Two variants of hemoglobin D in the algerian population: Hemoglobin D ouled rabah β19 (B1) Asn → Lys and hemoglobin D Iran β22 (B4) Glu → Gln

Élion, Jacques; Belkhodja, O; Wajcman, Henri; Labie, Dominique

doi:10.1016/0005-2795(73)90117-7

Cited by 37 publications

(8 citation statements)

References 10 publications

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“…In the Twareg Kel Kummer of Mali, over 20 % of the population have a fl-chain mutation which has recently been identified. It is an HbD Ouled Rabah: f119asn-'lysdescdbed by Elion, Belkhodja, Wajcman and Labie, 1973. Hence, Hb C seems to originate from the Volta plateau, where the highest frequency is encountered: from the Volta plateau, it may have spread out in all directions (figure 2).…”

Section: Discussionmentioning

confidence: 91%

Comparative study of haemoglobin types of two populations of eastern Senegal—Bedik and Niokholonko

Mauran-Sendrail

Bouloux

Gomila

et al. 1975

Annals of Human Biology

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The haemoglobin types of 1487 of the East Senegal Bedik and Niokholonko populations have been studied. There are significant differences between them, the most likely explanation of which is that the populations are of different origins. The Bedik appear to be the most ancient known settlers in East Senegal: they possess only A and S haemoglobins. The Niolholonko came later, probably from Mali: they have a lower frequency of S genes but AC and AD phenotypes are also encountered among them.

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Section: Discussionmentioning

confidence: 91%

Comparative study of haemoglobin types of two populations of eastern Senegal—Bedik and Niokholonko

Mauran-Sendrail

Bouloux

Gomila

et al. 1975

Annals of Human Biology

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“…It is interesting that both clinical and hematological abnormalities observed in our patient, as well as her sisters, are consistent with previous observations reported in double heterozygosities for Hb D-thalassemia. [17][18][19] Although the non-alpha to alpha ratio was not performed on either parent, the laboratory data suggested that the father was responsible for transmitting the alpha gene to the α-thalassemia genes in his three daughters, while the mother proved to be the source of the Hb D gene (32%). With normal MCV, however, α-thalassemia was difficult to rule out in her case.…”

Section: Discussionmentioning

confidence: 99%

Hemoglobin D Trait with Alpha Thalassemia in a Saudi Family

Al-Otaibi

Ahmed

2000

Ann Saudi Med

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In 1951, Itano 1 encountered a new hemoglobin variant, which co-migrated with hemoglobin S (Hb S) at alkaline pH, but failed to sickle. It was labeled as hemoglobin D (Hb D), and was subsequently found to have the structure α-2-β-2-121 Glu→Gln, where glutamine replaced the normal β-121 glutamic acid. 2The electrophoretic mobilities of Hb D and Hb S are identical at alkaline pH, however, Hb S can be differentiated from Hb D by its decrease solubility in the reduced state and its associated presence with sickling. Furthermore, Hb D can be separated from Hb S on citrate agar gel electrophoresis at pH 6.2.3 It was later found that the Hb D gene can be detected by DNA amplification and globin chain analysis.3-5 Several cases of Hb D have been reported and were labeled as Hb D Punjab or Hb D Los Angeles. [6][7][8][9][10]

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“…It has been suggested that the Hb D that is present at appreciable frequency in the Arabo-Berbers of Algeria (Cabannes, 1965) may in fact be an alpha-chain variant (de Traverse and Coquelet, 1961;Konigsberg et al, 1965). More recently, however, two new variants of Hb D have been reported in the Algerian population, one Hb D Ouled Rabah (/19 Asn--Lys) and the other D Iran (/322 Glu-÷ Gln) (Elion et al, 1973) the latter having also been reported in an Iranian (Rahbar, 1973) and in a Pakistani family (Rohe, Sharma, and Ranney, 1973).…”

Section: Hb D Punjab In the United Kingdommentioning

confidence: 99%