Sickle cell anemia and resistance to malaria: Narrative review

Revista de la Facultad de Ciencias de la Salud de la Universidad del Cauca

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Title Sickle cell anemia and resistance to malaria: Narrative review
Anemia falciforme y la resistencia a la malaria. Revisión narrativa
 
Creator Roldán-Isaza, Mariana
Herrera-Almanza, Laura
Hernández-Martínez, Alejandro
Martínez-Sánchez , Lina María
 
Subject malaria
anemia
sickle cell
Hemoglobin
Sickle
malaria
anemia de células falciformes
Hemoglobina Falciforme
 
Description Sickle cell disease (SCD) is an autosomal recessive hemoglobinopathy, caused by the mutation of the β-globin chain gene that results in the replacement of valine by glutamic acid at the position of the sixth amino acid in the hemoglobin. There are various molecular and cellular mechanisms by which its pathophysiology is explained and thanks to its current understanding, new pharmacological agents are under clinical and preclinical research. Sickle hemoglobin (HbS), which is the consequence of this mutation, is related as a form of protection against malaria in heterozygotes; however, homozygous status (HbSS) may be associated with increased susceptibility to malaria. This protection relationship in heterozygotes is evidenced in lower levels of parasitaemia and later onset, that various theories had tried to explain. Therefore, this article aims to review the relationship between SCD and the protection it generates in malaria infection, in addition to exposing the pathophysiology and treatment of SCD to achieve a broader understanding of the disease.
La enfermedad de células falciformes (SCD, por sus siglas en inglés) es una hemoglobinopatía autosómica recesiva, producida por la mutación del gen de la cadena β-globina que genera la sustitución de valina por el ácido glutámico en la posición del sexto aminoácido de la hemoglobina. Existen diversos mecanismos moleculares y celulares por los cuales se explica su fisiopatología y gracias a su actual entendimiento, se encuentran en investigación clínica y preclínica nuevos agentes farmacológicos.  La hemoglobina falciforme (HbS), que es la consecuencia de dicha mutación, se relaciona como una forma de protección contra la malaria en los heterocigotos; sin embargo, el estado homocigoto (HbSS) puede estar asociado con una mayor susceptibilidad a la malaria. Dicha relación de protección en heterocigotos se evidencia en niveles más bajos de parasitemia y de aparición más tardía, lo que se ha tratado de explicar por diversas teorías. Por tanto, este artículo tiene como objetivo revisar la relación entre la SCD y la protección que genera en infección por malaria, además de exponer la fisiopatología y el tratamiento de la SCD para lograr un entendimiento más amplio de la enfermedad.   
 
Publisher Universidad del Cauca
 
Date 2020-07-01
 
Type info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
 
Format application/pdf
 
Identifier https://revistas.unicauca.edu.co/index.php/rfcs/article/view/1510
10.47373/rfcs.2020.v22.1510
 
Source Revista de la Facultad de Ciencias de la Salud Universidad del Cauca; Vol. 22 No. 2 (2020): Colecistectomía laparoscópica; 34-42
Revista de la Facultad de Ciencias de la Salud Universidad del Cauca; Vol. 22 Núm. 2 (2020): Colecistectomía laparoscópica; 34-42
2538-9971
0124-308X
 
