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PubMed1996

A seven year anthropobiological survey on the distribution of abnormal hemoglobins in Cameroon.

Within the frame of an anthropobiological survey on some populations of Cameroon (1985-1991), Hb beta data were collected from numerous ethnic groups including Bakaka, Bamileke, Daba, Fali, Guiziga, Kanuri, Mada, Mafa, Mundang, Uldeme, Podokwo, Tali, Tupuri, Fulbe, Mandara, Ewondo and Bassa. Hb beta *S allele frequencies ranged from 0.008 +/- 0.003 (among Fali) to 0.152 +/- 0.020 (among Mandara) and 0.152 +/- 0.044 (among Podokwo), whereas Hb beta *S was found to be absent among Tupuri. Hb beta *C was observed among Bamileke (0.001 +/- 0.001), Fali (0.003 +/- 0.002), Fulbe (0.002 +/- 0.002), Mafa (0.005 +/- 0.005), Mundang (0.005 +/- 0.005), Tupuri (0.010 +/- 0.007) and Podokwo (0.015 +/- 0.015). The possible reasons for these variations in allele frequencies are discussed.

Alleles↗
PubMed1976

The immunologic identification of abnormal hemoglobins.

Guinea pig antisera against human hemoglobin contain antibodies to multiple antigenic determinants. Hemoglobin variants having single amino acid substitutions affecting these determinants are recognized as antigenically deficient in a radioimmunoassay system. The multivalent antisera may be made more selective by appropriate absorption with hemoglobin variants. Three such antisera containing antibodies specific, respectively, for the beta-chain of Hb A, Hb S, and Hb C are described. They can differentiate among the hemoglobins of individuals who possess these variants alone or in any paired combination. Their discriminating ability is not hindered by the presence of 1,000-fold concentrations of Hb F and may therefore be extended to the early prenatal diagnosis of sickling disorders. The antisera described also detect several other variants of Hb A. The approximate location of the substitution in variants so detected can be determined by a complementation test. This is based on the finding that two antigenically deficient hemoglobins will complement each other in mixture provided their amino acid substitutions involve different determinants.

Fetal Blood↗
PubMed1980

[Polycythemia resulting from abnormal hemoglobin with increased affinity for oxygen. Two cases (author's transl)].

An abnormal hemoglobin with increased oxygen affinity has to be suspected in all the cases of polycythemia where no direct signs of "polycythemia vera", or any of the classical reasons for erythropoietic stimulation can be demonstrated. This fact is documented by two new observations, one concerning a 44 year-old man with Hb Kempsey, another concerning a 58 year-old woman with Hb Malmö. The diagnosis is based on a scrupulous electrophoretic study involving an isoelectric focusing on polyacrylamide gel, and, on the study of the oxygen binding properties of the red blood cells. This polycythemia being a compensatory mechanism allowing a normal oxygen delivery to the tissues has to be respected and a compromise must be found with the cardiovascular risk.

Adult↗
PubMed1979

[Hemoglobin J Amiens beta 17 (A 14) Lys replaced by Asn. Coincidence of a functionally silent new abnormal hemoglobin and a polycythemia vera (author's transl)].

A new abnormal hemoglobin, Hb J Amiens beta 17 (A 14) Lys replaced by Asn, has been discovered during the exploration of a recent polycythemia in a 65-year-old patient of Spanish extraction. Oxygen affinity of washed red blood cells was found to be normal at pH 7.13 (P 50 = 30.0 mmHg, N = 29.5 +/- 1). Cooperativity is unchanged, and no instability was detected. From this study, it is concluded that there is no relation between this functionally silent hemoglobin and the polycythemia. In fact, the recent appearance of the polycythemia, the involvement of the other blood cell lines, particularly the thrombocytosis, the high score of leukocyte alkaline phosphatases, and the results of the bone marrow biopsy led to the diagnosis of polycythemia vera.

Aged↗