Fast Facts: Type 1 Diabetes in Adults

J. Brake, P. Weston, R. Zaidi

Description

'Fast Facts: Type 1 Diabetes in Adults' provides a practical overview of this chronic autoimmune condition. Written by and for health professionals working in primary care, this colourful and accessible handbook highlights important practice points that cover: • the identification and management of adults with type 1 diabetes • the prevention and treatment of complications • advances in technology and future treatments An indispensable read for anyone wanting to get up to speed with best practice in primary care. Table of Contents: • Overview • Diagnosis • Management • Hypoglycemia • Education • Special circumstances • Complications • Living with the condition • Technology • Future treatments

Sujets

• Médecine
• Spécialités médicales
• Diabetes mellitus
• Diabetes
• Endocrinology

Informations

• Publié par: S. Karger AG
• Date de parution: 07 octobre 2021
• Nombre de lectures: 0
• EAN13: 9783318069167
• Langue: English
• Poids de l'ouvrage: 3 Mo

Extrait

Fast Facts: Type 1 Diabetes in Adults
First published 2021
Text 2021 Reza Zaidi, Philip Weston, Julie Brake
2021 in this edition S. Karger Publishers Ltd
S. Karger Publishers Ltd, Elizabeth House, Queen Street, Abingdon, Oxford OX14 3LN, UK
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All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the express permission of the publisher.
The rights of Reza Zaidi, Philip Weston and Julie Brake to be identified as the authors of this work have been asserted in accordance with the Copyright, Designs Patents Act 1988 Sections 77 and 78.
The publisher and the authors have made every effort to ensure the accuracy of this book, but cannot accept responsibility for any errors or omissions.
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Registered names, trademarks, etc. used in this book, even when not marked as such, are not to be considered unprotected by law.
A CIP record for this title is available from the British Library.
ISBN: 978-3-318-07000-2
Zaidi R (Reza)
Fast Facts: Type 1 Diabetes in Adults/ Reza Zaidi, Philip Weston, Julie Brake
Medical illustrations by Graeme Chambers, Belfast, UK.
Typesetting by Amnet, Chennai, India.
Printed in the UK with Xpedient Print.
List of abbreviations
Foreword
Introduction
Overview
Diagnosis
Management
Hypoglycemia
Education
Special circumstances
Complications
Living with the condition
Technology
Future treatments
Useful resources
Index
List of abbreviations
ACE: angiotensin-converting enzyme
AGP: ambulatory glucose profile
App: application
BMI: body mass index
CGM: continuous glucose monitoring
CKD: chronic kidney disease
C-peptide: connecting peptide
CVD: cardiovascular disease
DCCT: Diabetes Control and Complication Trial
DIY: do-it-yourself
DKA: diabetic ketoacidosis
DR: diabetic retinopathy
DVLA: Driver and Vehicle Licensing Agency
EDIC: Epidemiology of Diabetes Interventions and Complications
eGFR: estimated glomerular filtration rate
ESRD: end-stage renal disease
GAD: glutamic acid decarboxylase 65
GLP-1: glucagon-like peptide 1
GLUT: glucose transporter
HbA1c: glycated hemoglobin
HLA: human leukocyte antigen
IA-2: insulinoma-associated protein 2
ICR: insulin to carbohydrate ratio
IFCC: International Federation of Clinical Chemistry and Laboratory Medicine
IL: interleukin
ISF: insulin sensitivity factor
JDRF: Juvenile Diabetes Research Foundation
MDI: multiple-dose injection
MHC: major histocompatibility complex
NHS: National Health Service
NICE: National Institute for Health and Care Excellence
RNA: ribonucleic acid
SGLT2: sodium glucose co-transporter 2
SMBG: self-monitoring of blood glucose
Th: T helper cell
TNF : tumor necrosis factor
YDMV: your diabetes may vary
Foreword
Life expectancy for adults living with type 1 diabetes has increased over recent years but remains significantly shorter than for people without diabetes. Type 1 diabetes care has evolved at pace, yet the basic tenets remain the same: better self-management, improved peer support and access to good specialist care. New knowledge and treatment opportunities have arisen over the last decade, alongside developments in technology that have improved the ability of patients to self-manage their glucose levels and their condition. Nonetheless, important deficiencies in care remain, and it is essential that those involved in the care of adults with type 1 diabetes ensure that systems are in place to provide support, education and training for insulin users, as well as other biomedical services and interventions. Such systems include not only specialist care but also primary care, where a significant part of care is delivered. Fast Facts: Type 1 Diabetes in Adults provides busy primary care providers with concise, practical advice that is evidence-based and in line with current guidelines, enabling them to support adults with type 1 diabetes to avoid complications and live full, largely unrestricted lives.
Professor Partha S Kar OBE
National Specialty Advisor, Diabetes at NHS England
Consultant in Diabetes and Endocrinology at Portsmouth Hospitals NHS Trust
Introduction
