Abstract
Development of reliable, easy-to-use, rapid diagnostic tests (RDTs) to detect glucose-6-phosphate dehydrogenase (G6PD) deficiency at point of care is essential to deploying primaquine therapies as part of malaria elimination strategies. We assessed a kit under research and development called CareStart™ G6PD deficiency screening test (Access Bio, New Jersey, USA) by comparing its performance to quantitative G6PD enzyme activity using a standardized spectrophotometric method (‘gold standard’). Blood samples (n = 903) were collected from Cambodian adults living in Pailin province, western Cambodia. G6PD enzyme activities ranged from 0 to 20.5 U/g Hb (median 12.0 U/g Hg). Based on a normal haemoglobin concentration and wild-type G6PD gene, the normal values of G6PD enzymatic activity for this population was 3.6 to 20.5 U/g Hg (95th percentiles from 5.5 to 17.2 U/g Hg). Ninety-seven subjects (10.7%) had <3.6 U/g Hg and were classified as G6PD deficient. Prevalence of deficiency was 15.0% (64/425) among men and 6.9% (33/478) among women. Genotype was analyzed in 66 G6PD-deficient subjects and 63 of these exhibited findings consistent with Viangchang genotype. The sensitivity and specificity of the CareStart™ G6PD deficiency screening test was 0.68 and 1.0, respectively. Its detection threshold was <2.7 U/g Hg, well within the range of moderate and severe enzyme deficiencies. Thirteen subjects (1.4%, 12 males and 1 female) with G6PD enzyme activities <2 U/g Hg were falsely classified as “normal” by RDT. This experimental RDT test here evaluated outside of the laboratory for the first time shows real promise, but safe application of it will require lower rates of falsely “normal” results.
Highlights
In the context of malaria elimination, vector control measures e.g. long lasting bednets and indoor residual spraying along with prompt diagnosis and treatment of malaria infected patients are the most effective tools currently available [1]
Primaquine, at the transmission blocking dose, has been shown to cause haemolysis in P. falciparum-infected African children without glucose-6-phosphate dehydrogenase (G6PD) deficiency [8] and to cause a greater initial fall in haemoglobin following treatment compared to Artemisinin Combined Therapies (ACTs) alone [3]
Significant differences were found between villages (P,0.01): the lowest mean was observed in Phitas Sbov (7.4 U/g Hg, SD = 3.9 U/g Hg) and the highest in Pech Kiri (11.7 U/g Hg, SD = 5.2 U/g Hg)
Summary
In the context of malaria elimination, vector control measures e.g. long lasting bednets and indoor residual spraying along with prompt diagnosis and treatment of malaria infected patients are the most effective tools currently available [1]. Antimalarial drugs are seen as crucial to eliminate malaria and the focus is on the role of drugs to block malaria transmission by killing gametocytes and reducing the pool of liver hypnozoites of Plasmodium vivax and P. ovale [2]. Primaquine, at the transmission blocking dose (single dose, 0.75 mg/kg), has been shown to cause haemolysis in P. falciparum-infected African children without G6PD deficiency [8] and to cause a greater initial fall in haemoglobin following treatment compared to ACT alone [3]. High dose primaquine caused haemolysis in healthy, G6PD normal individuals [9] This dose of primaquine causes only slight drops in haemoglobin in healthy African-American volunteers having the A- variant, but in healthy volunteers having the B- Mediterranean variant, a hemolysis of 25% of red blood cells occurs [10]. Risk of hemolysis with primaquine varies with status of both infection and G6PD deficiency variant
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