To the Editor: I wish to report a case of quinine-induced disseminated intravascular coagulation (DIC) and haemolytic–uraemic syndrome (HUS).

A 78-year-old woman presented with nausea, vomiting, diarrhoea, fever and confusion three hours after taking 150 mg of quinine for leg cramps. Five months earlier she had been admitted overnight for similar symptoms after quinine ingestion, her symptoms resolving over 12 hours without sequelae. Before this she had ingested quinine infrequently for the preceding five years without complication.

Her past history included hypertension, hypercholesterolaemia and glaucoma; medications were simvastatin, lisinopril and latanoprost eye drops. On presentation her temperature was 40ºC, blood pressure was 150/90 mmHg; physical examination was otherwise unremarkable. Initial investigations showed serum creatinine concentration, 0.11 mmol/L (reference range, 0.05–0.10 mmol/L); platelet count, 124 × 109/L (reference range, 150–400 × 109/L); prothrombin time, 21.2 seconds (reference range, 11s–16s); activated partial thromboplastin time, 66.3 seconds (reference range, 25s–42s); fibrinogen concentration, 2.1 g/L (reference range, 1.5–4.0 g/L); and D-dimer level, > 4.0 mg/L (reference range, < 0.35 mg/L). No haemolysis was present on the initial blood film.

The patient rapidly developed oliguric renal failure, progressive coagulopathy and thrombocytopenia. There was no focus of infection, and blood, urine and faecal cultures were negative. Urine microscopy showed 3 × 106 leukocytes per litre (reference range, < 10 × 106/L), 270 × 106 erythrocytes per litre (reference range, < 10 × 106/L) and granular casts. Her urine output improved following infusions of saline, dopamine and high dose frusemide, but renal function continued to deteriorate. The coagulopathy had resolved by 48 hours after taking the quinine, but thrombocytopenia and renal function continued to worsen, with a platelet count of 18 × 109/L and a serum creatinine concentration of 0.58 mmol/L, evidence of haemolysis with fragmentation of red blood cells, elevated concentrations of lactate dehydrogenase (2450 U/L; reference range, 110–250 U/L) and bilirubin (32 µmol/L; reference range, < 20 µmol/L), and low haptoglobin concentration (< 0.06 g/L; reference range, 0.3–2.15 g/L), consistent with haemolytic–uraemic syndrome.

The patient was treated with four cycles of plasma exchange with 3 L volumes, corticosteroids and two cycles of haemodialysis over 11 days. Renal function gradually improved, although the serum creatinine concentration remained elevated at 0.17 mmol/L two months later.

The most common adverse reaction to quinine is thrombocytopenia. Six cases of DIC and 10 cases of HUS following quinine ingestion have been previously reported.1-5 This is the first report of both DIC and HUS occurring together after exposure to quinine. Many of the case reports describe multiple presentations before quinine was identified as the precipitant. It is important that prescribers are aware of this rare but serious reaction which may occur following exposure to quinine, and that a history of ingestion is sought in anyone presenting with otherwise unexplained DIC or HUS.