CHOLINESTERASE RBC

Erythrocyte cholinesterase is measured to diagnose organophosphate and carbamate toxicity and to detect atypical forms of the enzyme. Cholinesterase is irreversibly inhibited by organophosphate insecticides and reversibly inhibited by carbamate insecticides. Serum or plasma pseudocholinesterase is a better measure of acute toxicity, while erythrocyte levels are better for chronic exposure. (Serum level returns to normal prior to normalizing of red cell level). The cholinesterase activity in human red cells is highly but not exclusively specific for acetylcholine. It is referred to as true or specific cholinesterase. Cholinesterase activity present in the serum/plasma hydrolyses both choline and aliphatic esters, has a broader range of esterolytic activity, and is referred to as "pseudo-" or "nonspecific" cholinesterase. It hydrolyses acetylcholine only slowly. The systematic name for acetylcholinesterase is acetylcholine acetylhydrolase. Systematic name for cholinesterase (serum/plasma) is acylcholine acylhydrolase. The different nature of the cholinesterases was first described in 1940.[1] The plasma enzyme is synthesized by the liver, the red cell enzyme during erythropoiesis. The enzyme is a large complex protein. There is evidence that it has a multiple subunit structure, four peptide chains that form two dimers. Because of the many constituent amino acids, many molecular variants are possible. The RBC level is INCREASED in hemolytic states such as the thalassemias, spherocytosis, hemoglobin SS, and acquired hemolytic anemias. It is DECREASED in paroxysmal nocturnal hemoglobinuria and in relapse of megaloblastic anemia. (It returns to normal with therapy.) Potent inhibitors of cholinesterase may present important clinical toxicological problems. Systemic insecticides (eg, organophosphates or carbamates) are examples. Both RBC acetylcholinesterase and plasma cholinesterase are usually inhibited. The effect on the plasma enzyme is more marked, however, and serum levels are usually used in diagnosis and assessment of recovery. Recovery is best determined by looking for a plateau in erythrocyte cholinesterase activity. Toxic potency may vary, plasma versus red cell cholinesterase, such that in some cases, erythrocyte levels may be needed for diagnosis and/or monitoring. If there is suspicion that a decrease in cholinesterase activity may not relate to the inhibitor effect of an organophosphate, then red cell level of acetylcholinesterase should be obtained. If both serum and RBC levels are significantly decreased, findings are those of exogenous toxic effect.