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Titlebook: Congenital Hyperinsulinism; A Practical Guide to Diva D. De León-Crutchlow,Charles A. Stanley Book 2019 Springer Nature Switzerland AG 2019

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楼主: ominous
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Management of Diabetes and Pancreatic Insufficiency After Pancreatectomy,occur. Initially after surgery, patients may experience persistent hypoglycemia, persistent diabetes mellitus, or transient diabetes followed by hypoglycemia. Insulin is indicated in patients with hyperglycemia in the immediate post-op period to maintain normal glucose levels. For persistent diabete
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Neurodevelopmental Outcomes,evelopmental abnormalities (26–48%) and seizures (13–29%) in the hyperinsulinism population. Individuals are at risk of poor neurodevelopmental outcomes regardless of the duration of the hyperinsulinism or treatment modality. All children with hyperinsulinism require screening for developmental issu
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Diazoxide-Responsive Forms of Congenital Hyperinsulinism,xide to avoid fluid overload and pulmonary hypertension. Genetic forms of diazoxide-responsive hyperinsulinism include a distinctive form caused by dominant activating mutations in glutamate dehydrogenase (GDH). Leucine-induced and fasting hypoglycemia, mild hyperammonemia, and neurologic abnormalit
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Diazoxide-Unresponsive Forms of Congenital Hyperinsulinism,etic etiology. The overall goal in the management of infants with diazoxide-unresponsive HI is to identify those with focal HI and to find an effective treatment regimen for those that cannot be cured by surgery (diffuse HI).
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Management of Diabetes and Pancreatic Insufficiency After Pancreatectomy,e manner, exocrine pancreatic insufficiency may have a delayed onset after a subtotal pancreatectomy, and symptoms often arise only after nutritional sequela have occurred. Thus, careful screening for exocrine insufficiency with stool studies and labs should occur at baseline and at regular interval
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https://doi.org/10.1007/978-3-322-81157-8xide to avoid fluid overload and pulmonary hypertension. Genetic forms of diazoxide-responsive hyperinsulinism include a distinctive form caused by dominant activating mutations in glutamate dehydrogenase (GDH). Leucine-induced and fasting hypoglycemia, mild hyperammonemia, and neurologic abnormalit
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