Cholinesterase (Pseudocholinesterase) and Dibucaine Inhibition


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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.

  • Normal range:

    • 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


Increased In

  • Type IV hyperlipoproteinemia

  • DM

  • Hyperthyroidism

  • Insecticide exposure (organophosphates)

  • Nephritic syndrome

  • Psychosis

  • Breast cancer

Decreased In

  • Genetic PChE variants

  • Severe pernicious anemia (PA), aplastic anemia

  • Cirrhosis

  • CHF (causing liver disease)

  • Hepatic carcinoma

  • Malnutrition

  • Acute infections and burns

  • AMI, pulmonary embolism

  • Muscular dystrophy

  • After surgery

  • 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.