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Atypical antipsychotics (SGA) are used as first choice but this group of drugs may cause relatively more metabolic problems. Diabetic ketoacidosis (DCA) known as an acute, life-threatening complication of diabetes, can be triggered by use of SGA. In this presentation, we present a 17- year-old male patient who had DCA that thought to be triggered by olanzapine treatment.
Case presentation: E. has been followed up and treated for about 6 years in child and adolescent psychiatry outpatient clinic. He had no history of smoking, alcohol or substance abuse in any period of his life. There was no history of psychiatric disease in the family. His aunt has a history of type 2 diabetes. The first time he consulted us was about 2 years ago with the complaint of irritability, harm to his family and sleep problems. In this interview, we learned that she had been treated with risperidone 2 mg/day but had no benefit. Mental status examination revealed any hypomanic, manic, psychotic symptoms and signs. Aripiprazole 5 mg/day treatment was arranged and he benefited from drug. Patient was admitted again after 2.5 months and family had complaints of “inability to sleep, fears, biting himself, talking to himself”. Avolition, dirtiness obsessions and cleaning compulsions, visual, auditory and auditory hallucinations were determined in the examination. Patient was referred to child neurology and psychiatric hospitalization was recommended. However family did not want hospitalization and no pathology was found in her neurological examination. Patient was planned to have olanzapine 5 mg, 2 times a day. Approximately 1.5 months later, the patient re-admitted to us, he was so irritable, anxious, unsleeping and suggested to continuation of olanzapine in morning 5 mg and evening 10 mg. In third week of treatment, patient was admitted to the emergency room with nausea, vomiting, abdominal pain and blurred consciousness. In the evaluation; blood glucose 434 mg/dl, urine glucose 3+, protein 2+, ketone 3+, pH 6.0; The blood gas pH was found to be 7.146 and it was accepted to the pediatric intensive care unit with diagnosis of diabetic ketoacidosis. Olanzapine treatment was discontinued and he was discharged with insulin therapy. The patient is still followed up with aripiprazole 15 mg/day treatment. How SGA lead to hyperglycemia remains unclear. Due to the weight gain effects of olanzapine, increasing peripheral and hepatic insulin resistance and stimulating X receptor are most known factors contributing to this effect. This mechanism does not seem possible to explain the rapid onset of diabetes. Some clinical trials with olanzapine have shown biphasic changes in insulin secretion in patients. Olanzapine acts on direct beta cells in the early period of treatment and that insulin secretion decreases significantly may accompany this metabolic condition. As in our patient, it is stated that this possibility increases in case of genetic predisposition. Particular attention should be paid to use of olanzapine, which may cause metabolic side effects more frequently in young patients with familial predisposition.