Language spa
 
Relation https://revistas.unicauca.edu.co/index.php/rfcs/article/view/1510/1379
/*ref*/Atiku SM, Louise N, Kasozi DM. Severe oxidative stress in sickle cell disease patients with uncomplicated Plasmodium falciparum malaria in Kampala, Uganda. BMC Infect Dis. 2019;19(1):600. doi: 10.1186/s12879-019-4221-y.
/*ref*/Adjei GO, Goka BQ, Enweronu-Laryea CC, Rodrigues OP, Renner L, Sulley AM, et al. A randomized trial of artesunate-amodiaquine versus artemether-lumefantrine in Ghanaian paediatric sickle cell and non-sickle cell disease patients with acute uncomplicated malaria. Malar J. 2014;13:369. doi: 10.1186/1475-2875-13-369.
/*ref*/Eleonore NLE, Cumber SN, Charlotte EE, Lucas EE, Edgar MML, Nkfusai CN,et al. Malaria in patients with sickle cell anaemia: burden, risk factors and outcome at the Laquintinie hospital, Cameroon. BMC Infect Dis. 2020;20(1):40. doi:10.1186/s12879-019-4757-x.
/*ref*/Diakité SA, Ndour PA, Brousse V, Gay F, Roussel C, Biligui S, et al. Stage-dependent fate of Plasmodium falciparum-infected red blood cells in the spleen and sickle-cell trait-related protection against malaria. Malar J. 2016;15(1):482.
/*ref*/Milner DA Jr. Malaria Pathogenesis. Cold Spring Harb Perspect Med. 2018;8(1). pii: a025569. doi: 10.1101/cshperspect.a025569.
/*ref*/Bwire GM, Majigo M, Makalla R, Nkinda L, Mawazo A, Mizinduko M, et al. Immunoglobulin G responses against falciparum malaria specific antigens are higher in children with homozygous sickle cell trait than those with normal hemoglobin. BMC Immunol. 2019;20(1):12. doi: 10.1186/s12865-019-0294-z.
/*ref*/Komba AN, Makani J, Sadarangani M, Ajala-Agbo T, Berkley JA, Newton CR, et al. Malaria as a cause of morbidity and mortality in children with homozygous sickle cell disease on the coast of Kenya. Clin Infect Dis. 2009;49(2):216-22. doi: 10.1086/599834.
/*ref*/Albiti AH, Nsiah K. Comparative haematological parameters of HbAA and HbAS genotype children infected with Plasmodium falciparum malaria in Yemen. Hematology. 2014;19(3):169-74. doi: 10.1179/1607845413Y.0000000113
/*ref*/Oniyangi O, Omari AA. Malaria chemoprophylaxis in sickle cell disease.Cochrane Database Syst Rev. 2019;2019(11). doi: 10.1002/14651858.CD003489.pub2
/*ref*/Gupta NK, Gupta M. Sickle cell anemia with malaria: a rare case report. Indian J Hematol Blood Transfus. 2014;30 (1):38–40. doi:10.1007/s12288-012-0181-8
/*ref*/Rojas-Martínez A., Calderón E., Vidal M.A., Arroyo F., García-Hernández R., Torres L.M. Crisis drepanocítica y tratamiento del dolor. Rev. Soc. Esp. Dolor. 2015; 22 (4): 165-167. doi.org/10.4321/S1134-80462015000400004.
/*ref*/Azar S, Wong TE. Sickle Cell Disease: A Brief Update. Med Clin North Am. 2017;101(2):375-393. doi: 10.1016/j.mcna.2016.09.009
/*ref*/Eller R, da Silva D.B. Evaluation of a neonatal screening program for sickle-cell disease. J Pediatr (Rio J). 2016; 92 (4): 409-413. doi: 10.1016/j.jped.2015.10.002.
/*ref*/Castro IPS, Viana MB. Cognitive profile of children with sickle cell anemia compared to healthy controls. J Pediatr (Rio J). 2018. https://doi.org/10.1016/j.jped.2018.04.012
/*ref*/World Health Organization. World Malaria Report 2019. [Consultado el 24 Abr 2020] Disponible en: https://www.who.int/malaria/media/world-malaria-report-2019/es/.
/*ref*/Aneni EC, Hamer DH, Gill CJ. Systematic review of current and emerging strategies for reducing morbidity from malaria in sickle cell disease. Trop Med Int Health. 2013;18(3):313-27. doi: 10.1111/tmi.12056.
/*ref*/Kato GJ, Gladwin MT, Steinberg MH. Deconstructing sickle cell disease: reappraisal of the role of hemolysis in the development of clinical subphenotypes. Blood Rev 2007;21(1):37–47.
/*ref*/Díaz-Morejón L, Rodríguez-Jorge B, García-Sánchez D, León-Rayas Y, Aguilar-Lezcano L, Santacruz-Leonard M. Anemia drepanocítica: características generales de los pacientes a su diagnóstico. Revista Finlay [Internet]. 2019; 9(1): [aprox. 6 p.]. Disponible en: http://www.revfinlay.sld.cu/index.php/finlay/article/view/681
/*ref*/Ayala Viloria Alfonso J, González Torres Henry J, David Tarud Gabriel J. Anemia de células falciformes: una revisión. Salud, Barranquilla [Internet]. 2016;32 (3): 513-527. Disponible en: http://www.scielo.org.co/scielo.php?script=sci_arttext&pid=S0120-55522016000300014&lng=en.
/*ref*/Zúñiga C. Pamela, Martínez G. Cindy, González R. Lina M., Rendón C. Diana S., Rojas R. Nicolás, Barriga C. Francisco et al. Enfermedad de células falciformes: Un diagnóstico para tener presente. Rev. chil. pediatr. [Internet]. 2018; 89(4): 525-529. Disponible en: https://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0370-41062018000400525&lng=es. doi: 10.4067/S0370-41062018005000604
