To the Editor: Recently, we treated a patient with fatal paramethoxyamphetamine (PMA) poisoning. We believe this is the first PMA poisoning to be reported in the Australian Capital Territory.

PMA (street name, “death”) was first reported in the early 1970s during the emergence of recreational use of 3,4-methylenedioxymethamphetamine (MDMA [“ecstasy”]).1,2 Hyperthermia, coma and seizures are features of MDMA and PMA poisoning, but they are more severe with PMA ingestion; features of hypoglycaemia, hyperkalaemia and QRS interval prolongation are suggestive of PMA poisoning.3

Our patient was a 20-year-old man who was conveyed to the emergency department by ambulance after presumed MDMA ingestion. On presentation, he was unconscious (Glasgow Coma Score, 4/15) and had the following signs: temperature, 42.8°C; heart rate, 90 beats/min; QRS interval, 160 ms (reference range [RR], < 100 ms); blood pressure, 171/148 mmHg; oxygen saturation, 76% (RR, 95%–100%); and respiratory rate, 40 breaths/min.

After intubation, external cardiac compressions and multiple DC shocks were required to restore circulation. The initial serum potassium level was 8.9 mmol/L (RR, 3.2–5.0 mmol/L). Hypoxaemia persisted, and a chest x-ray showed extensive bilateral airspace consolidation.

The patient’s associates alleged that he habitually used equine clenbuterol and ovine androgen preparations in addition to ecstasy.

The subsequent days were notable for resistant shock, rhabdomyolysis, cardiomyolysis and severe coagulopathy refractory to therapy. Oliguric renal failure necessitated extracorporeal blood purification. Hepatic failure and hypoglycaemia were pronounced. The most extreme biochemical derangements recorded in this case are listed in the Box.

Five days after admission, the patient’s pupils were sluggishly reactive. Oculocephalic and oculocaloric reflexes were present but abnormal, while gag and cough reflexes were absent. A cerebral computed tomography scan showed extensive cerebral oedema.

By Day 8, the patient had fixed pupils and worsening haemodynamic instability. He died 10 days after ingestion of PMA.

The patient’s antemortem blood concentration of PMA was 2.3 mg/L — 2.0 mg/L above the typical fatal threshold of 0.3 mg/L previously reported.2-4 MDMA, methylenedioxyamphetamine (MDA) and methylecgonine were also detected at low levels.

Since 2005, the Pharmacy Guild of Australia has instituted its “Pseudo Watch” program to reduce diversion of pseudoephedrine to illicit methamphetamine manufacture by a combination of retail restrictions and recording details of purchasers judged genuine. Supporting legislation varies by state.5 However, PMA is made from the readily available and unmonitored precursor, anethole. Further, PMA has a slower onset of action than MDMA, leading to the possibility of additional doses being ingested while awaiting effects.

We believe medical practitioners should consider PMA poisoning in cases of severe reactions to ecstasy, especially those in which hypoglycaemia and hyperkalaemia are present. A “market” shift in drug use towards the more lethal PMA because of reduced availability of pseudoephedrine would be a cause for concern.