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The first case of loss of bile as a result of the formation of an external biliary fistula was described in 1670 by Thilesus, and the formation of fistulas and bile loss, which is observed in 1/3 of patients with perforation of the gallbladder, was described in 1890 by Courvoisier. The loss of bile as a result of the formation of biliary fistulas was studied by I.L. Bregadze, Yu.V. Astrozhnikov and others.
Currently, many researchers distinguish: Preaholiya, latent and explicit (chronic) acholia, depending on the stage of development of the acholia syndrome. Mild, moderate and severe acholia, depending on the severity of the disease. Acholia compensated, subcompensated or decompensated, depending on the patient's condition. According to the presence of concomitant lesions of organs and systems, hepatopathy, encephalopathy, angiopathy, etc.
The bile produced by the cells of the liver parenchyma (hepatocytes) is secreted into the bile canaliculi and then into the gradually enlarging bile ducts.
Enveloping food masses with undissolved fat, as a result of which proteolytic and amylolytic enzymes are not able to break down proteins and carbohydrates. Normally acidic gastric sodaRye is neutralized by bile, which maintains an alkaline environment in the duodenum that is optimal for duodenal juice enzymes. Reducing the adsorption of enzymes from the contents of the intestine by intestinal cells, as a result of which parietal digestion is disturbed. Normally, the sorption properties of the intestinal epithelium are stimulated by bile acids.