(Aust Prescr 2001;24:3)
Letters, which may not necessarily be published in full, should be restricted to not more than 250 words. When relevant, comment on the letter is sought from the author. Due to production schedules, it is normally not possible to publish letters received in response to material appearing in a particular issue earlier than the second or third subsequent issue.
Editor, – I would like to correct an error in the article by Dr Wargon (Aust Prescr 2000;23:62-3).
The comment that an organophosphate insecticide 'acts by non-reversibly blocking acetylcholine' is not correct. These compounds act by non-reversibly blocking the enzyme acetylcholinesterase which is responsible for degrading acetylcholine at nerve terminals. The effect of this enzyme inhibition is an excess acetylcholine activity rather than any blocking of the effects of this neurotransmitter.
Maldison (malathion) initially undergoes bioactivation in the insect to the active compound which, by my understanding, acts predominantly in the insect's central nervous system.
Pyrethroids (also mentioned in the article) act on voltage-dependent sodium channels in the nerve cell membranes.
With some of these drugs, this results in repetitive nerve firing and release of excess acetylcholine at the nerve terminal. The end result with some pyrethroids is therefore similar to that with the organophosphates.
Excess muscarinic activity resulting from the clinical use of reversible anticholinesterases (e.g. neostigmine) is a common problem which is overcome in anaesthetic practice by the concurrent administration of an antimuscarinic drug (e.g. atropine) that does block the action of acetylcholine at muscarinic receptors. This is important to prevent the severe bradycardia that would otherwise occur.
Kerry Brandis
Director of Anaesthesia
Gold Coast Hospital
Southport, Qld
