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Subject: Cholinesterase (Pseudocholinesterase) and Dibucaine Inhibition
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Cholinesterase is an enzyme that catalyzes the hydrolysis of the neurotransmitter Ach into choline and acetic acid, a reaction necessary to allow a cholinergic neuron to return to its resting state after activation.
Serum cholinesterase, often called pseudocholinesterase or PChE, is distinguished from acetylcholinesterase (AChE or “true cholinesterase”) by both location and substrate.
PChE is found primarily in the liver.
AChE, also known as RBC cholinesterase, erythrocyte cholinesterase, or Ach acetylhydrolase, is found primarily in the blood and neural synapses.
The difference between the two types of cholinesterase has to do with their respective preferences for substrates: AChE hydrolyzes Ach more quickly, and PChE hydrolyzes butyrylcholine more quickly.
Phenotype interpretation is based on the total PChE activity and the percent of inhibition caused by dibucaine. Although there are >25 different phenotypes, most are extremely rare. Patients with unusual phenotypes cannot metabolize succinylcholine or mivacurium in the normal fashion; therefore, these patients can have prolonged paralysis following the use of these drugs.
Other names: choline esterase II, SChE, Ach acylhydrolase, butyrylcholinesterase (BChE), dibucaine inhibition, and plasma cholinesterase.
Pseudocholinesterase, total: 2,900–7,100 U/L
Dibucaine inhibition: 70–90% (congenital deficiency 18–20%)
Monitoring exposure to organophosphorus insecticides
Monitoring patients with liver disease, particularly those undergoing liver transplantation
Identifying patients who are homozygous for the atypical gene and have low levels of PChE that are not inhibited by dibucaine
Identifying patients, who are heterozygous for the atypical gene and have lower than normal levels of PChE and varying levels of inhibition with dibucaine
Type IV hyperlipoproteinemia
Insecticide exposure (organophosphates)
Genetic PChE variants
Severe pernicious anemia (PA), aplastic anemia
CHF (causing liver disease)
Acute infections and burns
AMI, pulmonary embolism
Chronic renal disease
PChE levels are not to be confused with AChE levels. PChE levels are earlier indicators than AChE levels of organophosphate exposure.
Patients with normal PChE activity show 70–90% inhibition by dibucaine, whereas patients homozygous for the abnormal allele show little or no inhibition (0–20%) and usually low levels of enzyme. Heterozygous patients have intermediate PChE levels and response to inhibitors.
Dibucaine inhibition is no value over total PChE, for the diagnosis of organophosphorus pesticide exposure.
Anabolic steroids, carbamates, cyclophosphamide, estrogens, glucocorticoids, lithium, neuromuscular relaxants, oral contraceptives, organophosphorus insecticides, and radiographic agents decrease the circulating levels.
Serum separator tubes, citrate anticoagulants, detergents, and heavy metals also decrease the serum levels.