Product Description:
Hardcover: 381 pages
Publisher: S. Karger AG (Switzerland); 1 edition (June 2005)
Language: English
ISBN-10: 3805577664
ISBN-13: 978-3805577663
Editors:
F. Chiarelli Chieti
K. Dahl-Jørgensen Oslo
W. Kiess Leipzig
Diabetes mellitus is one of the most frequent chronic diseases affecting children and adolescents. The number of young children being diagnosed with type 1 diabetes is increasing worldwide and an epidemic of type 2 diabetes already at a young age is being observed in most societies around the world. In this book, leading experts from the USA, Europe and Israel provide a state-of-the-art summary of today's knowledge in the field of pediatric and adolescent diabetes. A number of excellent chapters deliver insight into the basic understanding of which factors contribute to or prevent the development of diabetes in young people. Other contributions provide tools for the clinician to manage the care of the child and adolescent with diabetes. In addition, knowledge from the latest scientific studies on the molecular biology of diabetes is also presented. It provides a summary of the most recent scientific discoveries related to pediatric and adolescent diabetes.
Contents:
Preface
- Etiopathogenetic Aspects of Type 1 Diabetes
- Susceptibility to Type 1 Diabetes: Genes and Mechanisms
- Autoimmunity in Type 1 Diabetes mellitus
- Neonatal Diabetes mellitus
- Diagnosis and Management of MODY in a Pediatric Setting
- Diabetic Ketoacidosis
- Insulin Treatment
- Medical Nutrition Therapy of Children and Adolescents with Diabetes
- Continuous Subcutaneous Insulin Infusion in Childhood and Adolescence
- Quality Management in Pediatric Diabetology
- Sports and Physical Activity in Children and Adolescents with Type 1 Diabetes mellitus
- Invasive and Noninvasive Means of Diabetes Self-Management
- Adolescence
- Diabetic Nephropathy in Children and Adolescents
- Diabetic Autonomic and Peripheral Neuropathy
- Macrovascular Disease
- Hypoglycemia in Children and Adolescents with Type 1 Diabetes
- Diabetic Retinopathy in Children and Adolescents with Type 1 Diabetes
- Complications and Consequences
- Type 2 Diabetes mellitus in Childhood
- Beta-Cell Function Replacement by Islet Transplantation and Gene Therapy
Subject Index
Chapter 1:
Etiopathogenetic Aspects of Type 1 Diabetes
Mikael Knip
Hospital for Children and Adolescents, University of Helsinki, Helsinki, and Department of Paediatrics, Tampere University Hospital, Tampere, Finland
Type 1 diabetes is perceived as a chronic immune-mediated disease with a subclinical prodromal period characterized by selective loss of insulin-producing B-cells in the pancreatic islets in genetically susceptible subjects. The most important genes contributing to disease susceptibility are located in the HLA class II locus on the short arm of chromosome 6 [1]. Nevertheless, only a relatively small proportion, i.e. less than 10%, of genetically susceptible individuals progress to clinical disease. This implies that additional factors are needed to trigger and drive B-cell destruction in genetically predisposed subjects. Clinical type 1 diabetes represents end-stage insulitis, and it has been estimated that at the time of diagnosis only 10–20% of the insulin-producing B-cells are still functioning. Environmental factors have been implicated in the pathogenesis of type 1 diabetes both as triggers and potentiators of B-cell destruction [2–4], although the contribution of any individual exogenous factor has not been definitely proven so far.
Natural History of Type 1 DiabetesThe clinical presentation of type 1 diabetes is preceded by an asymptomatic period of variable duration [5]. Aggressive B-cell destruction may lead to disease manifestation within a few months in young children, while in other individuals the process will continue for years, in some cases even for more than 10 years, before the eventual presentation of clinical disease. The appearance of diabetes-associated autoantibodies is the first detectable sign of emerging B-cell autoimmunity. There are four disease-related
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