• Ammonia in serum

    Ammonia is a product of protein metabolism, formed in all tissues. The largest amount of ammonia( 80%) is formed inside the intestines under the influence of bacteria. Nitrogenous compounds such as amino acids, uric acid, urea in the presence of bacterial enzymes( protease, urease, amine oxidase) are metabolized to ammonia. Ammonia is also formed in the cells of the intestinal mucosa from glutamine. Metabolism of ammonia to urea occurs in the liver during the ornithine cycle. This process can be disrupted both as a result of hyperproduction of ammonia in the intestine, so, due to a decrease in its conversion of

    to urea in liver pathology. The reference values ​​of ammonia in the blood serum are presented in the table.

    Table Reference values ​​for the concentration of ammonia( ammonia nitrogen) in the blood serum

    Table Reference values ​​for the concentration of ammonia( ammonia nitrogen) in the serum

    The determination of the concentration of ammonia in the blood in liver diseases is assigned the role of an indicatorshunting the liver( that is, a substance that normally comes from the intestine into the portal vein system and into the liver).In pathological conditions, with the development of venous collaterals, ammonia enters the system of general blood flow, bypassing the liver, and becomes, thus, an indicator of portal blood loss.

    In addition to shunted hyperammonemia, enzyme monomeremia is also observed. The latter develops when the systems involved in the conversion of ammonia( enzymes of the urea formation cycle) are disrupted. Basically, these disorders are registered in children and adolescents and are observed much less frequently by shunt. There are congenital and acquired enzymopathies leading to hyperammonemia. Congenital hyperlysinemia( defect of lysine dehydrogenase), propionic acidemia( defect of carboxylic acid of propionic acid), methylmalonium acidemia( defect of methylmalonyl mutase) and ornithmia( defect of ornithine kinase acid transaminase) belong to the congenital. Acquired fermentopathy refers to Reye's syndrome, in which there is a particularly high monemia-hyperemic( 3-5 times higher than normal).

    Increase in the concentration of ammonia in blood serum naturally occurs with cirrhosis of the liver. With cirrhosis of the liver without encephalopathy, the concentration of ammonia in the blood usually increases by no more than 25-50% compared with the upper limit of the norm, and with the development of encephalopathy - by 50-100%.

    Often an increase in the concentration of ammonia is noted in viral hepatitis. Expressed hyperamonia in these patients occurs with the development of acute liver failure, which is explained by the development of massive necrosis of the liver. Synthesis of urea from ammonia is disrupted if more than 80% of the parenchyma of the liver is damaged. An increase in ammonia in the blood of is also observed in liver cancer, chronic active hepatitis, fatty degeneration, and the intake of certain drugs( barbiturates, narcotic analgesics, furosemide, etc.).