Biomarkers of Exposure in OP poisoning Bishan Rajapakse 1, Nicholas Buckley 2 1 SACTRC Clinical Researcher, PhD Candidate, ANU 2 Professor of Medicine,

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Presentation transcript:

Biomarkers of Exposure in OP poisoning Bishan Rajapakse 1, Nicholas Buckley 2 1 SACTRC Clinical Researcher, PhD Candidate, ANU 2 Professor of Medicine, University of New South Wales, Professorial Medical Unit

Biomakers of Exposure Red blood cell acetylcholinesterase (RBC-AChE) Butrylcholinesterase, or Plasma cholinesterase (PChE) Both biomarkers of exposure for anticholinesterase pesticides and nerve agents

Normal Range Wide normal range PChE varies according to other features such as liver failure and infection Approximately 1:2000 people have no PChE

Red blood cell aceytlcholinesterase (RBC-AChE) Plasma cholinesterase or butrylcholinesterase (PChE) Description Biomarkers of exposure for anticholinesterase agents eg OP pesticides, nerve agents, carbamates. Features Good marker of inhibition of synaptic AChE and severity of poisoning Poor info about clinical severity but can be used confirm exposure. Function No physiological function knownBreaks down suxamethonium - (depolarising muscle blocker) Effect of oximes Reactivation occurs with oximesLimited reactivation with oximes Normal range 31.4 U/g Hb taken as normal limit - Normal > 75%, mild inhibition (30-75%), mod inhibition (10- 29%), severe inhibition (<10%) Wide normal range - infection and liver disease can affect levels. Also about 1:2000 have absence of the enzyme

Increase in RBC-AChE after bolus dose of pralixoxime Decreasing response after 4th dose (at 24 hours) Oximes stopped thereafter

RBC-AChE increases after Pralidoxime Response continues even at 4th dose (24hours) Further ongoing oxime therapy may be of benefit

Rapid spontaneous reactivation of RBC-AChE and PChE indicates acute carbamate poisoning No pralidoxime given