Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2016 Nov;26(6):517-522.
doi: 10.4314/ejhs.v26i6.3.

Coinheritance of B-Thalassemia and Sickle Cell Anaemia in Southwestern Nigeria

Osunkalu Vincent  1 , Bamisaye Oluwaseyi  2 , Babatunde James  3 , Lawal Saidat  4
Affiliations

Coinheritance of B-Thalassemia and Sickle Cell Anaemia in Southwestern Nigeria

Osunkalu Vincent et al. Ethiop J Health Sci. 2016 Nov.

Abstract

Background: Genes for haemoglobin S are found in high frequencies in Nigeria. However, there is little information on beta thalassemia in sickle cell anaemia in this population. The clinical presentation of HbS- β thalassemia is enormously variable, ranging from an asymptomatic state to a severe disorder similar to homozygous sickle cell disease.

Materials and methods: Haemoglobin A2 and HbF were determined in sickle cell anaemia patients attending LAUTECH Teaching Hospital, Osogbo, by elution after electrophoresis and alkaline denaturation methods respectively. Haematological parameters were estimated using Sysmex KX-21N and percentage target cells using Leishman's staining technique.

Results: Exactly 6% f the SCA patients were found to have elevated HbA2 (>3.3%) and HbF (>1.3%). These patients also had normal erythrocyte indices, increased platelet count, a significantly higher HCT and an increased % target cell.

Conclusion: These findings confirm that the frequency of beta thalassaemia in sickle cell patients in Nigeria is higher than previously thought. It is therefore important to consider the possibility of this variant in patients with sickle cell anaemia since their course may differ from that of patients with homozygous sickle cell anaemia.

Keywords: Haemoglobin A2; Haemoglobin F; Sickle cell anaemia; β-Thalassemia.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

References

    1. Weatherall DJ, Clegg JB. The Thalassaemia syndromes. 4th ed. Oxford: Blackwell Science; 2010. pp. 237–286.
    1. Renzo G, Raffaella O. Beta Thalassemia. Orphanet J Rare Dis. 2010;5:11. - PMC - PubMed
    1. Forget BG. Molecular mechanisms of beta thalassemia. In: Steinberg MH, Forget BG, Higgs DR, Nagel RL, editors. Disorders of hemoglobin: genetics, pathophysiology, and clinical management. 1st ed. Vol. 12. Cambridge: Cambridge University Press; 2001. pp. 252–276.
    1. Flint J, Harding RM, Boyce AJ, et al. The population genetics of the hemoglobinopathies. Bailliere's Clinical Hematology. 1998;11:1–50. - PubMed
    1. WHO Regional Committee for Africa, author. 56th Annual Session Final Report. 2006. [11-8-12]. Available online.