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Causes of increased and decreased cholinesterase
Last reviewed: 06.07.2025
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Reference values (norm) of cholinesterase activity in blood serum are 5300-12900 IU/l.
There are two different enzymes of this type in human tissues: acetylcholinesterase (the "true" cholinesterase), which is localized primarily in nervous tissue, skeletal muscles, and, in low concentrations, in erythrocytes; and serum, or pseudocholinesterase, which is widespread, present in the liver, pancreas, and secreted by the liver into the blood. Serum cholinesterase is an enzyme that catalyzes the hydrolysis of acetylcholine.
Determination of cholinesterase activity in serum is of greatest clinical interest for the diagnosis of poisoning with organophosphorus toxic substances and insecticides, as well as an indicator of the state of the protein-synthetic function of the liver and for the detection of atypical variants of the enzyme (dibucaine-resistant form).
Poisoning with organophosphorus substances and insecticides is accompanied by a marked decrease in cholinesterase activity. It decreases sharply in severe chronic liver diseases, especially in cirrhosis. A significant decrease in cholinesterase activity is also observed in widespread blastomatous liver lesions. In the initial stages of obstructive jaundice, a decrease in cholinesterase activity is very rarely detected.
A sharp decrease in cholinesterase activity is a typical manifestation of impaired protein-synthetic function of the liver in patients with viral hepatitis during the development of acute liver failure, and the degree of its decrease is inversely proportional to the severity of the disease. The lowest indicators are noted in patients several days before the development of hepatic coma. However, the long half-life of serum cholinesterase (7-10 days) reduces its capabilities in the diagnosis of acute liver failure.
In myocardial infarction, a sharp decrease in cholinesterase activity is observed by the end of the first day of the disease, which is caused by shock, leading to severe liver damage.
Recently, the study of this enzyme has been widely used to control the use of muscle relaxants in surgical practice. Curare-like substances (suxamethonium iodide, etc.), used in surgery to relax muscles, are usually quickly destroyed, mainly by serum cholinesterase. Severe consequences of using these agents (prolonged apnea, cholinergic shock) are possible both with acquired cholinesterase deficiency (more often with chronic liver diseases) and with its congenital defect.
In nephrotic syndrome, an increase in cholinesterase activity is observed, which is associated with an increase in the synthesis of albumins by the liver due to the rapid loss of finely dispersed protein fraction in the urine. An increase in cholinesterase activity is also sometimes observed in obesity and exudative enteropathy.
A slight increase in cholinesterase activity is sometimes possible with arterial hypertension, diabetes mellitus, tetanus, chorea, manic-depressive psychosis, depressive neuroses, and anxiety.