Medical expert of the article
New publications
The causes of increase and decrease in cholinesterase
Last reviewed: 19.10.2021
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
The reference values (norm) of cholinesterase activity in serum are 5300-12900 IU / l.
Two different enzymes of this type are present in human tissues: acetylcholinesterase ("true" cholinesterase), localized mainly in the nervous tissue, skeletal muscles and, in low concentration, in erythrocytes; and whey, or pseudocholinesterase, which is widely distributed, present in the liver, pancreas, secreted by the liver in the blood. Serum cholinesterase is an enzyme that catalyzes the hydrolysis reaction of acetylcholine.
Determination of cholinesterase activity in the serum is of the greatest clinical interest for the diagnosis of organophosphorous poisoning and insecticide poisoning, as well as an indicator of the status of the protein-synthetic function of the liver and for the detection of atypical variants of the enzyme (dibucaine-resistant form).
Poisoning with organophosphorous substances and insecticides is accompanied by a marked decrease in cholinesterase activity. It sharply decreases in severe chronic liver diseases, especially with cirrhosis. A significant decrease in cholinesterase activity is also observed with widespread blastomatous liver lesions. In the initial stages of obstructive jaundice, the decrease in cholinesterase activity is very rarely detected.
A sharp decrease in cholinesterase activity is a typical manifestation of a violation of protein-synthetic liver function in patients with viral hepatitis in the development of acute hepatic insufficiency, while the degree of its decrease is inversely proportional to the severity of the disease. The lowest values are noted in patients a few days before the development of the hepatic coma. Nevertheless, the long half-life of serum cholinesterase (7-10 days) reduces its ability to diagnose acute hepatic insufficiency.
With myocardial infarction, a sharp decrease in cholinesterase activity is noted towards the end of the first day of the disease, which is caused by a shock leading to severe liver damage.
Recently, the study of this enzyme is widely used to monitor the use of relaxants in surgical practice. Kurarepodobnye substances (suxamethonium iodide, etc.), used in surgery to relax the muscles, are usually quickly destroyed, mainly by cholinesterase of blood serum. Severe consequences of the use of these drugs (prolonged sleep apnea, cholinergic shock) are possible both with the acquired cholinesterase insufficiency (more often with chronic liver diseases) and with its inherent defect.
With nephrotic syndrome, an increase in cholinesterase activity is observed, which is associated with an increase in the synthesis of albumin by the liver due to the rapid loss of the finely dispersed fraction of proteins in the urine. An increase in cholinesterase activity is also sometimes observed with obesity and exudative enteropathy.
A slight increase in cholinesterase activity is sometimes possible with arterial hypertension, diabetes, tetanus, chorea, manic-depressive psychosis, depressive neuroses, anxiety.