Abstract
Before the discovery of insulin and the critical role of the pancreas vis-à-vis diabetes mellitus pathophysiology, childhood diabetes or what we now call type 1 or autoimmune diabetes mellitus was almost universally fatal. In limited-resource countries (LRC) around the world, this remains sadly true because of the expense and unavailability of medical care, medical information, and/or medications. In 1889, Minkowski and Mering identified the pancreas as the likely source of the problem in pancreatectomized dog experiments, and Langerhans, working with Virchow, identified the islands of pancreatic tissue now named after Langerhans as the likely source of the problem. Prior to that, Cawley, Boucherdat, Zuelzer, Gley, de Meyer, Schafer, Scott, Kleiner, and Paulescu all worked on this problem with varying results until Banting, Best, MacLeod, and Collip in Toronto in 1921 successfully treated pancreatectomized dogs with an alcohol-based pancreatic extract and then were the first to do the same with children and adults with diabetes, starting with Leonard Thompson in early 1922. Urinary and blood glucose levels were reduced, and clinical symptoms decreased concurrently. The magnificent medical historical work by Professor Michael Bliss, also from Toronto, as well as an excellent US NPR Television documentary, describes the trials and tribulations of this event that culminated in the “fastest Nobel Prize” awarded. Progressive biopharmaceutical advances have modified insulin from pigs and cows and then genetically engineered insulin to work much faster and also much slower to provide more modernized ways of providing insulin. Insulin pens then replaced vial and syringe administration, and then insulin pumps coupled with continuous blood glucose sensors have made delivery more physiologic in addition to more attention paid to nutrition advice, education, and psychosocial support around the world. Programs to assist delivery of expensive insulin to LRC administered by Insulin for Life, Life for a Child (LFAC), Changing Diabetes in Children (CDIC) coupled with support by ISPAD (International Society for Pediatric and Adolescent Diabetes) have continued to make such advances available thorough wonderful philanthropy in insulin manufacturers and manufacturers of blood glucose monitoring equipment and insulin pump/sensor suppliers.
Highlights
Insulin AnalogsDuring the 1980s and 1990s, insulin analogs became available as molecular scientists deciphered the actual alpha and beta chain molecular structure of insulin and its connecting peptide from the proinsulin molecule
Before the discovery of insulin and the critical role of the pancreas vis-à-vis diabetes mellitus pathophysiology, childhood diabetes or what we call type 1 or autoimmune diabetes mellitus was almost universally fatal
In financially distressed parts of the world where medical care is minimally available or just too expensive or too far away, not much has changed about diabetes mellitus for children and adolescents until programs such as Changing Diabetes in Children and Life for a Child as well as Insulin for Life offered hope and insulin—sometimes offering trained diabetes staff, glucose meters, test strips, and lancets—in recent years [1]
Summary
Hoechst began clinical trials in 1998 with what was called HOE 901, later glargine insulin. Increase the bedtime glargine or detemir; With the expectation that only 10–20% of pediatric and adolescent patients provided bedtime glargine or detemir alone will have sufficient basal insulin effect to last a full 24 h, expect that some morning glargine or detemir will be added based on late afternoon–evening hyperglycemia; When the morning basal insulin is added, expect the evening glargine or detemir dose to be decreased by approximately an equal amount; Understand that sometimes the reverse pattern occurs and more morning glargine or detemir is needed than evening basal analog; in some individuals, the morning and bedtime long-lasting analog doses are equal, but this is a smaller portion of patients; Once the overall pattern of basal insulins is established, go back and fine-tune to adjust the prandial fast-acting analogs by looking at pre and postprandial glycemic excursions with reminders about appropriate pre-meal timing of analog doses to actual timing of when food is ingested (usually about 15 min); Sometimes there is a need to change the bedtime basal insulin to suppertime when there is a more prolonged peak from the glargine or detemir; If there is a large morning or afternoon snack, these may need prandial bolus insulin analog coverage according to activity and BG results; Many no longer need mid-morning, mid-afternoon, or even bedtime snacks because of the relatively peakless nature of the basal insulin compared to the stronger NPH peaks used previously, and so calories can be cut back, and these snacks eliminated. As Sperling elegantly has written [51], the difficulties of type 1 diabetes remain with the inherent variability of food ingested, changes in activity from day-to-day, vagaries of insulin absorption and effect metabolically, counter-regulatory responses, and the ongoing potential dangers and fears of hypoglycemia; what he has called the Scylla and Charybdis of blood glucose control in children but this is somewhat lessened with the newest analogs compared to earlier preparations
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