A Cross Sectional Study of Association of HLA typing with Haemoglobin Level in Sickle Cell Anaemia
Journal of Pharmaceutical Research International,
Page 523-531
DOI:
10.9734/jpri/2021/v33i44B32704
Abstract
Background: Sickle-cell Disease (SCD) is the most common blood cell disorder affecting millions of people. In severe cases, regular blood transfusion is an essential practice to relieve clinical symptoms. However, since regular blood transfusion can lead to alloimmunization to foreign human leukocyte antigens (HLA), this may result in severe anemia due to red blood cell destruction. Therefore, this study aimed to determine the association between the hemoglobin level and the presence of HLA genotypes among Sickle Cell Anemia patients.
Methodology: A total of 64 SCD patients and 21 healthy donors seen at King Abdulaziz hospital between November 2019 and February 2021 were recruited for this study. Demographic data including ABO/Rhesus blood groups, hemoglobin concentration, were among the clinical information obtained. HLA genotyping was performed using Polymerase Chain Reaction-Sequence Specific Oligonucleotide (PCR-SSO). The data were cleaned using the Microsoft Excel and analysed using the statistical packages for Social Sciences (SPSS) version 24.
Results: The incidence of SCD is not strictly gender-related because of its transmission as an autosomal recessive disorder. Sixty-four individuals (33 females; 31 males) having SCD were analyzed. O blood group recorded the highest prevalence compared to other ABO blood groups in SCD patients. After analysing allelic association, HLA-A*02 was more frequent in SCD patients compared to control. After further allelic combination analysis of patients and compared with the control group, HLA-DQB1*02 was majorly involved in overexpression and decreasing hemoglobin level and significantly different among control and experimental groups.
Conclusion: Rhesus-positive blood types were more associated with the SCA. HLA- type II alleles could influence the clinical course of sickle cell disease and HLA-DQB1*02 was significantly different among SCD group and control individuals, which signifies the concept that the allele was overexpressed among patients resulting in low Hb level.
Keywords:
- Sickle cell anemia
- HLA typing
- anemia
How to Cite
References
Keidan AJ, Sowter MC, Johnson CS, Noguchi CT, Girling AJ, Stevens SM, et al. Effect of polymerization tendency on haematological, rheological and clinical parameters in sickle cell anaemia. Br J Haematol. 1989;71(4):551-7.
Leikin SL GD, Kinney TR, Sloane D, Klug P, Rida W. Mortality in children and adolescents with sickle cell disease. Pediatrics 1989;84(3):500-508. . Pediatrics. 1989:500-8.
Platt OS, Thorington BD, Brambilla DJ, Milner PF, Rosse WF, Vichinsky E, et al. Pain in sickle cell disease. Rates and risk factors. N Engl J Med. 1991;325(1):11-6.
Platt OS, Brambilla DJ, Rosse WF, Milner PF, Castro O, Steinberg MH, et al. Mortality in sickle cell disease. Life expectancy and risk factors for early death. N Engl J Med. 1994;330(23): 1639-44.
Serjeant GR CC, Lethbridge R, Morris J, Singhal A, Thomas PW. The painful crisis of homozygous sickle cell disease: Clinical features. . British Journal of Haematology. 1994:586-91.
Hoppe C, Klitz W, Vichinsky E, Styles L. HLA type and risk of alloimmunization in sickle cell disease. Am J Hematol. 2009;84(7):462-4.
Tamouza R NM-, Busson M, Marzais F, Girot R, Labie D. Infectious complications in sickle cell disease are influenced by HLA class II alleles. Immunology. 2002:194-9.
VM I. A specific chemical difference between the globins of normal human and sickle-cell anæmia hæmoglobin. Nature 1956;178(4537):792-794. Nature. 1956:792-4.
Satapornpong P, Jinda P, Jantararoungtong T, Koomdee N, Chaichan C, Pratoomwun J, et al. Genetic Diversity of HLA Class I and Class II Alleles in Thai Populations: Contribution to Genotype-Guided Therapeutics. Front Pharmacol. 2020;11:78.
Gluckman E CB, Bernaudin F, Labopin M, Volt F, Carreras J, Pinto Simões B, Ferster A, Dupont S, de la Fuente J, Dalle JH, Zecca M, Walters MC, Krishnamurti L, Bhatia M, Leung K, Yanik G, Kurtzberg J, Dhedin N, Kuentz M, Michel G, Apperley J et al. Sickle cell disease: an international survey of results of HLA-identical sibling hematopoietic stem cell transplantation. Blood. 2017;129(11):1548-56.
Ceglie G DMM, Tarissi De Jacobis I, de Gennaro F, Quaranta M, Baronci C, Villani A and Palumbo G. Gender-Related Differences in Sickle Cell Disease in a Pediatric Cohort: A Single-Center Retrospective Study. Front Mol Biosci. 2019;6(140).
Ilesanmi OO. Pathological basis of symptoms and crises in sickle cell disorder: implications for counseling and psychotherapy. Hematol Rep. 2010;2(1):e2.
Gladwin MT, Schechter AN, Ognibene FP, Coles WA, Reiter CD, Schenke WH, et al. Divergent nitric oxide bioavailability in men and women with sickle cell disease. Circulation. 2003;107(2):271-8.
Alagwu EA AD, Ngwu EE, Uloneme GC. ABO/Rhesus Blood Group and Correlation with Sickle Cell Disease and Type-II Diabetes Mellitus in South East and South-South of Nigeria. Pharmaceutical and Biosciences Journal; 2016.
Armando R. Orlina PJU, Mabel Koshy. Post‐transfusion alloimmunization in patients with sickle cell disease. American Journal of Hematology. 1978;2:101-6.
Alberú J M-BL, de Leo C, Vargas-Rojas MI, Marino-Vázquez LA, Crispín JC. A non-allogeneic stimulus triggers the production of de novo HLA antibodies in healthy adults. Transpl Immunol. 2007;18(2):166-71.
Gladstone DE ZA, Fuchs EJ, Luznik L, Kasamon YL, King KE, Brodsky RA, Jones RJ, Leffell MS. Partially mismatched transplantation and human leukocyte antigen donor-specific antibodies. Biol Blood Marrow Transplant. 2013;19(4):647-52.
Beck S TJ. The human major histocompatibility complex: lessons from the DNA sequence. Annu Rev Genomics. 2000:117-37.
HA E. HLA Polymorphism and Disease Susceptibility. Computational Genetics and Genomics: Humana Press; 2005.
JB. World distribution of HLA alleles and implications for disease. Ciba Found Symp. 1996;197(233).
A. Driss KOA, J.M. Hibbert, B.E. Gee, T.V. Adamkiewicz, J.K. Stiles. Sickle Cell Disease in the Post Genomic Era: A Monogenic Disease with a Polygenic Phenotype. Genomics Insights. 2009; 23-48.
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