) in antipsychotic-naïve youth. Outcomes for these first-episode psychosis patients will be explored in the context metabolic changes during their first three months of treatment. Methods Participants (n = 10) aged 14–29 years were followed throughout their first three months of treatment with an antipsychotic medication (of physician’s/patient’s choice). Participants were evaluated on metabolic indices including weight, waist circumference, and BMI, as well as QoL [Pediatric Quality of Life Index (PedsQL) and PedsQL General Well-Being Scale] and clinical presentation [Clinical Global Impression (CGI) scale]. Descriptive statistics and nonparametric tests were conducted to compare significant changes across these variables. Results Significant changes in metabolic indices were observed over the first three months of treatment, as measured in weight gain (p = 0.02), increased waist circumference (p = 0.02) and increased BMI (p = 0.01). Physicians rated clinical improvement in participants, CGI score (p = 0.03). However, patient-rated QoL remained unchanged within all subcategories, including psychosocial (p = 0.52) and general well-being (p = 0.35). Discussion It appears that antipsychotic-related metabolic side effects may not impede upon early clinical improvement or impact QoL. In addition, there does not appear to be a relationship between clinical presentation and QoL as our small sample show QoL remains neutral or positive. Taken together, these findings suggest that clinical presentation and metabolic side effects may not be influential in early psychosis. From a clinical perspective, these early pilot data add to the literature highlighting the significant, early, antipsychotic-induced metabolic side effects in youth, and also encouraging clinicians to attend to the interplay between treatment and related QoL. This study is limited by its small sample size and naturalistic treatment allocation. These participants will be followed longitudinally to monitor development of adverse metabolic outcomes as well as changes in QoL in later stages of treatment/illness. The field must to understand how treatment and management of metabolic side effects can be augmented to promote clinical improvement and QoL, given the prevalence of adolescent patients who eventually wish to discontinue antipsychotic drugs because of metabolic side effects.


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