This form of diabetes, previously encompassed by the terms insulin–dependent diabetes, Type 1 diabetes, or juvenile– onset diabetes, results from autoimmune mediated destruction of the beta cells of the pancreas. The rate of destruction is quite variable, being rapid in some individuals and slow in others. The rapidly progressive form is commonly observed in children, but also may occur in adults. The slowly progressive form generally occurs in adults and is sometimes referred to as latent autoimmune diabetes in adults (LADA). Some patients, particularly children and adolescents, may present with ketoacidosis as the first manifestation of the disease. Others have modest fasting hyperglycaemia that can rapidly change to severe hyperglycaemia and/or ketoacidosis in the presence of infection or other stress. Still others, particularly adults, may retain residual beta–cell function, sufficient to prevent ketoacidosis, for many years. Individuals with this form of Type 1 diabetes often become dependent on insulin for survival eventually and are at risk for ketoacidosis. At this stage of the disease, there is little or no insulin secretion as manifested by low or undetectable levels of plasma C–peptide.
Markers of immune destruction, including islet cell autoantibodies, and/or autoantibodies to insulin, and autoantibodies to glutamic acid decarboxylase (GAD) are present in 85–90 % of individuals with Type 1 diabetes mellitus when fasting diabetic hyperglycaemia is initially detected. The peak incidence of this form of Type 1 diabetes occurs in childhood and adolescence, but the onset may occur at any age, ranging from childhood to the ninth decade of life. There is a genetic predisposition to autoimmune destruction of beta cells, and it is also related to environmental factors that are still poorly defined. Although patients are usually not obese when they present with this type of diabetes, the presence of obesity is not incompatible with the diagnosis. These patients may also have other autoimmune disorders such as Graves’ disease,
Hashimoto’s thyroiditis, and Addison’s disease.
Markers of immune destruction, including islet cell autoantibodies, and/or autoantibodies to insulin, and autoantibodies to glutamic acid decarboxylase (GAD) are present in 85–90 % of individuals with Type 1 diabetes mellitus when fasting diabetic hyperglycaemia is initially detected. The peak incidence of this form of Type 1 diabetes occurs in childhood and adolescence, but the onset may occur at any age, ranging from childhood to the ninth decade of life. There is a genetic predisposition to autoimmune destruction of beta cells, and it is also related to environmental factors that are still poorly defined. Although patients are usually not obese when they present with this type of diabetes, the presence of obesity is not incompatible with the diagnosis. These patients may also have other autoimmune disorders such as Graves’ disease,
Hashimoto’s thyroiditis, and Addison’s disease.
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