Background: Here, we report a case of central pontine demyelinization in a type-2 diabetes patient with hyperglycemia\nafter a binge-eating attack in the absence of a relevant hyponatremia.\nCase presentation: A 55-year-old, male type-2 diabetic patient with liver cirrhosis stage Child-Pugh B was admitted due\nto dysmetria of his right arm, gait disturbance, dizziness, vertigo, and polyuria, polydipsia after a binge-eating attack of\nsweets (a whole fruit cake and 2 Liters of soft drinks). A recently initiated insulin therapy had been discontinued for\n8 months. A serum glucose measurement obtained 5 days prior to hospitalisation was 38.5 mmol/l (694 mg/dl). The\npatient graved for sweets since stopping alcohol consumption 8 months earlier. On admission, venous-blood glucose\nwas 29.1 mmol/l (523.8 mg/dl), glycated hemoglobin was 168.0 mmol/mol or 17.6%. No supplementation of sodium\nchloride was reported. Laboratory exams revealed an elevated serum ammonia level (127.1 �¼mol/l), rendering a hepatic\nencephalopathy very likely. After initiation of insulin therapy, capillary glucose normalized, and serum sodium rose from\n133 on admission to 144 mmol/l during the hospital stay. In retrospect, the mild hyponatremia on admission was\nclassified as pseudohyponatremia due to hyperglycemia. The patient had an insulin resistance (HOMA-IR 7.8 (normal\nrange < 2.5)). A T2-weighted magnetic resonance imaging (MRI) of the head and a cranial computed tomography scan\nwere obtained demonstrating a symmetric central pontine demyelinization. After 26 days in hospital, the patient was\ndischarged with an inkretin-mimetic therapy (dulaglutide SC, 1.5 mg/week) and an intensified conventional insulin\ntherapy (insulin aspart: 14 units/d in euglycemia, insulin glargin 20 units/d).\nConclusions: Central pontine and/or cerebellar myelinolysis can be caused by sudden, severe, and sustained\nhyperglycemia, especially when another risk factor (in this case, liver cirrhosis) is present. Functional neurological\ndeficits in the context of hyperglycemia should prompt for the consideration of this differential diagnosis in all\ndiabetes patients.
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