Rapid-onset clozapine-induced loss of glycaemic control: Case report
Alejandro Porras-Segovia,
Amir Krivoy,
Mark Horowitz,
George Thomas,
Mark Bolstridge,
Dragos Ion,
Sukhwinder S. Shergill
Affiliations
Alejandro Porras-Segovia
University of Granada, Granada, Spain
Amir Krivoy
Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; National Psychosis Unit, Bethlem Royal Hospital, South London and Maudsley NHS Foundation Trust London, London, UK
Mark Horowitz
National Psychosis Unit, Bethlem Royal Hospital, South London and Maudsley NHS Foundation Trust London, London, UK
George Thomas
Hull York Medical School, University of York, York, UK
Mark Bolstridge
National Psychosis Unit, Bethlem Royal Hospital, South London and Maudsley NHS Foundation Trust London, London, UK
Dragos Ion
National Psychosis Unit, Bethlem Royal Hospital, South London and Maudsley NHS Foundation Trust London, London, UK
Sukhwinder S. Shergill
Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; National Psychosis Unit, Bethlem Royal Hospital, South London and Maudsley NHS Foundation Trust London, London, UK
Clozapine has proved to be an effective antipsychotic for the treatment of refractory schizophrenia – characterised by the persistence of symptoms despite optimal treatment trials with at least two different antipsychotics at adequate dose and duration – but its use is hampered by adverse effects. The development of clozapine-induced diabetes is commonly considered to arise as part of a metabolic syndrome, associated with weight gain, and thus evolves slowly. We present the case of an individual with refractory schizophrenia and metformin-controlled diabetes who developed rapid-onset insulin-dependent hyperglycaemia immediately after starting clozapine. Given the refractory nature of his illness, the decision was made to continue clozapine and manage the diabetes. This case supports the existence of a more direct mechanism by which clozapine alters glycaemic control, aside from the more routine slow development of a metabolic syndrome.
