Transfusion Practice, Post-Transfusion Complications and Risk Factors in Sickle Cell Disease in Senegal, West Africa

Moussa Seck1,3, Alioune Badara Senghor2, Mossane Loum3, Sokhna Aissatou Touré3, Blaise Félix Faye1,3, Alioune Badara Diallo3, Mohamed Keita3, Seydi Elimane Bousso3, Sérigne Mourtalla Guèye2,3, Macoura Gadji1,2, Abibatou Sall1,4, Awa Oumar Touré1,5 and Saliou Diop1,2,3.

Department of Hematology, Cheikh Anta Diop University, Dakar, Senegal.
2 National Blood Transfusion Center, Dakar, Senegal.
3 Clinical Hematology Department, CNTS, Dakar, Senegal.
4 Hematology Laboratory, Dalal Jamm Hospital, Dakar, Senegal.
5 Hematology Laboratory, Aristide Le Dantec Hospital, Dakar, Senegal.

Correspondence to: Seck Moussa (Seck M). Department of Hematology, Cheikh Anta Diop University, Dakar, Senegal. Clinical Hematology Department, CNTS, Dakar, Senegal. BP 5002 Dakar-Fann. Phone: (+221) 77 557 28 86

Published: January 1, 2022
Received: September 3, 2021
Accepted: December 8, 2021
Mediterr J Hematol Infect Dis 2022, 14(1): e2022004 DOI 10.4084/MJHID.2022.004

This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Context and Objectives: Blood transfusions (BT) remain a mainstay of therapy for patients with sickle cell disease (SCD) but pose significant clinical challenges. We aim to assess infectious markers, red cell alloimmunization, and iron overload secondary to BT in SCD patients.
Materials and Methods: This case-control study included 253 SCD (153 SCD-transfused and 100 SCD non-transfused). We evaluated the transfusion practice (modalities, indications), post-transfusion complications (infections, alloimmunization, iron overload), and risk factors of these complications (socio-demographic, clinical, biological).
Results: Median age was 28.5 years (5 - 59). The sex ratio was 0.86. Homozygous SCD was the most common (95.3%). Simple BT was performed in 92.8% and transfusion exchange in 18.9%. Transfusion indications were dominated by acute anemia (57.06%) and vaso-occlusive crisis (VOCs) (14%). Red blood cell concentrates (RBCSs) were administered to 93.46%. The median RBCs received per patient was 10 (2 - 48). The prevalence of VHC in SCD-transfused was 1.33% and 2% for VHB. Anti-HIV antibodies were not found. Red cell alloimmunization frequency was 16%. The most common alloantibodies were anti-rhesus (34.19%) and anti-Kell (23.67%). Iron overload was detected in 7.84%. The number of RBCs transfused was the only risk factor for alloimmunization (p = 0.03) and iron overload (p = 0.023). BT frequency was not related to infectious transmission.
Conclusion: BT therapy is still a risk for SCD polytransfused patients despite advances in blood safety. Although infectious transmission has rare, the risk of alloimmunization and iron overload is high in these patients.


SCD is one of the most common worldwide hereditary disorders characterized by the substitution of hemoglobin A (HbA) with the abnormal HbS. In Africa, 10% to 40% are carriers of HbS, and each year 200 000 to 300 000 newborns have the homozygous form.[1] SCD is characterized by high morbidity and significant mortality at the onset of acute or chronic complications whose treatment often resorts to BT.[2]
BT is currently a major therapeutic option indispensable in the management of severe forms of SCD.[3,4] It exists in three methods to treat SCD anemia: simple BT, punctual transfusion exchange, and long-term transfusion exchange.[5,6]
Despite the benefits, multi-transfused patients are at an increased risk of complications of red cell alloimmunization, iron overload, and blood-transmitted infections.[7,8,9] The frequency of these complications correlates with RBCs  units transfused.[3,4] The presence of one of these complications is a major risk factor for morbidity and mortality in SCD patients requiring specialized therapeutic management.[8,10] Preventing these complications can be achieved by optimization of BT indications, extensive phenotyping of RBCs and patient’s blood group, and strengthening infectious blood safety.[11,12] Systematic screening for these complications in SCD-polytransfused is recommended by screening for irregular agglutinins, for infectious transmitted (HIV, VHB, VHC) before and after BT, and ferritin assay even if serum ferritin constitutes an indirect marker to detect post-transfusion iron overload.[13,14,15] In Africa, there are many shortcomings in transfusion availability and safety. These constraints could have consequences in polytransfused patients such as SCD patients. Unfortunately, data on the frequency of post-transfusion complications are scarce, especially in Senegal. 
The objective of this study was to report on the practical aspects of BT and post-transfusion complications in SCD patients.

