Hyperinsulinism is a pathological condition of the body, caused by an absolute or relative excess of insulin, causing a strong decrease in blood sugar, resulting in glucose deficiency and oxygen starvation of the brain, leading to a violation of the higher nervous activity in the first place.

Etiology and pathogenesis. The most common cause of pancreatic hypoglycemia is hyperinsulinism, caused by adenoma (often benign, less often malignant) and rarely, diffuse adenomatous hyperplasia of p-cell pancreatic islets. Non-pancreatic hypoglycemia develops due to liver and gastrointestinal diseases (liver cirrhosis, cholangitis, cholecystitis, etc.), endo-crine system (damage to the pituitary, thyroid and adrenal glands), metabolic disorders (renal glucose, malnutrition, pregnancy and lactation, etc.). Non-pancreatic hypoglycemia can occur in disorders of the central and autonomic nervous systems, as well as in extra pancreatic tumors.

Hyperinsulinism can be absolute, that is, associated with any pathology of the insular apparatus (primary organic hyperinsulinism; in children with congenital non-tolerance of the amino acid leucine, stimulating insulin secretion, etc.) and relative, not related to pathology insular apparatus of the pancreas (secondary, functional, symptomatic hyperinsulinism). Relative hyperinsulinism is due to the increased sensitivity of the organism to insulin normally secreted by p-cells of the pancreatic islets.

Insufficient blood sugar (neurogenic anorexia, pyloric stenosis, renal glucosuria, high exercise, etc.) or impaired compensatory mechanisms involved in the regulation of carbohydrate metabolism and insulin inactivation (marked hypofunction of the anterior lobe) can lead to a relative excess of insulin. hypophysis, adrenal cortex, thyroid gland, functional liver insufficiency, liver cirrhosis, C (C, C) injury.

Hypoglycemic conditions can sometimes occur with the development of Zollinger-Ellison syndrome (ulcerous, non-p-cell adenoma emanating from pancreatic islets) in patients with its combination with insulin-secreting adenoma of pancreatic islets. Diffuse adenomatosis of the insular apparatus of the pancreas was observed in this syndrome in 10% of cases. Hypoglycemic conditions can also occur when patients develop extrapancreatic tumors located in the abdominal or thoracic cavity and in the retroperitoneal space. Histologically, these tumors are divided into mesodermal (fibrosarcoma, retroperitoneal neural mesothelioma, etc.) and epithelial (hepatoma, adrenal carcinoma, etc.).

When extrapancreatic In hypothelium, hypoglycemic states develop, probably due to the release of some substances other than insulin and potentiating the action of insulin by these tumors. It is assumed that these substances are a component of nucleic acids or tryptophan conversion products. The development of hypoglycemia in these patients, apparently, in some cases is also associated with an increase in metabolism in the tumor and an increase in the absorption of glucose from the blood, as well as with the release of substances with an insulin-like property by the tumor.

local_offerevent_note March 3, 2019

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