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      Acute onset clozapine-induced hyperglycaemia: A case report

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          Abstract

          Clozapine is an atypical antipsychotic which is described to have higher efficacy among all available antipsychotic medications. Clozapine is reserved especially for resistant schizophrenia due to its side effects. Clozapine-induced metabolic syndrome and hyperglycaemia are common long-term side effects and are responsible for increased mortality in patients with schizophrenia. In this case, a patient with resistant schizophrenia was presented with acute-onset hyperglycaemia and delirium with the use of clozapine within a week. Withdrawal of clozapine in the patient led to the improvement in delirium and hyperglycaemia without the use of any hypoglycaemic agent. This case supports the notion that in certain cases clozapine can induce hyperglycemia through possible direct pathophysiological mechanisms within a shorter time frame.

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          Clozapine, diabetes mellitus, weight gain, and lipid abnormalities: A five-year naturalistic study.

          D. Hayden, C. G. Gray, Henry Nasrallah … (2000)
          The goal of this 5-year naturalistic study of patients treated with clozapine was to examine the incidence of treatment-emergent diabetes mellitus in relation to other factors, including weight gain, lipid abnormalities, age, clozapine dose, and treatment with valproate. Data on age, gender, race, diagnosis, family history of diabetes, and age at clozapine initiation were collected from medical records of 82 outpatients with schizophrenia or schizoaffective disorder. Clozapine dose, data on use of valproate, and laboratory test results were recorded at 6-month intervals. The mean age at the time of clozapine initiation of the 82 patients was 36.4 years; 26.8% of the patients were women, and 91.5% were Caucasian. The mean baseline weight was 175.5 lb, and the mean body mass index was 26.9 kg/m(2). Thirty patients (36.6%) were diagnosed with diabetes during the 5-year follow-up. Weight gain, use of valproate, and total daily dose of clozapine were not significant risk factors for developing diabetes mellitus. Patients experienced significant weight gain that continued until approximately month 46 from initiation of clozapine. There was a nonsignificant increase in total serum cholesterol and a significant increase in serum triglycerides level. The results support the hypotheses that patients treated with clozapine experience significant weight gain and lipid abnormalities and appear to be at increased risk for developing diabetes.
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            Treatment-resistant schizophrenia: current insights on the pharmacogenomics of antipsychotics

            John Lally, Fiona Gaughran, Philip Timms … (2016)
            Up to 30% of people with schizophrenia do not respond to two (or more) trials of dopaminergic antipsychotics. They are said to have treatment-resistant schizophrenia (TRS). Clozapine is still the only effective treatment for TRS, although it is underused in clinical practice. Initial use is delayed, it can be hard for patients to tolerate, and clinicians can be uncertain as to when to use it. What if, at the start of treatment, we could identify those patients likely to respond to clozapine – and those likely to suffer adverse effects? It is likely that clinicians would feel less inhibited about using it, allowing clozapine to be used earlier and more appropriately. Genetic testing holds out the tantalizing possibility of being able to do just this, and hence the vital importance of pharmacogenomic studies. These can potentially identify genetic markers for both tolerance of and vulnerability to clozapine. We aim to summarize progress so far, possible clinical applications, limitations to the evidence, and problems in applying these findings to the management of TRS. Pharmacogenomic studies of clozapine response and tolerability have produced conflicting results. These are due, at least in part, to significant differences in the patient groups studied. The use of clinical pharmacogenomic testing – to personalize clozapine treatment and identify patients at high risk of treatment failure or of adverse events – has moved closer over the last 20 years. However, to develop such testing that could be used clinically will require larger, multicenter, prospective studies.
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              Potential mechanisms of atypical antipsychotic-induced metabolic derangement: clues for understanding obesity and novel drug design.

              Roberto Coccurello, Anna Moles (2010)
              Beside the therapeutic improvement over first-generation antipsychotics, the fact that prescription of atypical agents is also associated to the emergence of severe metabolic derangement in patients is not a mystery anymore. Body weight gain, dyslipidemia, adiposity, impaired glucose homeostasis, insulin and leptin resistance and new-onset type II diabetes are all part of a syndromic cluster of vast medical concern. Thus, clinical reports and rodent models of atypical antipsychotic-associated metabolic impairment have growth in parallel as separate territories. This review focuses on the attempt to take a snapshot of the present developing moment and to describe to what extent clinical data are reflected by the findings derived from animal studies. This aim is pursued through different steps that, starting from the criteria necessary to characterize the "atypicality" of atypical drugs, then explore the consistency among clinical and animal-based data. The endpoint of this survey consists in the analysis of the potential mechanisms underlying the metabolic derangement induced by this class of drugs. It is, indeed, our opinion that some atypical antipsychotics should be viewed as potent obesogenic factors that can be exploited as valuable tools to shed light into the elusive dilemma of obesity. For this reason, recently identified obesogenic and diabetogenic mechanisms are the background on which the present work is built and some novel forthcoming lines of investigation suggested. 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Gen Psychiatr
                Journal ID (iso-abbrev): Gen Psychiatr
                Journal ID (hwp): gpsych
                Journal ID (publisher-id): gpsych
                Title: General Psychiatry
                Publisher: BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                ISSN (Electronic): 2517-729X
                Publication date Collection: 2019
                Publication date (Electronic): 11 April 2019
                Volume: 32
                Issue: 2
                Electronic Location Identifier: e100045
                Affiliations
                [1 ] departmentDepartment of Psychiatry , Shyam Shah Medical College Rewa , Rewa, India
                [2 ] departmentDepartment of Psychiatry , Mahatma Gandhi Memorial Medical College , Indore, India
                Author notes
                [Correspondence to ] Dr Dheerendra Kumar Mishra; mdheerendra.ssmc@ 123456gmail.com
                Author information
                http://orcid.org/0000-0002-5068-2922
                Article
                Publisher ID: gpsych-2018-100045
                DOI: 10.1136/gpsych-2018-100045
                PMC ID: 6551436
                PubMed ID: 31179433
                SO-VID: 5e681ba1-fe94-43c4-b126-3efadd71f133
                Copyright © © Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
                License:

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0

                History
                Date received : 26 December 2018
                Date revision received : 06 February 2019
                Date accepted : 10 February 2019
                Categories
                Subject: Case Report
                Subject: 1506
                Custom metadata
                special-feature unlocked

                Keywords: clozapine,adverse effects,hyperglycemia,delirium,acute onset
                Data availability:
                Keywords: clozapine, adverse effects, hyperglycemia, delirium, acute onset

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