Cholinesterase, Blood

Cholinesterase is an enzyme that hydrolyzes the acetylcholine released at central and peripheral sites. Two types of cholinesterase are present; acetylcholinesterase, or true cholinesterase, and pseudocholinesterase. Acetylcholinesterase is found in large amounts in red cells and neurons. Pseudocholinesterase (PCHE) is present in serum, plasma, liver, pancreas, heart, and other tissues. Pseudocholinesterase is also known as butrylcholinesterase (BuChE) or plasmacholinesterase. 

Both plasma and tissue cholinesterase activity are markedly inhibited by organophosphate pesticides and herbicides, such as diazinon and malathion. Theoretically, acetylcholinesterase is the best enzyme to follow because its presence in red cells more accurately reflects enzyme concentration in the central nervous system. However, plasma PCHE can be measured more easily and is suppressed enough to be useful in the diagnosis of acute organophosphate toxicity. PCHE levels correlate fairly well with cholinergic signs and symptoms. Headache and fatigue are common in mild poisoning in which PCHE activity is inhibited 20 to 50%. Weakness, muscle fasciculation, and difficulty talking are symptomatic of moderate poisoning, in which PCHE activity is reduced 80 to 90%. In severe poisoning, when enzyme activity is inhibited more than 90%, patients present with coma, flaccid paralysis, and cyanosis.  

Pregnancy and liver disease can also cause a decrease in cholinesterase activity. Caution must be exercised when diagnosing pesticide or herbicide intoxication in the presence of these medical conditions.  

PCHE is also useful to evaluate patients who have experienced prolonged apnea after exposure to succinylcholine, a muscle relaxant used in surgery. Normally, cholinesterase rapidly hydrolyzes succinylcholine. Less than <1% of individuals have either atypical or Kalow variants that do not hydrolyze succinylcholine efficiently. Individuals, who are either homozygotes or compound heterozygotes, have very low levels of pseudocholinesterase activity that is not inhibited by dibucaine. These patients may develop prolonged muscle relaxation and apnea after the administration of succinylcholine.  

Reference ranges are:

Patients with normal pseudocholinesterase activity exhibit 70 to 90% enzyme inhibition with dibucaine while patients, who are homozygous or compound heterozygous for one of the variants, have <20% inhibition.

Pseudocholinesterase is measured by an enzyme assay. One red top tube of blood is required.

References

Trujillo R, West WP. Pseudocholinesterase Deficiency. [Updated 2023 Jul 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK541032/

Andersson ML, Møller AM, Wildgaard K. Butyrylcholinesterase deficiency and its clinical importance in anaesthesia: a systematic review. Anaesthesia. 2019 Apr;74(4):518-528.

Lurati AR. Organophosphate exposure with pseudocholinesterase deficiency. Workplace Health Saf. 2013 Jun;61(6):243-5.