E-Book, Englisch, 408 Seiten, ePub
Ziegler / Gries / Andersen Textbook of Diabetic Neuropathy
1. Auflage 2002
ISBN: 978-3-13-257865-4
Verlag: Thieme
Format: EPUB
Kopierschutz: 6 - ePub Watermark
E-Book, Englisch, 408 Seiten, ePub
ISBN: 978-3-13-257865-4
Verlag: Thieme
Format: EPUB
Kopierschutz: 6 - ePub Watermark
Awareness of neuropathy as a chronic complication of diabetes is constantly increasing. Diabetes centers adopt methods to diagnose neuropathy without neurological training. This trend calls for instructions on how to use and interpret diagnostic methods. This book includes recent research and covers clinical, technical, and public health aspects of neuropathy, bringing together the top experts in the field.
Zielgruppe
Ärzte
Autoren/Hrsg.
Fachgebiete
Weitere Infos & Material
1 Diabetes Mellitus: An Introduction
2 Structure and Function of the Nervous System
3 Epidemiology of Diabetic Neuropathy
4 Pathogenesis and Pathology of Diabetic Neuropathy
5 Clinical Features and Treatment of Diabetic Neuropathy
6 Socioeconomic Aspects
7 Recommendations for Structured Care
Guidelines for the Diagnosis and Outpatient Management of Diabetic Peripheral Neuropathy
1 Diabetes Mellitus: An Introduction F.A. Gries, J. Eckel, P. Rösen, and D. Ziegler The aim of this introduction is to provide a general understanding of diabetes mellitus and its impact on the diabetic individual. It will focus on aspects of epidemiology, pathobiochemistry, prevention, and therapy. Given the scope covered, selectivity and bias of topics and citations have been accepted as unavoidable. Definition The term “diabetes mellitus” comprises a number of chronic diseases characterized by hyperglycemia due to absolute or relative insulin deficiency. Hyperglycemia is only the most obvious biochemical marker of complex metabolic disorders that affect carbohydrate, lipid, protein, and electrolyte metabolism and may impair numerous organs and functions of the organism. Diagnosis The diagnosis of diabetes mellitus is based on classical symptoms (weight loss, polyuria, thirst, muscular weakness and fatigue) and persistent hyperglycemia. Glucosuria and elevated glycosylated hemoglobin (HbAlc) levels should not be used for diagnosis. The criteria for diagnosis of hyperglycemia and the classification of diabetes mellitus are not uniformly accepted. Some physicians use the criteria of the United States National Diabetes Data Group of 1979 [1], which was endorsed by the World Health Organization Study Group on Diabetes Mellitus in 1985 [2], while others prefer the criteria of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus of the American Diabetes Association 1998 [3] (Table 1.1). The criteria published in 1998 tend to diagnose diabetes in younger and more obese subjects than the WHO 1985 criteria, while subjects with postprandial hyperglycemia, microalbuminuria, and those with other predictors of cardiovascular disease are less likely to receive this diagnosis despite the fact that they are at similar risk of premature death [4–8]. Classification The diabetes mellitus classification of 1979 [1] was based “in large part on the pharmacological treatment used in its management.” This was reflected in the terms “insulin-dependent diabetes mellitus” (IDDM) and “non-insulin-dependent diabetes mellitus” (NIDDM) and the further subdivision of patients with the latter into obese and nonobese. The typing of 1998 is based on etiology and pathogenetic mechanisms (Table 1.2). About 50 different types of diabetes mellitus have been identified, the majority of cases being type 1, type 2, or gestational diabetes mellitus. Table 1.1 Criteria for the diagnosis of diabetes according to the World Health Organization [2] and the American Diabetes Association [3] World Health Organization American Diabetes Association Clinical: Increased thirst and urine volume, unexplained weight loss, established by casual blood glucose Polyuria, polydipsia and unexplained weight loss plus casual plasma or capillary blood glucose = 200 mg/dl (11.1 mmol/l) or or Biochemical: Casual venous plasma glucosea > 200mg/dl (11.1 mmol/l), fasting venous or capillary plasma glucose b = 140 mg/dl (7.8 mmol/l) and 2 h venous or capillary plasma or capillary whole blood glucose c = 200 mg/dl (11.1 mmol/l) after glucose loadd Fasting plasma glucose = 126 mg/dl (7.0 mmol/l) or capillary blood glucose = 110 mg/dl or 2 h plasma or capillary blood glucose = 200 mg/dl (11.1 mmol/l) during an oral glucose tolerance test a Values for capillary plasma > 220 mg/dl, for venous whole blood >180 mg/dl. for capillary whole blood > 200 mg/dl b Value for venous and capillary whole blood = 120 mg/dl c Value for venous whole blood = 180 mg/dl d Performed as described by WH01985 [2] using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water There is a great similarity between type 1 diabetes and IDDM and between type 2 diabetes and NIDDM. However, these pairs of terms should not be used indiscriminately as being respectively synonymous. Type 1 diabetes mellitus may for a limited time after manifestation remain non-insulin-dependent, particularly when it begins in an adult (latent autoimmune diabetes in adults. LADA; see page 10). On the other hand, NIDDM, like any type of diabetes mellitus, may become insulin-dependent at an advanced or critical stage. Epidemiology Epidemiological research on diabetes mellitus is hampered by methodological problems. The criteria and methods for both the diagnosis and the classification of diabetes mellitus have changed over time. Population-based studies are rare, studies based on subgroups are usually biased, and even random samples are not always representative. The epidemiology of diabetes mellitus shows considerable regional variation, so that when data from different regions are compared, the ethnicity, gender, and age structure of the groups that had been studied need to be considered-but frequently these have not been communicated. These problems are more relevant to studies on type 2 respectively NIDDM than type 1 respectively IDDM. Type 1 Diabetes/IDDM The incidence of IDDM varies considerably with geography and ethnicity. In Japan, China, and in African Americans the incidence (number of new cases per 100 000 person-years) in the age group of 0-14 years is below 5. In most European regions it is about 1020 per 100 000 person-years, and in Finland and Sardinia it is above 30 [2,9,10,11]. The highest incidence of IDDM is found in children below the age of 15, but IDDM or type 1 diabetes may become manifest at any age. The estimated incidence in adults is about half that observed in children of the respective population. However, the figure may be much higher if cases of LADA are included, which may comprise about 10% of all patients initially diagnosed as having type 2 diabetes mellitus [12]. Worldwide a trend to increasing incidence in children and adolescents has been observed [13–15]. According to a Finnish study the incidence is increasing more in younger than older age groups [16]. Firstborn children are at highest risk. The risk increases with the age of the mother [17]. Table 1.2 Shortened version of the classification of diabetes according to the Expert Committee on the Diagnosis and Classification of Diabetes mellitus [3] I. Type 1 diabetes (ß-cell destruction, usually leading to absolute insulin deficiency) A. Immune-mediated B. Idiopathic II. Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance) III. Other specific types A. Genetic defects of ß-cell function B. Genetic defects in insulin action C. Disease of the exogenic pancreas D. Endocrinopathies E. Drug- or chemical-induced F. Infections G. Uncommon forms of immune-mediated diabetes H. Other genetic syndromes sometimes associated with diabetes IV. Gestational diabetes (GDM) Reliable data about the prevalence of IDDM/type 1 diabetes mellitus are not available. Type 1 diabetes is associated with genetic as well as environmental factors. The rising incidence can hardly be explained by a change in the gene pool, so environmental factors must be playing a major role. However, it is impossible at present to decide what these environmental factors are. The life expectancy of IDDM subjects is reduced. The number of lost years of life depends on the age at diagnosis (it is highest in early-onset IDDM) and on the quality of care as well as on chronic complications [18–20]. In the USA, mortality “among males was 5.4 times higher and in females it was 11.5 times higher than in the total US population.” “Among people with age at diagnosis < 30 years, IDDM reduces life expectancy by at least 15 years.” In 70-90% the cause of death is related to diabetes [21]. In long-term type 1 diabetes vascular complications are the most important predictors and causes of death[22–24] (Table 1.3). In the USA, ketosis has been the cause of death in about 10% of people with IDDM who died at 0-44 years of age. Hypoglycemia may be the undiagnosed cause of sudden death. It was noted as an underlying cause of death in about 1 of 300 deaths due to diabetes [25]. Others have estimated that 2-4% of all deaths in IDDM subjects are due to hypoglycemia [26]. Type 2 Diabetes/NIDDM Type 2 diabetes mellitus is by far the most common type of diabetes. By extrapolation from the incidence of diabetic retinopathy in recently diagnosed subjects it may be concluded that the disease will manifest a couple of years before it is diagnosed. Most cases are diagnosed in individuals...
