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International Journal of Clinical and Experimental Medicine Research

ISSN Online: 2575-7970 ISSN Print: 2575-7989 CODEN: IJCEMH
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ArticleOpen Access http://dx.doi.org/10.26855/ijcemr.2021.04.011

Association between Sickle Cell Crisis and Other Types of Hemoglobin among Sudanese Children with Sickle Cell Anemia

Arwa Abdelbagi Mohammed1,*, Fathelrahman Mahadi Hassan2, Abdelgadir Ahmed Abdelgadir1, Amged Hussein Abdelrhman1

1Department of Hematology and Immunohematology, Omdurman Islamic University, Sudan.  2Department of Clinical Laboratory Sciences, Collage of Applied Medical Science, Imam Abdulrahman Bin Faisal Universitym, Dammam, KSA.

*Corresponding author: Arwa Abdelbagi Mohammed

Published: April 07, 2021

Abstract

Background: Sickle cell anemia (SCA) is a common genetic disorder that causes considerable morbidity and mortality throughout the world. The study was performed in 82 Sudanese participants with sickle cell disease as study population with both sexes, age (2-12 years). Materials and Methods: Venous blood was collected using sterile disposable plastic syringe after cleaning the vein puncture area with 70% ethanol, the blood was added to the EDTA and gently mixed, then CBC was performed using (Sysmex-3000 plus) and (Electrophoresis) was done. Results: The results of this study show that most patients had raised level of hemoglobin F according to gender found that there were 43 males and 28 females had raised level of HbF, 7 males and 2 females were normal, and 36% of patients had raised level of HbA2 in both gender (20 males) (10 females). Conclusion: HbF in sickle cell anemia patients was found to be 85.3% (raised), HbS in sickle cell anemia patients was found to be 100% (raised) and HbA2 in sickle cell anemia patients was found to be 30.5% (Normal).

Keyword

Sudanese Children, Sickle Cell Crisis, other Types of Hemoglobin

References

[1] Acquaye, J. K., Omer, A., Ganeshaguru, K., et al. (1985). Non-benign sickle cell anaemia in western Saudi Arabia. Br J Haematol, 60(1): 99-108. 

[2] Rdachi, K., Kim, J., Asakura, T., Schwartz, E. (1990). Characterization of two types of fetal hemoglobin: alpha2 G gamma2 and alpha2 Agamma2. Blood, 75(10): 2070-2075.

[3] Adams, R. J., Ohene-Frempong, K., Wang, W. (2001). “Sickle cell and the brain”. Hematology Am Soc Hematol Educ Program, (1): 31-46. Doi: 10.1182/asheducation-(2001).1.31. PMID 11722977. 

[4] Dams, R. J. (2007). “Big strokes in small persons”. Arch. Neurol., 64(11): 1567-74. doi:10.1001/archneur.64.11.1567. PMID 17998439. 

[5] Aidoo, M., Terlouw, D. J., Kolczak, M. S., McElroy, P. D., Terkuile, F. O., Kariuki, S., Nahlen, B. L., Lal, A. A., Udhayakumar, V. (2002). “Protective effects of the sickle cell gene against malaria morbidity and mortality”. The Lancet, Apr 13, 359 (9314): 1311-2.

[6] Aldrich, T. K., Nagel, R. L. (1998). “Pulmonary Complications of Sickle Cell Disease.” In Reynolds, H. Y., Bone, R. C., Dantzker, D. R., George, R. B., Matthay, R. A. Pulmonary and Critical Care Medicine (6th Ed.). St. Louis: Mosby. (1998) pp. 1-10. ISBN 0-8151-1371-4.

[7] Al-Jam'a, A. H., Al-Dabbous, I. A., Chirala, S. K., et al. (2000). Splenic function in sickle cell anemia patients in Qatif, Saudi Arabia. Am J Hematol, 63(2): 68-73. 

[8] Allison, A. C. (2009). “Genetic control of resistance to human malaria”. Current Opinion in Immunology, 21(5): 499-505. doi:10.1016/j.coi.2009.04.001. PMID 19442502. 

[9] Almeida, A., Roberts, I. (2017). “Bone involvement in sickle cell disease”. Br. J. Haematol., 129(4): 482-90. doi:10.1111/j.1365-2141.2005.05476.x. PMID 15877730. 

[10] Akinsheye, I., Alsultan, A., Solovieff, N., Ngo, D., Baldwin, C. T., Sebastiani, P., Chui, D. H., Steinberg, M. H. (2018). Blood 7: 118(1): 19-27. doi: 10.1182/blood-2011-03-325258. Epub 2011 Apr 13 Fetal hemoglobin in sickle cell anemia.

[11] Ahmed, S., Saleem, M., Modell, B., Petrou, M. (2002). Screening Extended Families for Genetic Hemoglobin Disorders in Pakistan. N Engl J Med., 347: 1162-8.

[12] Khair, F. M. (2019). The genetic origin of SCD in Sudan haplotype determine of homozygous patient. MD thesis: Khartoum Univ. Br. J. Haematol., 129(4): 482-90. doi:10.1111/j.1365 2141.2005.05476.x. PMID 15877730.

Copyright

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How to cite this paper

Association between Sickle Cell Crisis and Other Types of Hemoglobin among Sudanese Children with Sickle Cell Anemia

How to cite this paper: Arwa Abdelbagi Mohammed, Fathelrahman Mahadi Hassan, Abdelgadir Ahmed Abdelgadir, Amged Hussein Abdelrhman. (2021) Association between Sickle Cell Crisis and Other Types of Hemoglobin among Sudanese Children with Sickle Cell Anemia. International Journal of Clinical and Experimental Medicine Research5(2), 166-184.

DOI: http://dx.doi.org/10.26855/ijcemr.2021.04.011