Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose-6-phosphate dehydrogenase-normal adult volunteers infected with mosquito-bone Chesson strain vivax malaria were treated with chloroquine and primaquine during the initial attack. Administration of 60 mg (base) of primaquine daily for 7 days was as effective in preventing relapse as is the regimen customarily used for the radical cure of infections produced by this strain, namely, 30 mg daily for 14 days. However, it is stressed that because of the risk of primaquine-induced hemolysis in individuals having genetically-transmitted erythrocyte abnormalities this high dosage should not be used routinely.
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PMID:Radical cure of Chesson strain vivax malaria in man by 7, not 14, days of treatment with primaquine. 32 72

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzymopathy. Because its gene locus is on the X-chromosome it is more common in males than females in all populations. Prevalence rates vary from 62% among Kurdish Jews to the very low rates (0.1% or less in Japan, for example), which are compatible with sporadic cases arising from spontaneous mutations. However, there is at least one population in which G6PD deficiency has not been found, namely the indigenous (Amerindian) population of America. Approximately 400 variants have been described. Despite the clinical burden imposed by this enzymopathy, polymorphic frequencies have been reached in many populations. There is abundant epidemiological evidence that this has happened because of a biological advantage conferred on heterozygotes in falciparum malaria endemic areas. This advantage may apply to quartan malaria as well. Clinical severity varies, from the rare chronic nonspherocytic haemolytic anaemia to progressively milder forms like the Mediterranean and A- types. The other clinical syndromes, i.e. neonatal jaundice and haemolysis caused by infections, foods, drugs and chemicals, are not always predictable. This is because only a fraction of such enzymopathic persons develop these syndromes after exposure to the relevant stimulus. Modern techniques of molecular biology may elucidate why this is so. There is some emerging evidence that the genetic burden or survival value associated with G6PD deficiency may be relevant not only in tropical and infectious diseases, but also in their chemotherapy (e.g. malaria) as well as in the control of a long-recognized environmental pollutant such as lead.
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PMID:Glucose-6-phosphate dehydrogenase deficiency. 151 Nov 80

Glucose-6-phosphate dehydrogenase (G6PD) and hemoglobin E (HbE) were studied among 708 malarial patients and control groups of Ao Nagas from the Mokokchung District of Nagaland in the extreme northeast of India. The data suggest that malaria is an important ecologic factor in maintaining the high frequency of G6PD deficiency and HbE among the Ao Nagas. Although migrations from adjoining populations that have a high frequency of both these traits could have contributed to the presence of these genes in the Ao Nagas, malaria also could be an essential determinant in maintaining the current high frequency in present-day Ao Nagas.
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PMID:Prevalence of malaria in Ao Nagas and its association with G6PD and HbE. 155 89

Glucose-6-phosphate dehydrogenase (G6PD; EC 1.1.1.49)-deficient red blood cells from male hemizygotes and female heterozygotes from the island of Sardinia were studied for their ability to support growth in vitro of the malaria-causing organism Plasmodium falciparum. Parasite growth was approximately one-third of normal in both hemi- and heterozygotes for G6PD deficiency. In Sardinians with the beta 0-thalassemia trait, parasite growth was normal except when G6PD deficiency occurred together with the thalassemia trait. The data support the hypothesis that G6PD deficiency may confer a selective advantage in a malarious area; the female heterozygote may be at a particular advantage because resistance to malaria equals that of male hemizygotes, but the risk of fatal hemolysis may be less. However, more female heterozygotes must be studied to confirm this hypothesis. No protective effect of beta 0-thalassemia trait could be demonstrated in vitro.
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PMID:Glucose-6-phosphate dehydrogenase deficiency inhibits in vitro growth of Plasmodium falciparum. 633 74

Glucose-6-phosphate dehydrogenase (G6PD) deficiency, the most common enzymopathy of humans, affects over 400 million people. The geographical correlation of its distribution with the historical endemicity of malaria suggests that this disorder has risen in frequency through natural selection by malaria. However, attempts to confirm that G6PD deficiency is protective in case-control studies of malaria have yielded conflicting results. Hence, for this X-linked disorder, it is unclear whether both male hemizygotes and female heterozygotes are protected or, as frequently suggested, only females. Furthermore, how much protection may be afforded is unknown. Here we report that, in two large case-control studies of over 2,000 African children, the common African form of G6PD deficiency (G6PD A-) is associated with a 46-58% reduction in risk of severe malaria for both female heterozygotes and male hemizygotes. A mathematical model incorporating the measured selective advantage against malaria suggests that a counterbalancing selective disadvantage, associated with this enzyme deficiency, has retarded its rise in frequency in malaria-endemic regions. Although G6PD deficiency is now regarded as a generally benign disorder, in earlier environmental conditions it could have been significantly disadvantageous.
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PMID:Natural selection of hemi- and heterozygotes for G6PD deficiency in Africa by resistance to severe malaria. 2343 53

Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency surveys in Afghan refugees and a local community in the North-West Frontier Province, Pakistan, showed that this trait was most common among Pathan and Uzbak refugees (15.8% and 9.1% respectively). The prevalence among Pakistani Pathans was 7.0%, and that in Tajik and Turkoman refugees was 2.9% and 2.1% respectively. Hospital studies showed that the type of G-6-PD deficiency in Pathans could cause severe haemolytic crises. The potentially fatal side effects of primaquine treatment in the Pathan communities, and the high risk of re-infection, render the anti-relapse treatment policy for Plasmodium vivax obsolete. However, epidemic conditions of P. falciparum malaria may justify the use of primaquine as a gametocidal drug, administered as a single dose, during the transmission season. These findings necessitate revision of the recommendations for the use of primaquine in the area.
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PMID: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. 774 10

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is seen at a higher frequency in many national and ethnic groups in areas of current or former malaria endemicity. A screening programme undertaken to evaluate the gene frequencies for this deficiency in the highly inbred South Indian population of Karnataka revealed that of the 5140 neonates screened, 7.8% were G6PD deficient with no correlation between the reported level of inbreeding and enzyme deficiency. An interesting finding was the equal number of male (198) and female (207) individuals, with G6PD activity of less than 3 IU. The possible implications of this finding with regard to the expression of G6PD gene is discussed.
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PMID:An unusual distribution of glucose-6-phosphate dehydrogenase deficiency of south Indian newborn population. 800 21

Glucose-6-phosphate dehydrogenase (G6PD) is a cytoplasmic enzyme that is essential for a cell's capacity to withstand oxidant stress. G6PD deficiency is the commonest enzymopathy of humans, affecting over 400 million persons worldwide. The geographical correlation of its distribution with the historical endemicity of malaria suggests that 66PD deficiency has risen in frequency through natural selection by malaria. This is supported by data from in vitro studies that demonstrate impaired growth of P. falciparum parasites in G6PD-deficient erythrocytes. Attempts to confirm that G6PD deficiency is protective in field studies of malaria have yielded conflicting results, but recent results from large case control studies conducted in East and West Africa provide strong evidence that the most common African G6PD deficiency variant, G6PD A-, is associated with a significant reduction in the risk of severe malaria for both G6PD female heterozygotes and male hemizygotes. The effect of female homozygotes on severe malaria remains unclear but can probably be assumed to be similar to that of comparably deficient male hemizygotes.
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PMID:Glucose-6-phosphate dehydrogenase deficiency and malaria. 969 35

Glucose-6-phosphate dehydrogenase A- (G6PD A-) deficiency is a common enzymopathy in Africa that sporadically leads to manifest haemolytic anaemia. It is not exactly known how far the haematological status of individuals with either homozygous or heterozygous G6PD A- deficiency differs from that of individuals with normal G6PD activity. In a field study in Nigeria, we determined G6PD gene variants, the corresponding G6PD and pyruvate kinase (PK) activities, and basic haematological parameters in clinically healthy individuals, who were, in part, asymptomatically infected by malaria parasites. Red blood cell counts and haemoglobin levels were lower in G6PD A- deficient than in G6PD normal subjects. PK activities were higher in G6PD deficients, indicating a younger red cell population in these individuals. These findings suggest that G6PD A- deficiency is accompanied by chronic subclinical haemolysis. As a consequence, the reduced life span of red cells leads to an impaired diagnosis of G6PD heterozygosity when applying routine biochemical methods.
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PMID:Red cell glucose-6-phosphate dehydrogenase status and pyruvate kinase activity in a Nigerian population. 1074 71

Glucose-6-phosphate dehydrogenase (G6PD) deficiency was evaluated in 1676 schoolboys in northern Vietnam. The trait was nearly absent in boys of the Kinh (0.5%) and the Mong (0.7%) ethnic groups that traditionally have lived outside malaria transmission areas. Prevalences among ethnic groups living in the foothills, the breeding area of the main malaria vector Anopheles minimus, ranged from 9.7% to 31%. These findings support the hypothesis of a selective advantage of the trait in Plasmodium falciparum-endemic areas.
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PMID:Glucose-6-phosphate dehydrogenase deficiency in northern Vietnam. 1074 83


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