ESPE Abstracts (2018) 89 P-P2-108

Severe Stress-Induced Subcutaneous and Intravenous Insulin Resistance in an Eight Year Old Boy with T1DM, Necessitating Seven Months of IV Insulin, Reversed after Psychiatric Treatment

CCN van Ommena,b, JJG Hoorweg-Nijmanb, H Stuarta,b, PKH Deschampsc & AA Verrijn Stuarta,b


aPediatric Endocrinology, Department of Pediatrics, University Medical Center Utrecht, Utrecht, Netherlands; bDiabetes Centraal, St. Antonius Hospital, Utrecht, Netherlands; cDepartment of Psychiatry, University Medical Center, Utrecht Brain Center, Utrecht, Netherlands


Background: Persistent severe insulin resistance (IR) in T1DM is infrequent, complex to handle and disabling. Genetic and epigenetic factors play a significant role in the pathophysiology of IR. This case report discusses the potential role of habitual and stress-inducing environmental factors in a school-aged boy with a neurodevelopmental disorder.

Case report: We present an eight year old boy with a three year history of T1DM (GAD positive) regulated by uneventful continuous subcutaneous insulin infusion (CSII) treatment for three years. Though initially increased behavioral dysregulation was partly attributed to T1DM, he was diagnosed with a neurodevelopmental disorder with symptoms of autism, deficient anxiety and attention regulation at age six. Therapy consisted of behavioral interventions and atypical antipsychotics. Shortly after start of aripiprazol, mild ketoacidosis developed. After appropriate treatment, metabolic control could only be maintained by intravenous insulin (iv) therapy. Attempts during prolonged admission and while on iv insulin to restart CSII were unsuccessful with subcutaneous (sc) insulin up to 6 U/kg per day and injections sc with Insulin Degludec, Insulin Aspart, Insuman Infusat (to exclude allergy), and Insulin Glulisin as well as addition of metformin all failed to reinstall glycemic control. Technical problems and manipulations were excluded; carbohydrate and exercise management did not affect IR and he did not have signs of lipodystrophy or acanthosis nigricans. Extensive laboratory investigations revealed normal cortisol, catecholamine- and glucagon levels; positive anti-insulin and negative insulin receptor antibodies. Antipsychotics, as potential trigger for IR, were discontinued; thereafter behavioral problems deteriorated despite initiation of carbamazepine treatment. Five months after onset of IR, admission to a child psychiatry inpatient unit was decided on. A 24/7 structured, behavioral approach combined with ongoing strict T1DM regulation led to a successful, lasting transfer to CSII treatment.

Discussion: In this now 10 year old boy with T1DM and a neurodevelopmental disorder we hypothesize a role for stress-induced IR. Antipsychotic treatment alterations may have initiated the onset of sc and iv IR. However, cessation of antipsychotic treatment did not re-install glycemic control; suggestive of a role for stress-induced IR. With structured behavioral approach in a child psychiatry unit combined with continuation of strict regulation of nutrition and insulin therapy the IR disappeared. He still frequently presents with ketoacidosis but not with lasting IR.

Conclusion: IR appeared to be at least in part stress dependent and an integrated therapeutic approach led to better behavioral as well as glycemic control.

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