Cholinesterase Cholinesterases hydrolyze acetylcholine and also other choline esters and thereby regulate nerve impulse transmission at the nerve synapse and neuromuscular junction. There are two types of cholinesterases: acetylcholinesterase, also known as “true cholinesterase,” and pseudocholinesterase. True cholinesterase exists primarily in the RBCs and nerve tissue. It is not in the serum. Pseudocholinesterase, on the other hand, exists in the serum. Deficiencies in either of these enzymes can be acquired or congenital.
Because succinylcholine (the most commonly used muscle relaxant during anesthesia induction) is inactivated by pseudocholinesterase, people with an inherited pseudocholinesterase enzyme deficiency exhibit increased and/or prolonged effects of succinylcholine. Patients with a genetic variant of pseudocholinesterase may have a nonfunctioning form of pseudocholinesterase and will also experience prolonged effects of succinylcholine administration. Prolonged muscle paralysis and apnea will occur after anesthesia in these patients. This situation can be avoided by measuring serum cholinesterase (pseudocholinesterase) on all patients with a family history of prolonged apnea after surgery. Because patients with a nonfunctioning variant of pseudocholinesterase will have normal total quantitative pseudocholinesterase levels and yet have prolonged paralytic effects of succinylcholine, usually a second test (dibucaine inhibition) is also performed. Dibucaine is a local anesthetic that inhibits the function of normal pseudocholinesterase. The dibucaine inhibition number is the percent of pseudocholinesterase activity that is inhibited when dibucaine is added to the patient’s serum sample. If total pseudocholinesterase is normal, and dibucaine numbers are low, the presence of a nonfunctioning pseudocholinesterase variant is suspected and the patient will be at risk for succinylcholine-induced prolonged paralysis.
A common form of acquired cholinesterase deficiency, either true or pseudocholinesterase, is caused by overexposure to pesticides or organophosphates. Persons with jobs associated with chronic exposure to these chemicals are often monitored by the frequent testing of RBC cholinesterase levels. Other potential causes of reduced cholinesterase levels include chronic liver diseases, malnutrition, and hypoalbuminemia. Increased cholinesterase levels, when found in the amniotic fluid, represent strong evidence for a neural tube defect.
Normal Serum Cholinesterase: 8 to 18 units/mL.
Normal Red Blood Cell Cholinesterase: 5 to 10 units/mL.
Normal Dibucaine Inhibition: 79%-84%
Because succinylcholine (the most commonly used muscle relaxant during anesthesia induction) is inactivated by pseudocholinesterase, people with an inherited pseudocholinesterase enzyme deficiency exhibit increased and/or prolonged effects of succinylcholine. Patients with a genetic variant of pseudocholinesterase may have a nonfunctioning form of pseudocholinesterase and will also experience prolonged effects of succinylcholine administration. Prolonged muscle paralysis and apnea will occur after anesthesia in these patients. This situation can be avoided by measuring serum cholinesterase (pseudocholinesterase) on all patients with a family history of prolonged apnea after surgery. Because patients with a nonfunctioning variant of pseudocholinesterase will have normal total quantitative pseudocholinesterase levels and yet have prolonged paralytic effects of succinylcholine, usually a second test (dibucaine inhibition) is also performed. Dibucaine is a local anesthetic that inhibits the function of normal pseudocholinesterase. The dibucaine inhibition number is the percent of pseudocholinesterase activity that is inhibited when dibucaine is added to the patient’s serum sample. If total pseudocholinesterase is normal, and dibucaine numbers are low, the presence of a nonfunctioning pseudocholinesterase variant is suspected and the patient will be at risk for succinylcholine-induced prolonged paralysis.
A common form of acquired cholinesterase deficiency, either true or pseudocholinesterase, is caused by overexposure to pesticides or organophosphates. Persons with jobs associated with chronic exposure to these chemicals are often monitored by the frequent testing of RBC cholinesterase levels. Other potential causes of reduced cholinesterase levels include chronic liver diseases, malnutrition, and hypoalbuminemia. Increased cholinesterase levels, when found in the amniotic fluid, represent strong evidence for a neural tube defect.
Causes of False Cholinesterase Test Findings
- Pregnancy normally decreases Cholinesterase levels in blood.
- It is important to recognize that pseudocholinesterase levels cannot be measured in postoperative patients in the recovery room if the patient is not regaining muscular function, because often one or more of the above drugs may be given during the surgery and could invalidate the results.
- Drugs that may cause decreased values include Atropine, Caffeine, Codeine, Estrogens, Morphine Sulfate, Neostigmine, Oral contraceptives, Hhenothiazines, Quinidine, Theophylline, Steroids, and Vitamin K. It is recomended to withhold these drugs for 12 to 24 hours before the test since they may alter the results of the test.
Normal Cholinesterase Findings
Normal Serum Cholinesterase: 8 to 18 units/mL.
Normal Red Blood Cell Cholinesterase: 5 to 10 units/mL.
Normal Dibucaine Inhibition: 79%-84%
Causes of High Cholinesterase Levels
- Reticulocytosis: Increased RBC precursors are associated with higher levels of true cholinesterase.
- Increased Cholinesterase Levels are observed without any known pathophysiological causes in patients with Hyperlipidemia, Nephrosis, and Diabetes.
Causes of False Cholinesterase Test Findings
- Poisoning from organic phosphate insecticides: These chemicals inhibit the activity of cholinesterases.
- Cholinesterases are not synthesized in persons with Congenital Enzyme Deficiency and patients who have Hepatocellular Disease.
- Malnutrition and other forms of hypoalbuminemia: Albumin is important in the transport and function of cholinesterases.
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