{"title":"Diabetes mellitus","authors":"Gary Butler, Jeremy Kirk","doi":"10.1093/med/9780198786337.003.0005","DOIUrl":null,"url":null,"abstract":"\n\n\n • Diabetes mellitus is a chronic hyperglycaemia state, caused by defects in:\n \n\n\n ◦ insulin secretion\n \n\n ◦ insulin action\n \n\n ◦ both.\n \n\n • Type 1 diabetes accounts for ~95% of cases.\n \n\n\n ◦ Rising incidence in UK (25/100,000 children/year) now appears to be stabilizing.\n \n\n ◦ Peaks at younger age (4–6 years of age) and also puberty.\n \n\n • Therapy:\n \n\n\n\n\n ■ With subcutaneous insulin (multiple daily injections, continuous subcutaneous insulin infusion (CSII) (less used now, twice- and thrice-daily mixtures)) to mimic physiological secretion, maintain euglycaemia, minimize hypoglycaemic episodes and diabetic ketoacidosis.\n \n\n ◦ Monitoring:\n \n\n\n ■ Minimum of five self-monitored blood glucose measurements a day recommended. Continuous glucose monitoring increasingly utilized, especially with CSII.\n \n\n ■ Overall control assessed using glycated haemoglobin.\n \n\n • Outcome:\n \n\n\n ■ Clear evidence that good diabetic control associated with reduction in complications (micro- and macrovascular).\n \n\n ■ Screening recommended at an early stage to detect complications and prevent progression.\n \n\n • Type 2 diabetes:\n \n\n\n ◦ Increasingly recognized in children/adolescents.\n \n\n ◦ Increased incidence in:\n \n\n\n ■ females\n \n\n ■ ethnic minorities\n \n\n ■ overweight/obese\n \n\n ■ those with family history.\n \n\n ◦ Part of metabolic syndrome: T2DM/insulin resistance, hypertension, hyperlipidaemia, cardiovascular disease, adrenarche/polycystic ovarian syndrome.\n \n\n ◦ A combination of insulin resistance and (relative) insulin deficiency; oral hypoglycaemics may be appropriate (at least initially).\n \n\n • Other forms of diabetes (uncommon):\n \n\n\n ◦ Maturity-onset diabetes of the young (MODY):\n \n\n\n ■ autosomal dominant inheritance; dependent on type, variable\n \n\n ■ response to oral hypoglycaemics\n \n\n ■ development of microvascular complications.\n \n\n ◦ Association with syndromes, e.g. Wolfram, Walcott–Rallison, Prader–Willi syndrome.\n \n\n ◦ Cystic fibrosis-related diabetes:\n \n\n\n ■ not autoimmune in origin, due to combination of insulin deficiency/resistance\n \n\n ■ increasing incidence with age\n \n\n ■ treatment is with insulin.","PeriodicalId":217485,"journal":{"name":"Paediatric Endocrinology and Diabetes","volume":"125 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/9780198786337.003.0005","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
• Diabetes mellitus is a chronic hyperglycaemia state, caused by defects in:
◦ insulin secretion
◦ insulin action
◦ both.
• Type 1 diabetes accounts for ~95% of cases.
◦ Rising incidence in UK (25/100,000 children/year) now appears to be stabilizing.
◦ Peaks at younger age (4–6 years of age) and also puberty.
• Therapy:
■ With subcutaneous insulin (multiple daily injections, continuous subcutaneous insulin infusion (CSII) (less used now, twice- and thrice-daily mixtures)) to mimic physiological secretion, maintain euglycaemia, minimize hypoglycaemic episodes and diabetic ketoacidosis.
◦ Monitoring:
■ Minimum of five self-monitored blood glucose measurements a day recommended. Continuous glucose monitoring increasingly utilized, especially with CSII.
■ Overall control assessed using glycated haemoglobin.
• Outcome:
■ Clear evidence that good diabetic control associated with reduction in complications (micro- and macrovascular).
■ Screening recommended at an early stage to detect complications and prevent progression.
• Type 2 diabetes:
◦ Increasingly recognized in children/adolescents.
◦ Increased incidence in:
■ females
■ ethnic minorities
■ overweight/obese
■ those with family history.
◦ Part of metabolic syndrome: T2DM/insulin resistance, hypertension, hyperlipidaemia, cardiovascular disease, adrenarche/polycystic ovarian syndrome.
◦ A combination of insulin resistance and (relative) insulin deficiency; oral hypoglycaemics may be appropriate (at least initially).
• Other forms of diabetes (uncommon):
◦ Maturity-onset diabetes of the young (MODY):
■ autosomal dominant inheritance; dependent on type, variable
■ response to oral hypoglycaemics
■ development of microvascular complications.
◦ Association with syndromes, e.g. Wolfram, Walcott–Rallison, Prader–Willi syndrome.
◦ Cystic fibrosis-related diabetes:
■ not autoimmune in origin, due to combination of insulin deficiency/resistance
■ increasing incidence with age
■ treatment is with insulin.