G6PD Mediterranean accounts for the high prevalence of G6PD deficiency in Kurdish Jews

Abstract

The Jews of Kurdistan are a small inbred population with a high incidence of beta-thalassaemia and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Recently, it was reported that the beta-thalassaemia in this population shows an unusual mutational diversity; 13 different mutations were identified, of which 4 had not previously been observed in any other population. In contrast, we now report that the G6PD deficiency, which has the highest known incidence in the world, and which affects about 70% of males, is almost entirely attributable to a single widespread mutation, G6PD Mediterranean.

Molecular Characterization of G6PD Deficient Variants in Nineveh Province, Northwestern Iraq

“…The Mediterranean variant (563C?T) was found to be the most frequent variant in many parts of the world including Mediterranean countries, Middle East and Indian subcontinent with figures reaching to 97 % in Kurdish Jewish, [16][17][18][19][20][21]. This variant is the most common variants in other parts of Iraq [6][7][8].…”

Differing Pathogenesis of Perinatal Bilirubinemia in Glucose-6-Phosphate Dehydrogenase-Deficient Versus-Normal Neonates

“…PCR followed by allele-specific oligonucleotide hybridization was used to determine the presence or absence of nt 563, the nucleotide mutated in G-6-PD Mediterranean (16) and which is seen in the Sephardic-Jewish population studied (9,17). Details of the procedure have been published elsewhere (9).…”

Coexistence of five G6PD variants indicates ethnic complexity of Phuket islanders, Southern Thailand

“…High frequency of some G6PD variants in particular populations was once attributed to heterozygous advantage against malaria (Luzzatto et al 1969), and epidemiological evidence indicates that G6PD deficiency confers some resistance to P. falciparum, the primary human malaria (Ruwende et al 1995). In fact, there is a global geographic correlation, in general, between the frequency of G6PD deficient variants and the local history of malarial disease (Allison 1960;Oppenheim et al 1993). In other words, G6PD deficiency is a genetic witness of the past exposure to malaria in a population.…”