Materials and Methods

The study included 253 SCD patients (homozygous SS, heterozygous SC, Sβ0 thalassemia, Sβ+ thalassemia) consisting of 153 transfused and 100 non-transfused SCD.
SCD-transfused had undergone at least two transfusions during follow-up; blood samples were taken at least one month before from any vaso occlusives crisis (VOCs) or infections. VOCs were defined as bone pain that lasted 48 hours or required hospitalization. All patients were diagnosed by hemoglobin electrophoresis at alkaline pH, regularly monitored every three months, and a medical record included socio-demographic, clinical, and biological data. Informed consent was obtained for all patients before the samples.
This case-control study was carried out at the Clinical Hematology Department (Dakar, Senegal) over six months. Three samples (5ml) were taken; EDTA samples for detection and identification of irregular antibodies, citrate samples for viral hepatitis B (HBsAg), hepatitis C (VHC antibodies), and HIV (HIV 1 and 2 antibodies, and P24 antigen), and a serum sample for ferritin assay. Blood samples collected were immediately centrifuged at 3500 rpm. The serum was aliquoted and stored at -80°C.
Viral markers screening (HBsAg, VHC antibodies, HIV antibodies) was performed using chemiluminescence methods (Architect i1000sr, Abbott, USA). Searching for irregular antibodies was carried out by gel filtration test (Bio-Rad reagents, USA). Ferritin assay was performed by immunoassay (PLC Axsym, Abbott, USA). The reference values of ferritin level were defined between 7 and 250 ng/ml (Women) and 20-300 ng/ml (Men). Iron overload was defined when ferritin level was greater than or equal to 1000 ng/ml.
Socio-demographic variables were age and sex. Clinical variables consisted of the duration of follow-up, number of VOCs, acute complications (acute anemia, priapism, acute chest syndrome, infections, stroke), chronic complications (biliary lithiasis, leg ulcer, osteonecrosis, cardiac failure, renal failure). Laboratory variables consisted of blood count and hemoglobin electrophoresis data. Transfusion data were the frequency of transfusions, type of blood product, transfusion indications, and transfusion modalities. In addition, risk factors for the occurrence of transfusion complications were studied.
Data were collected and analyzed using Epi Info version 3.5.4. Means were calculated with a 95% confidence interval. Chi2 test was used to study the frequency data (significance of p <0.05). In addition, the correlation coefficient (r) between ferritin level and RBCs number received was determined (r between -1 and 1).
All patients signed an informed consent form prior to participation in the study. For minors, the signature was obtained from one of the parents.


SCD Patients Baseline Characteristics. The mean age was 28.5 years (5 - 59), and the sex ratio was 0.86. Homozygous SCD was more common (95.3%), Sβ0 thalassemia (2.62%), SC form (1.31%), and Sβ+ thalassemia (0.65%). The mean duration of follow-up was 9.1 years (2 - 26). The mean number of VOCs per year was 2 (1 - 6). Acute complications consisted of anemia (63.98%), infections (26.69%), priapism (5.51%), stroke (2.12%), acute chest syndrome (0.85%) and renal failure (0.85%). Chronic complications were found in 39.87% of SCD-transfused and consisted of femoral head osteonecrosis (27.87%), biliary lithiasis (32.79%), leg ulcers (16.39%), pulmonary arterial hypertension (16.39%), and renal failure (6.56%). We had no statistical difference in baseline characteristics comparing transfused and non-transfused SCD patients (Table 1).

Table 1 Table 1. Baseline characteristics of SCD-transfused and SCD non-transfused patients.

Blood Transfusion Practice. According to transfusion methods, simple transfusion was performed in 92.81%, transfusion exchange in 18.95%; 14.37% of the patients were submitted to a blood transfusion program. Transfusion indications consisted of acute anemia (57.06%), prolonged VOCs (14%), pregnancy management (10.5%), surgery (7%), leg ulcers (4.2%), infections (2.8%), priapism (1.4%), acute chest syndrome (2.1%) and stroke (0.7%). RBCs were administered to 93.46% and whole blood to 6.54%. Mean number of RBCs transfused by patient was 10 (2 - 48); 43.14% had received between 2 and 5 RBCs (Figure 1).

Figure 1 Figure 1. SCD-Transfused patients and number of RBCS received.

Post-Transfusion Red Cell Alloimmunization (RCA). The prevalence of RCA was 16%. Anti-Rhesus and anti-Kell alloantibodies were predominant with 34.19% and 23.67% respectively (Table 2).
According to the distribution of alloantibodies, 14 SCD-transfused had a single alloantibody (58.3%), 5 patients had two alloantibodies (20.83%) and 5 other patients had three alloantibodies (20.83%).

Table 2 Table 2. Frequency and specificity of anti-erythrocyte alloantibodies..

Post-Transfusion Iron Overload. Median value of ferritin level was 339.5 ng/ml (16 - 5941). Twelve patients (7.84%) had ferritin levels more than 1000 ng/ml and received more than 20 RBCSs. We observed that ferritin level was correlated of blood transfusions frequency (r = 0.8) (Figure 2).

Figure 2 Figure 2. