Evaluation of cardiac function tests in Sudanese adult patients with sickle cell trait
DOI:
https://doi.org/10.13181/mji.v25i3.1412Keywords:
cardiac function tests, CK-MB, homocysteine, hs-CRP, NT-proBNP, sickle cell traitAbstract
Background: Cardiac dysfunctions have been recognized as a common complication of sickle cell anaemia (SCA), and together with pulmonary disorder accounts for many deaths in these patients. However, sickle cell traits appear clinically normal, although they have genetic abnormality. The aim of this study was to assess the effect of sickle cell trait on cardiac prognostic markers by measuring high density lipoprotein (HDL-C), low density lipoprotein (LDL-C), cardiac creatine kinase (CK-MB), ultra-sensitive C reactive protein (us-CRP), total homocysteine (Hyc), and N-terminal pro-brain natriuretic peptide (NT-pro BNP) tests in adult Sudanese patients with sickle cell trait.
Methods: A cross-sectional study was performed in 200 healthy volunteers as a control group and 200 diagnosed patients with sickle cell trait. It was carried out in Khartoum Specialized Hospital, Al-Bayan Hospital, Obayed Clinical Center and Dr. Nadir Specialized Hospital, Sudan between January 2015 and January 2016. All participants were between 20-32 years old. LDL-C, HDL-C, CK-MB, NT-proBNP and hs-CRP concentrations were measured by Hitachi 912 full-automated Chemistry Analyzer (Roche Diagnostics, Germany) as manufacturer procedure, while homocysteine level was measured by ELISA technique using special kit.
Results: When compared to control group, the levels of LDL-C, hs-CRP and NT-proBNP revealed significant increase in patients’ sera (p<0.001), while Hyc and CK-MB levels were increased insignificantly in patients with SCT (p=0.069, p=0.054 respectively). On the other hand, comparison to control group, HDL-C showed insignificant reduction in patients (p=0.099).
Conclusion: The results suggest that sickle cell trait increased the risk of patient-related complication secondary to cardiac dysfunction.
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References
Eller R, da Silva DB. Evaluation of a neonatal screening program for sickle-cell disease. J Pediatr (Rio J). 2016;92(4):409-13. http://dx.doi.org/10.1016/j.jped.2015.10.002
Di Maria MV, Hsu HH, Al-Naami G, Gruenwald J, Kirby KS, Kirkham FJ, et al. Left ventricular rotational mechanics in Tanzanian children with sickle cell disease. J Am Soc Echocardiogr. 2015;28(3):340-6. http://dx.doi.org/10.1016/j.echo.2014.11.014
Weatherall DJ. The inherited diseases of hemoglobin are an emerging global health burden. Blood. 2010;115(22):4331-6. http://dx.doi.org/10.1182/blood-2010-01-251348
Rees DC, Williams TN, Gladwin MT. Sickle-cell disease. Lancet. 2010;376(9757):2018-31. http://dx.doi.org/10.1016/S0140-6736(10)61029-X
Ngolet LO, Engoba MM, Kocko I, Dokekias AE, Mombouli JV, Moyen GM. Sickle-cell disease healthcare cost in Africa: Experience of the Congo. Anemia. 2016;2016:2046535. http://dx.doi.org/10.1155/2016/2046535
Leonardo FC, Brugnerotto AF, Domingos IF, Fertrin KY, de Albuquerque DM, Bezerra MA, et al. Reduced rate of sickle-related complications in Brazilian patients carrying HbF-promoting alleles at the BCL11A and HMIP-2 loci. Br J Haematol. 2016;173(3):456-60. http://dx.doi.org/10.1111/bjh.13961
Piel FB, Adamkiewicz TV, Amendah D, Williams TN, Gupta S, Grosse SD. Observed and expected frequencies of structural hemoglobin variants in newborn screening surveys in Africa and the Middle East: deviations from Hardy-Weinberg equilibrium. Genet Med. 2016;18(3):265-74. http://dx.doi.org/10.1038/gim.2015.143
Tsitsikas DA, Sirigireddy B, Nzouakou R, Calvey A, Quinn J, Collins J, et al. Safety, tolerability, and outcomes of regular automated red cell exchange transfusion in the management of sickle cell disease. J Clin Apher. 2016;00:1-6. http://dx.doi.org/10.1002/jca.21447
Ndeezi G, Kiyaga C, Hernandez AG, Munube D, Howard TA, Ssewanyana I, et al. Burden of sickle cell trait and disease in the Uganda Sickle Surveillance Study (US3): a cross-sectional study. Lancet Glob Health. 2016;4(3):e195-200. http://dx.doi.org/10.1016/S2214-109X(15)00288-0
Faro GB, Menezes-Neto OA, Batista GS, Silva-Neto AP, Cipolotti R. Left ventricular hypertrophy in children, adolescents and young adults with sickle cell anemia. Rev Bras Hematol Hemot. 2015;37(5):324-8. http://dx.doi.org/10.1016/j.bjhh.2015.07.001
Gladwin MT, Sachdev V. Cardiovascular Abnormalities in sickle cell disease. J Am Coll Cardiol. 2012;59(13):1123-33. http://dx.doi.org/10.1016/j.jacc.2011.10.900
Abdelsalam KE. Combination of plasma ultra-sensitive CRP and homocysteine as diagnostic and predictive protocol for acute myocardial infarction. Int J Sci Res. 2015;4(4):1733-5.
Goodman J, Hassell K, Irwin D, Witkowski EH, Nuss R. The splenic syndrome in individuals with sickle cell trait. High Alt Med Biol. 2014;15(4):468-71. http://dx.doi.org/10.1089/ham.2014.1034
Rahimi Z, Vaisi-Raygani A, Pourmotabbed T. Association between apolipoprotein e4 allele, factor V Leiden, and plasma lipid and lipoprotein levels with sickle cell disease in Southern Iran. Mol Biol Rep. 2011;38(2):703-10. http://dx.doi.org/10.1007/s11033-010-0157-4
Galvão AF, Petta T, Flamand N, Bollela VR, Silva CL, Jarduli LR, et al. Plasma eicosanoid profiles determined by high-performance liquid chromatography coupled with tandem mass spectrometry in stimulated peripheral blood from healthy individuals and sickle cell anemia patients in treatment. Anal Bioanal Chem. 2016.408(13):3613-23. http://dx.doi.org/10.1007/s00216-016-9445-8
Krishnan S, Setty Y, Betal SG, Vijender V, Rao K, Dampier C, et al. Increased levels of the inflammatory biomarker C-reactive protein at baseline are associated with childhood sickle cell vasocclusive crises. Br J Haematol. 2010;148(5):797-804. http://dx.doi.org/10.1111/j.1365-2141.2009.08013.x
Okocha C, Manafa P, Ozomba J, Ulasi T, Chukwuma G, Aneke J. C-reactive protein and disease outcome in nigerian sickle cell disease patients. Ann Med Health Sci Res. 2014;4(5):701-5. http://dx.doi.org/10.4103/2141-9248.141523
Machado RF, Anthi A, Steinberg MH, Bonds D, Sachdev V, Kato GJ, et al. N-terminal pro-brain natriuretic peptide levels and risk of death in sickle cell disease. JAMA. 2006;296(3):310-8. http://dx.doi.org/10.1001/jama.296.3.310
Ndumele CE, Matsushita K, Sang Y, Lazo M, Agarwal SK, Nambi V, et al. N-Terminal Pro-Brain natriuretic peptide and heart failure risk among individuals with and without obesity: The Atherosclerosis Risk in Communities (ARIC) study. Circulation. 2016;133(7):631-8. http://dx.doi.org/10.1161/CIRCULATIONAHA.115.017298
Ali Z, Troncoso JC, Fowler DR. Recurrent cerebral venous thrombosis associated with heterozygote methylenetetrahydrofolate reductase C677T mutation and sickle cell trait without homocysteinemia: an autopsy case report and review of literature. Forensic Sci Int. 2014;242:e52-5. http://dx.doi.org/10.1016/j.forsciint.2014.07.007
Nnadi E, Manafa P, Okocha E, Chukwuma G, Aneke J. Evaluation of creatine kinase activity and inorganic phosphate concentration in adult Nigerian homozygous and heterozygous hemoglobin phenotypes. Ann Med Health Sci Res. 2014;4(5):697-700. http://dx.doi.org/10.4103/2141-9248.141518
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