{"title":"低血糖","authors":"G. Butler, J. Kirk","doi":"10.1093/med/9780198786337.003.0007","DOIUrl":null,"url":null,"abstract":"\n\n\n • Hypoglycaemia is defined as ‘A plasma glucose concentration low enough to cause symptoms and/or signs of impaired brain function’.\n \n\n • Cut-offs are contentious, ranging from <2.2 to <4.0 mmol/L, and are dependent on age, diagnosis, and also availability/usage of alternative metabolic fuels such as ketones.\n \n\n • May be transient or persistent, dependent on diagnosis.\n \n\n • Causes broadly due to:\n \n\n\n ◦ decreased glucose including prematurity, inborn errors of metabolism, hypopituitarism, adrenal insufficiency (primary and secondary), and prolonged fasting\n \n\n ◦ increased glucose utilization including infant of diabetic mother, hyperinsulinaemia, perinatal asphyxia, and various syndromes, e.g. Beckwith–Wiedemann.\n \n\n • Endocrine causes of hypoglycaemia include growth hormone deficiency, adrenal insufficiency (primary and secondary), and (?) hypothyroidism.\n \n\n • Metabolic disorders cause hypoglycaemia via impaired:\n \n\n\n ◦ mobilization of glucose stores\n \n\n ◦ gluconeogenesis\n \n\n ◦ alternative energy sources\n \n\n ◦ liver function.\n \n\n • Hyperinsulinaemic hypoglycaemia presents with increased glucose requirements (>8 mg/kg/minute) and non-ketotic hypoglycaemia. Diagnosis confirmed by demonstrating raised/detectable insulin/C-peptide during hypoglycaemia. Genotyping may assist with not only diagnosis but direct therapy (medical and surgical).","PeriodicalId":217485,"journal":{"name":"Paediatric Endocrinology and Diabetes","volume":"1 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2020-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Hypoglycaemia\",\"authors\":\"G. Butler, J. Kirk\",\"doi\":\"10.1093/med/9780198786337.003.0007\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"\\n\\n\\n • Hypoglycaemia is defined as ‘A plasma glucose concentration low enough to cause symptoms and/or signs of impaired brain function’.\\n \\n\\n • Cut-offs are contentious, ranging from <2.2 to <4.0 mmol/L, and are dependent on age, diagnosis, and also availability/usage of alternative metabolic fuels such as ketones.\\n \\n\\n • May be transient or persistent, dependent on diagnosis.\\n \\n\\n • Causes broadly due to:\\n \\n\\n\\n ◦ decreased glucose including prematurity, inborn errors of metabolism, hypopituitarism, adrenal insufficiency (primary and secondary), and prolonged fasting\\n \\n\\n ◦ increased glucose utilization including infant of diabetic mother, hyperinsulinaemia, perinatal asphyxia, and various syndromes, e.g. Beckwith–Wiedemann.\\n \\n\\n • Endocrine causes of hypoglycaemia include growth hormone deficiency, adrenal insufficiency (primary and secondary), and (?) hypothyroidism.\\n \\n\\n • Metabolic disorders cause hypoglycaemia via impaired:\\n \\n\\n\\n ◦ mobilization of glucose stores\\n \\n\\n ◦ gluconeogenesis\\n \\n\\n ◦ alternative energy sources\\n \\n\\n ◦ liver function.\\n \\n\\n • Hyperinsulinaemic hypoglycaemia presents with increased glucose requirements (>8 mg/kg/minute) and non-ketotic hypoglycaemia. Diagnosis confirmed by demonstrating raised/detectable insulin/C-peptide during hypoglycaemia. Genotyping may assist with not only diagnosis but direct therapy (medical and surgical).\",\"PeriodicalId\":217485,\"journal\":{\"name\":\"Paediatric Endocrinology and Diabetes\",\"volume\":\"1 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Paediatric Endocrinology and Diabetes\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1093/med/9780198786337.003.0007\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Paediatric Endocrinology and Diabetes","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/med/9780198786337.003.0007","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
• Hypoglycaemia is defined as ‘A plasma glucose concentration low enough to cause symptoms and/or signs of impaired brain function’.
• Cut-offs are contentious, ranging from <2.2 to <4.0 mmol/L, and are dependent on age, diagnosis, and also availability/usage of alternative metabolic fuels such as ketones.
• May be transient or persistent, dependent on diagnosis.
• Causes broadly due to:
◦ decreased glucose including prematurity, inborn errors of metabolism, hypopituitarism, adrenal insufficiency (primary and secondary), and prolonged fasting
◦ increased glucose utilization including infant of diabetic mother, hyperinsulinaemia, perinatal asphyxia, and various syndromes, e.g. Beckwith–Wiedemann.
• Endocrine causes of hypoglycaemia include growth hormone deficiency, adrenal insufficiency (primary and secondary), and (?) hypothyroidism.
• Metabolic disorders cause hypoglycaemia via impaired:
◦ mobilization of glucose stores
◦ gluconeogenesis
◦ alternative energy sources
◦ liver function.
• Hyperinsulinaemic hypoglycaemia presents with increased glucose requirements (>8 mg/kg/minute) and non-ketotic hypoglycaemia. Diagnosis confirmed by demonstrating raised/detectable insulin/C-peptide during hypoglycaemia. Genotyping may assist with not only diagnosis but direct therapy (medical and surgical).