Tafenoquine for preventing relapse in people with vivax malaria

Antimalarial drugs as a treatment of anaemia in children living in malaria-endemic areas

Rajapakse S1, Rodrigo C1, Fernando SD2

1. Faculty of Medicine, University of Colombo, Department of Clinical Medicine, Colombo, Sri Lanka
2. Faculty of Medicine, University of Colombo, Department of Parasitology, Colombo, Sri Lanka

Cochrane Database of Systematic Reviews 2015, Issue 4. Art. No.: CD010458.

To read the full review please follow this link: DOI: 10.1002/14651858.CD010458.pub2


Vivax malaria is caused by the parasite Plasmodium vivax. The disease includes a stage of liver infection and this can cause relapse unless treated. The only drug available until recently was primaquine, but this requires a 14-day course of treatment. Alternatives have been tried, one of which is tafenoquine, which does not need such a long course of treatment. Both primaquine and tafenoquine can cause haemolysis in people with glucose-6-phosphate dehydrogenase (G6PD) enzyme deficiency, which is a common genetic defect. We conducted a Cochrane Review on the effect of the drug tafenoquine on clearing the dormant P. vivax parasites in infected patients to prevent a relapse.

Review findings

Researchers in the Cochrane Collaboration examined the research published up to 13 April 2015. We identified three trials conducted in Thailand, India, Peru and Brazil on adults with confirmedP. vivax malaria that randomized 453 participants. All adults received chloroquine (to clear the parasites in the blood) and some groups received either tafenoquine, primaquine or no further treatment. All were observed for recurrences of P. vivax malaria (up to six months) and all trials tested people for G6PD enzyme, and excluded patients who were deficient.

Adults receiving tafenoquine at doses greater than 300 mg had fewer relapses than adults who had no further treatment (moderate quality evidence). Tafenoquine 600 mg may be better in relapse prevention than standard primaquine doses (low quality evidence). In patients who do not have G6PD deficiency, there may be little or no difference in adverse effects (low quality evidence).

The drug is untested in children and pregnant women. The shorter treatment course is a practical advantage, but the longer half-life could may have more substantive consequences if given inadvertently to people with G6PD deficiency.