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What causes diabetes in children?
Last reviewed: 23.04.2024
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Causes of diabetes in children
It is suggested that in the development of diabetes mellitus, both genetic predisposition and environmental factors are important. Hereditary predisposition to type 1 diabetes is associated with an unfavorable combination of normal genes located in different loci on different chromosomes, most of which control various parts of autoimmune processes in the body. More than 95% of patients with type 1 diabetes have HLA-DR3, -DR4 or -DR3 / DR4 alleles. A high degree of predisposition to type 1 diabetes mellitus is carried by combinations of certain allelic variants of HLA-DQh DR-genes.
In addition, various environmental factors are involved in the pathogenesis of diabetes. Most of these factors are unknown, but viral infections (enterovirus, rubella virus) and nutritional factors (eg, cow's milk in early childhood) can become triggers triggering an autoimmune process in predisposed individuals. The immunological process leading to the manifestation of type 1 diabetes mellitus begins years before the onset of clinical symptoms of the disease. During this pre-diabetic period, elevated titers of various autoantibodies to islet cells (ICA) and insulin (IAA) or to a protein found in islet cells, to GAD (glutamate decarboxylase) can be detected in the blood in patients.
Pathogenesis of diabetes mellitus
Six stages are distinguished in the development of the disease.
- I stage - the genetic predisposition associated with HLA.
- II stage - the effect of the factor provoking autoimmune insulitis.
- III stage - chronic autoimmune insulitis.
- Stage IV - partial destruction of beta cells. Reduced secretion of insulin to the introduction of glucose while maintaining basal glycemia (fasting).
- V stage - clinical manifestation of the disease with residual insulin secretion.
- Stage VI - complete destruction of beta cells, absolute insulin deficiency.
Deficiency of insulin leads to a decrease in the transport of glucose to liver cells, fat and muscle tissue, an increase in hyperglycemia. Mechanisms for the formation of endogenous glucose in the liver are activated to compensate for energy deficiency.
Under the influence of "counterinsular" hormones (glucagon, adrenaline, GCS), glycogenolysis, gluconeogenesis, proteolysis, lipolysis are activated. Increases in hyperglycemia, increased blood levels of amino acids, cholesterol, free fatty acids, exacerbated by energy deficits. At a glycemia level above 9 mmol / l, glucosuria appears. Osmotic diuresis develops, which in turn leads to polyuria. Dehydration and polydipsia. Insulin deficiency and hyperglucagonemia promote the conversion of fatty acids into ketones. Accumulation of ketones leads to metabolic acidosis. Ketones, excreted in urine along with cations, increase the loss of water and electrolytes. Increasing dehydration, acidosis, hyperosmolality and oxygen deficiency lead to the development of diabetic coma.