Editor—Robinson et al report a reduction in the amount of paracetamol ingested in overdose since the introduction of reduced pack sizes and blister packing of over the counter paracetamol in September 1998.
1 They found no change, however, in the incidence of hepatotoxicity. Their results contrast with those of other studies, which have shown a 21% reduction in episodes of hepatotoxicity and a 64% reduction in the development of severe hepatotoxicity.
2,3 As they have stated, hepatic failure is rare if <12 g of paracetamol is ingested.
4 But the median dose ingested in their study did not reach this level. It is thus unsurprising that the study included only five cases of hepatotoxicity; given this low number, it seems imprudent to claim that no change in incidence has occurred.
In addition, the paracetamol concentrations quoted in the paper are low, considering that concentrations >200 mg/l four hours after ingestion and >130 mg/l six hours after ingestion are used to guide the appropriate use of acetylcysteine treatment. Despite the low concentrations quoted, acetylcysteine was given to 25% and 31% of patients. This does not seem to accord with current practice recommendations.
Robinson et al conclude that the change in pack size had no effect on the incidence of severe liver failure. In our view, a stricter definition of paracetamol overdose is required if we are to make sense of the conflicting reports. Perhaps paracetamol overdose should be confined to subjects who claim to have taken an overdose and have a measurable serum concentration.
The burden of paracetamol poisoning on the NHS is high, with over 70

000 episodes a year in Britain.
5 It is worrying that the recent measures have not had a more dramatic effect on this serious problem. If, as Turvill et al say,
3 only a 21% reduction has been achieved then further measures such as limiting paracetamol to prescription only should be considered.