Type 1 diabetes is a chronic autoimmune condition characterized by insulin deficiency and resultant hyperglycemia that is distinct from the more prevalent type 2 diabetes. The nomenclature has evolved from the early 20th century use of insulin-sensitive diabetes mellitus , through juvenile-onset and insulin-dependent diabetes mellitus in the 1950s, to the adoption of the type 1 diabetes terminology in the late 1990s. Over the last three decades, our knowledge of type 1 diabetes has increased rapidly because of better understanding of genetics, epidemiology and cell dysfunction. Major developments in diagnostic methods, monitoring tools and insulin delivery options have improved outcomes for people living with the condition; however, wide gaps still exist in our understanding of the condition and ability to standardize care across levels of healthcare.
In this resource, we cover the key areas of type 1 diabetes in adults as seen through the lens of multidisciplinary specialist medical professionals and, most importantly, an expert member of a family living with and around the condition. There is particular emphasis on recent developments in insulin pharmacokinetics, monitoring and therapeutic technology, and models of education.
This handbook will be ideal for all care providers across the healthcare spectrum and adults living with type 1 diabetes looking to raise awareness and broaden their understanding of this omnipresent condition, therapeutic modalities and potential complications. Through this book, we hope to improve advocacy and care, and positively impact healthcare outcomes and the quality of life of people living with type 1 diabetes.
Acknowledgment. The authors thank Dr Joan St John, London North West University Healthcare NHS Trust and North West London Diabetes Transformation programme, for helpful comments on the manuscript.
1
Overview
Normal physiology of insulin synthesis and action
Insulin is synthesized in and secreted exclusively from cells within the islets of Langerhans in the pancreas. 1 Synthesis begins with a larger precursor, preproinsulin, which is cleaved by proteases into proinsulin. This is further cleaved by enzymes into insulin and connecting peptide (C-peptide) ( Figure 1.1 ). The active insulin molecule consists of two polypeptide chains linked by disulphide bridges; the A chain has 21 amino acids and the B chain 30 amino acids.
Glucose is the main stimulator of insulin release, which occurs in a biphasic pattern: the first acute phase lasts a few minutes, followed by a sustained second phase . Glucose metabolism in the cell is governed by glucokinase activity that, in turn, determines the glucose-insulin dose-response curve. Half-maximal stimulation of insulin release occurs at a glucose level of 8 mmol/L (144 mg/dL) with no secretion at levels of 5 mmol/L (90 mg/dL) and below.
Glucose transporters. Insulin binds to a glycoprotein cell surface receptor, initiating the phosphorylation of amino acids by the enzyme tyrosine kinase. Glucose molecules are transported into cells via specialized proteins, the glucose transporters (GLUTs). With the exception of GLUT-4, transport by GLUTs is non-insulin-mediated in the muscles and adipose tissue.
Blood glucose levels are tightly controlled in people without diabetes at around 5 mmol/L (90 mg/dL) by the balance of glucose entry into the circulation from the liver and intestinal absorption, and peripheral uptake by muscle and adipose tissue. Insulin is secreted at a low, basal level in the non-fed/fasted state and 80% of glucose consumption is by the brain in a non-insulin-dependent manner.
At mealtimes, insulin secretion is stimulated to increase peripheral uptake of glucose, and liver glycogen breakdown (glycogenolysis) and the formation of new glucose from substrates such as glycerol, lactate and amino acids (gluconeogenesis) is reduced ( Figure 1.2 ). Insulin also directly reduces lipolysis and promotes lipogenesis in white adipose tissue.

Figure 1.1 Insulin biosynthesis showing the cleavage of proinsulin into insulin and C-peptide. Letters denote the different peptide chains. Adapted from Bilous and Donnelly 2010. 1
Evolution of type 1 diabetes
Insulin deficiency is the hallmark of type 1 diabetes. 2 Type 1a is caused by immune destruction of cells of the islets of Langerhans by autoantibodies. Type 1b is a rare form of idiopathic insulin deficiency that lacks evidence of an autoimmune etiology.
The most widely accepted hypothesis for the evolution of type 1 diabetes describes genetically susceptible individuals being exposed to putative environmental factors at a certain point in their lives ( Figure 1.3 ). These trigger a destructive T cell-mediated autoimmune process, resulting in diffuse lymphocytic infiltration of the islets, known as insulitis, and cell loss over a period of time. This results in the loss of the first phase of insulin response to intravenous glucose, insulin deficiency and, eventually, overt clinical diabetes because of severe abnormalities in the metabolism of carbohydrates, fat and protein. Although symptoms of hyperglycemia appear when approximately 90% of the cells are destroyed, there is evidence that residual insulin production can last for months and, in some cases, years after diagnosis.

Figure 1.2 Profiles of insul