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    52 Acetylcholinesterase of erythrocytes (AChE)

    52 Acetylcholinesterase of erythrocytes (AChE)

    Erythrocyte acetylcholinesterase: red cell enzyme, marker of organophosphate exposure and its interpretation.

    Erythrocyte acetylcholinesterase (AChE) is the same enzyme that breaks down acetylcholine at nerve synapses, but located on the membrane of red blood cells. Its function there is not fully understood; it is considered a marker of the integrity of the red cell membrane, and its activity changes as red cells age. Clinically it is most important as a marker of exposure to cholinesterase inhibitors: organophosphate and carbamate pesticides and nerve agents inhibit AChE in synapses and on red cells in parallel, so red cell AChE reflects the degree of inhibition in the nervous system better than plasma cholinesterase.

    EnzymesRed blood cellsPoisoning
    Locationred cell membrane
    Main useorganophosphate exposure
    Compared withindividual baseline
    Related testplasma butyrylcholinesterase
    Acetylcholine cycle at a synapse: choline and acetyl coenzyme A form acetylcholine, which is released, activates receptors and is broken down by acetylcholinesterase into choline and acetate; choline is taken back up Acetylcholine cycle at the synapse choline + acetyl-CoA Acetylcholine released, binds receptors Acetylcholinesterase splits ACh in ≈ 1 ms ChAT choline taken back into the nerve ending (acetate released) Blocking acetylcholinesterase (nerve agents, organophosphates) causes acetylcholine excess.
    Figure 1. Synthesis, action and breakdown of acetylcholine. ChAT = choline acetyltransferase.

    Interpretation

    Because normal activity varies widely between people and methods, results are best compared with the person's own baseline value (for example in agricultural workers before the spraying season) or with the laboratory range. Red cell AChE recovers slowly, at the rate of new red cell production (about 1% per day), so it also reflects past exposure, whereas plasma butyrylcholinesterase recovers faster.

    Clinical significance

    Low activity

    Organophosphate or carbamate poisoning, chronic occupational exposure to pesticides, nerve agents; also reported in some haematological conditions (for example paroxysmal nocturnal haemoglobinuria) and conditions with membrane damage.

    High activity

    Young red cell population (reticulocytosis after bleeding or haemolysis); changes have also been described in several inflammatory, metabolic and neurological diseases.

    Acute organophosphate poisoning causes excess acetylcholine: small pupils, salivation, sweating, vomiting, diarrhoea, slow pulse, bronchial secretions, muscle twitching and weakness, and respiratory failure. It is an emergency treated with atropine, oxygen and supportive care.

    Seek emergency care

    after contact with or swallowing pesticides, especially with small pupils, heavy sweating and salivation, vomiting, muscle twitching, breathing difficulty or drowsiness.

    References

    1. Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet. 2008;371(9612):597–607. doi:10.1016/S0140-6736(07)61202-1
    2. Saldanha C. Human erythrocyte acetylcholinesterase in health and disease. Molecules. 2017;22(9):1499. doi:10.3390/molecules22091499

    This article is for general information and does not replace a consultation with a doctor. Laboratory results must be interpreted by a physician together with symptoms and other tests.

    Published on 29 April 2024