{"title":"窒息新生儿的短暂性高胰岛素血症。","authors":"K Schultz, G Soltész","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Hypoglycemia in birth asphyxiated infants is attributed to glycogen depletion. We observed three term AGA (Appropriate for Gestational Age) infants with birth asphyxia, who developed hyperinsulinemic hypoglycemia postnatally. All had inappropriately high serum insulin concentrations for their blood glucose levels, and needed glucose infusion rates of greater than 8 mg/kg/min for several days to maintain normoglycemia. All infants recovered spontaneously.</p>","PeriodicalId":76974,"journal":{"name":"Acta paediatrica Hungarica","volume":"31 1","pages":"47-52"},"PeriodicalIF":0.0000,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Transient hyperinsulinism in asphyxiated newborn infants.\",\"authors\":\"K Schultz, G Soltész\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Hypoglycemia in birth asphyxiated infants is attributed to glycogen depletion. We observed three term AGA (Appropriate for Gestational Age) infants with birth asphyxia, who developed hyperinsulinemic hypoglycemia postnatally. All had inappropriately high serum insulin concentrations for their blood glucose levels, and needed glucose infusion rates of greater than 8 mg/kg/min for several days to maintain normoglycemia. All infants recovered spontaneously.</p>\",\"PeriodicalId\":76974,\"journal\":{\"name\":\"Acta paediatrica Hungarica\",\"volume\":\"31 1\",\"pages\":\"47-52\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1991-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Acta paediatrica Hungarica\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta paediatrica Hungarica","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Transient hyperinsulinism in asphyxiated newborn infants.
Hypoglycemia in birth asphyxiated infants is attributed to glycogen depletion. We observed three term AGA (Appropriate for Gestational Age) infants with birth asphyxia, who developed hyperinsulinemic hypoglycemia postnatally. All had inappropriately high serum insulin concentrations for their blood glucose levels, and needed glucose infusion rates of greater than 8 mg/kg/min for several days to maintain normoglycemia. All infants recovered spontaneously.