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Background and PurposeHyperglycemia after acute ischemic stroke (AIS) is associated with poor outcomes. However, there is no consensus as to the optimal method for glycemic control. We designed an insulin infusion protocol for aggressive glucose control and investigated its efficacy and safety.MethodsWe applied our protocol to patients within 48 hours after AIS or transient ischemic attack (TIA) with an initial capillary glucose level of between 100 and 399 mg/dL (5.6-22.2 mmol/L). An insulin solution comprising 40 or 50 U of human regular insulin in 500 mL of 5% dextrose was administered for 24 hours. Capillary glucose was measured every 2 hours and the infusion rate was adjusted according to a nomogram with a target range of 80-129 mg/dL (4.4-7.2 mmol/L). Changes in glucose and overall glucose levels during insulin infusion were analyzed according to the presence of diabetes or admission hyperglycemia (admission glucose >139 mg/dL or 7.7 mmol/L) by the generalized estimating equation method.ResultsThe study cohort comprised 115 consecutive patients. Glucose was significantly lowered from 160±57 mg/dL (8.9±3.2 mmol/L) at admission to 93±28 mg/dL (5.2±1.6 mmol/L) during insulin infusion (p<0.05). Laboratory hypoglycemia (capillary glucose <80 mg/dL or 4.4 mmol/L) occurred in 91 (71%) patients, 11 (10%) of whom had symptomatic hypoglycemia. Although glucose levels were significantly lowered and maintained within the target range in all patients, overall glucose levels were significantly higher in patients with diabetes or hyperglycemia (p<0.05).ConclusionsOur insulin-infusion protocol was effective in glycemic control for patients with AIS or TIA. Further modification is needed to improve the efficacy and safety of this procedure, and tailored intervention should be considered according to glycemic status.

Acute hemorrhagic leukoencephalopathy is a rare condition associated with the influenza virus, but the role of influenza in this condition has not been clarified. We experienced a patient with influenza A and B virus co-infection who initially presented mild gastrointestinal symptoms and rapidly progressed to coma. Magnetic resonance imaging showed severe brain edema and multiple intracranial hemorrhagic lesions. The patient was treated with oseltamivir and corticosteroid, and her clinical course improved without neurological sequelae.

Paraproteinemia potentially causes peripheral neuropathy via an unknown underlying pathogenetic mechanism. We report a case of pathologically proven amyloid neuropathy with AL amyloidosis with an IgA kappa light chain, which was initially diagnosed as neuropathy associated with monoclonal gammopathy of undetermined significance. This case indicates that in cases of neuropathy with paraproteinemia, the other potential causes should be excluded by appropriate means, especially pathological evaluations.