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In impoverished rural settings, patients very often are not provided primaquine therapy as a direct consequence of a lack of access to G6PD screening.G6PD deficiency as the basis of hemolytic sensitivity to primaquine was described in 1956, and a variety of diagnostic tests for the disorder appeared within a decade.The most widely applied technology for G6PD screening—the fluorescent spot test (FST)—is impractical in that setting.At G6PD activity ≤40% of normal (n = 112), CSG test was not inferior to FST in detecting G6PD deficiency ( = 0.01) specificity, respectively.The combination of them explains more than 50 years without access to G6PD screening, which in turn accounts for the lack of access to primaquine therapy against vivax malaria for almost all those patients.We consider this deceptively simple problem the likely basis of most clinical attacks of vivax malaria and attendant burdens of morbidity and mortality.uses cookies to personalize content, tailor ads and improve the user experience.

We evaluated a new point-of-care G6PD screening kit (Care Start G6PD, CSG) against FST using graded Cu Cl treatments to simulate variable hemizygous states, and varying proportions of Cu Cl-treated RBC suspensions to simulate variable heterozygous states of G6PD deficiency.

In experiments double-blinded to Cu Cl treatment, technicians reading FST and CSG test (n = 269) classified results as positive or negative for deficiency.

At G6PD activity ≤40% of normal (n = 112), CSG test was not inferior to FST in detecting G6PD deficiency (P = 0.003), with 96% vs 90% (P = 0.19) sensitivity and 75% and 87% (P = 0.01) specificity, respectively.

to place dormant forms in the liver called hypnozoites.

These parasites typically cause 3 or more clinical attacks in relatively quick succession in the months after the primary attack, or may do so up to 1 or 2 years later.

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