/*ref*/Tisdale JF, Thein SL, Eaton WA. Treating sickle cell anemia. Science. 2020;367(6483):1198-1199. doi: 10.1126/science.aba3827.
/*ref*/Monus T, Howell CM. Current and emerging treatments for sickle cell disease. JAAPA. 2019;32(9):1-5. doi: 10.1097/01.JAA.0000578812.47138.99.
/*ref*/Fernandes Q. Therapeutic strategies in Sickle Cell Anemia: The past present and future. Life Sci. 2017; 178:100-108. doi: 10.1016/j.lfs.2017.03.025.
/*ref*/Nevitt SJ, Jones AP, Howard J. Hydroxyurea (hydroxycarbamide) for sickle cell disease. Cochrane Database Syst Rev. 2017;4:CD002202. doi: 10.1002/14651858.CD002202.pub2.
/*ref*/Hasson C, Veling L, Rico J, Mhaskar R. The role of hydroxyurea to prevent silent stroke in sickle cell disease: Systematic review and meta-analysis. Medicine (Baltimore). 2019;98(51):e18225. doi: 10.1097/MD.0000000000018225.
/*ref*/Cooper TE, Hambleton IR, Ballas SK, Johnston BA, Wiffen PJ. Pharmacological interventions for painful sickle cell vaso-occlusive crises in adults. Cochrane Database Syst Rev. 2019;2019(11). doi: 10.1002/14651858.CD012187.pub2.
/*ref*/Merlet AN, Messonnier LA, Coudy-Gandilhon C, Béchet D, Gellen B, Rupp T, et al. Beneficial effects of endurance exercise training on skeletal muscle microvasculature in sickle cell disease patients. Blood. 2019;134(25):2233-2241. doi: 10.1182/blood.2019001055.
/*ref*/Padaro E, Kueviakoe IMD, Agbétiafa K, Magnang H, Mawussi K, Layibo Y, Vovor A. Therapeutic phlebotomy during major sickle cell disease in Togo. Med Sante Trop. 2019;29(1):106-107. doi: 10.1684/mst.2019.0886.
/*ref*/Kapoor S, Little JA, Pecker LH. Advances in the Treatment of Sickle Cell Disease. Mayo Clin Proc. 2018;93(12):1810-1824. doi: 10.1016/j.mayocp.2018.08.001.
/*ref*/Ataga KI, Stocker J. The trials and hopes for drug development in sickle cell disease. Br J Haematol. 2015;170(6):768-80. doi: 10.1111/bjh.13548.
/*ref*/Ferreira FA, Benites BD, Costa FF, Gilli S, Olalla-Saad ST. Recombinant erythropoietin as alternative to red cell transfusion in sickle cell disease. Vox Sang. 2019;114(2):178-181. doi: 10.1111/vox.12750.
/*ref*/Demirci S, Uchida N, Tisdale JF. Gene therapy for sickle cell disease: An update. Cytotherapy. 2018 Jul;20(7):899-910. doi: 10.1016/j.jcyt.2018.04.003.
/*ref*/Olowoyeye A, Okwundu CI. Gene therapy for sickle cell disease. Cochrane Database Syst Rev. 2018;11:CD007652. doi: 10.1002/14651858.CD007652.pub6.
/*ref*/López C, Saravia C, Gomez A, Hoebeke J, Patarroyo MA. Mechanisms of genetically-based resistance to malaria. Gene. 2010;467(1-2):1-12. doi: 10.1016/j.gene.2010.07.008.
/*ref*/Miura K, Diakite M, Diouf A, Doumbia S, Konate D, Keita AS et al. Relationship between malaria incidence and IgG levels to Plasmodium falciparum merozoite antigens in Malian children: impact of hemoglobins S and C. PLoS One. 2013;8(3):e60182. doi: 10.1371/journal.pone.0060182.
/*ref*/Nasr A, Saleh AM, Eltoum M, Abushouk A, Hamza A, Aljada A, et al. Antibody responses to P. falciparum Apical Membrane Antigen 1(AMA-1) in relation to haemoglobin S (HbS), HbC, G6PD and ABO blood groups among Fulani and Masaleit living in Western Sudan. Acta Trop. 2018;182:115-123. doi: 10.1016/j.actatropica.2018.02.030.
/*ref*/Tan X, Traore B, Kayentao K, Ongoiba A, Doumbo S, Waisberg M, et al. Hemoglobin S and C heterozygosity enhances neither the magnitude nor breadth of antibody responses to a diverse array of Plasmodium falciparum antigens. J Infect Dis. 2011;204(11):1750-61. doi: 10.1093/infdis/jir638.
/*ref*/Beaudry JT, Krause MA, Diakite SA, Fay MP, Joshi G, Diakite M, et al. Ex-vivo cytoadherence phenotypes of Plasmodium falciparum strains from Malian children with hemoglobins A, S, and C. PLoS One. 2014;9(3):e92185. doi: 10.1371/journal.pone.0092185.
/*ref*/Diakité SA, Ndour PA, Brousse V, Gay F, Roussel C, Biligui S, et al. Stage-dependent fate of Plasmodium falciparum-infected red blood cells in the spleen and sickle-cell trait-related protection against malaria. Malar J. 2016;15(1):482.
/*ref*/Archer NM, Petersen N, Clark MA, Buckee CO, Childs LM, Duraisingh MT. Resistance to Plasmodium falciparum in sickle cell trait erythrocytes is driven by oxygen-dependent growth inhibition. Proc Natl Acad Sci U S A. 2018;115(28):7350-7355. doi: 10.1073/pnas.1804388115.
/*ref*/Duraisingh M, Lodish H. Sickle Cell MicroRNAs Inhibit the Malaria Parasite. Cell Host Microbe. 2012; 12(2): 127–128. doi: 10.1016/j.chom.2012.08.001
 
Rights Derechos de autor 2020 Universidad del Cauca
info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/4.0
 

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