Paracetamol

Clinical Chemistry

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Description

Paracetamol is a commonly used analgesic. If taken in excess it can lead to liver damage and renal impairment. Liver damage may be delayed following excessive paracetamol administration. The major paracetamol metabolites are the glucuronide and sulphate derivatives. A small proportion of a metabolite formed by microsomal oxidation is converted to glutathione and excreted subsequently as cysteine or mercapturate derivatives. If the glutathione stores of the liver become depleted in the prescence of large amounts of paracetamol, the oxidised metabolite combines with liver cell components causing hepatic necrosis. The hepatocellular damage can be reduced by giving the patient compounds containing thiol groups such as methionine and N-acetyl cysteine. Treatment is guided by plasma paracetamol concentration, amongst other parameters.

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Indications

Suspected paracetamol poisoning or overdose with unknown drugs.

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Sample Type

Serum, SST/Gel, minimum 2 mL (1 mL separated serum). Avoid haemolysis. Take sample prior to commencement of N-acetylcysteine

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Reference Range

Reference ranges are provided on the report. Alternatively, please contact the laboratory for current ranges.

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Turnaround Time

Within 1 hour

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Testing Frequency

As required

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External Notes

The latest Toxbase and Trust treatment guidelines should be followed in treating patients with suspected paracetamol overdose. Paracetamol levels are of no value in predicting liver damage if taken less than 4 hours after a suspected overdose. It should be noted that patient samples containing conjugates of paracetamol, which have been stored for more than two weeks at room temperature, may yield paracetamol as a result of degradation of the conjugates.

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