Malaria glucose-6-phosphate dehydrogenase deficiency

When advising potential travelers on prophylaxis for malaria, be aware of the incidence of chloroquine-resistant P. falciparum malaria and the countries where it is prevalent. In patients who have P. vivax or P. ovale malaria (note that some patients can have P. falciparum and one of these species), following the treatment of the acute phase of malaria and screening for glucose-6-phosphate dehydrogenase deficiency, patients should receive a regimen of primaquine for 14 days to ensure eradication of the hypnozoite stage of P. vivax or P. ovale. For detailed recommendations for prevention of malaria go to www.cdc.gov/travel/. 

G2. Ganczakowski, M., Town, M., Bowden, D. K Vulliamy, T. J., Kaneko, A., Clegg, J. B., Weatherall, D. J., and Luzzatto, L Multiple glucose 6-phosphate dehydrogenase-deficient variants correlate with malaria endemicity in the Vanuatu archipelago (southwestern Pacific). Am. J. Hum. Genet. 56,294-301 (1995). 

Jalloh A, Tantular IS, Pusarawati S, et al. Rapid epidemiologic assessment of glucose-6-phosphate dehydrogenase deficiency in malaria-endemic areas in Southeast Asia using a novel diagnostic kit. Trap Med Int Health. 2004 9 615-623. 

It is believed that the aglycone components of these substances, called divicine and isouramil, respectively, can oxidize GSH. Individuals who eat fresh fava beans are protected to a certain extent from malaria. A condition known as favism results when some glucose-6-phosphate dehydrogenase-deficient individuals develop a severe hemolytic anemia after eating the beans. Explain why. 

The highest prevalence rates for glucose 6-phosphate dehydrogenase deficiency are found in tropical Africa and Asia, in some areas of the Middle East and the Mediterranean, and in Papua New Guinea. The geographic distribution of this deficiency is similar to that of sickle cell trait, and is probably also related to the relative resistance it confers against the malaria parasite. 

Researchers beheve that carriers of a G6PD mutation may be partially protected against malaria, an infectious disease carried by a certain type of mosquito. A reduction in the amount of functional glucose-6-dehydrogenase appears to make it more difficult for this parasite to invade red blood cells. Glucose-6-phosphate dehydrogenase deficiency occurs most frequently in areas of the world where malaria is common. 

Ruwende C, HiU A. Glucose-6-phosphate dehydrogenase deficiency and malaria. J Mol Med. 1998 Jul 76(8) 581-8. Review. PubMed citation... 

Frequencies of sickle cell trait and glucose-6-phosphate dehydrogenase deficiency differ in highland and nearby lowland malaria-endemic areas of Kenya. 

Frequency of glucose-6-phosphate dehydrogenase deficiency in relation to altitude a malaria hypothesis. 

Haemoglobinuria after a single dose treatment with dapsone and pyrimethamine for falciparum malaria in a patient with glucose-6-phosphate dehydrogenase deficiency. 

Population studies in Cameroon hemoglobin S, glucose-6-phosphate dehydrogenase deficiency and falciparum malaria. 

Prevalence and clinical presentation of glucose-6-phosphate dehydrogenase deficiency in Pakistani Pathan and Afghan refugee communities in Pakistan implications for the use of primaquine in regional malaria control programmes. 

Resistance of glucose-6-phosphate dehydrogenase deficiency to malaria effects of fava bean hydroxypyrimidine glucosides on Plasmodium falciparum growth in culture and on the phagocytosis of infected cells. 

Glucose- 6-phosphate dehydrogenase Low or absent enzyme activity in about 10% of African populations. Hemolysis following intake of a number of drugs which have electrophilic reactive metabolites, but also, carriers of this enzyme deficiency have a partial protection from malaria. 

Deficiency of the first enzyme of the pentose phosphate pathway, glucose 6-phosphate dehydrogenase, is widespread.11 Its geographical distribution suggests that, like the sickle-cell trait, it confers some resistance to malaria. A partial deficiency of 6-phosphogluconolactonase (Eq. 17-12, step b) has also been detected within a family and may have contributed to the observed hemolytic anemia.1... 

Cappadoro, M., Giribaldi, G., O Brien, E., Turrini, F., Mannu, F., Ulliers, D., Simula, G., Luzzatto, L., and Arese, P. (1998). Early phagocytosis of glucose-6-phosphate dehydrogenase (G6PD)-deficient erythrocytes parasitized by Plasmodium falciparum may explain malaria protection in G6PD deficiency. Blood 92, 2527-2534. 

During World War II, American soldiers stationed in tropical countries received primaquine (25) as antimalarial prophylaxis it turned out that only soldiers of African descent developed hemolysis from the administration of primaquine. The explanation came aitr(26) The affected soldiers had a genetic deficiency of glucose-6-phosphate dehydrogenase this deficiency was frequent in Africans because it protected the carrier from malaria, but it was rare in countries without malaria. After discovery of the genetic deficiency of iso-niazid acetylation (5,27), other investigators found substantial interethnic differences in the frequency of this deficiency (28). The deficiency was rare in Eskimos (Inuit), relatively frequent in Europeans and Africans, and intermediate in East Asians. 

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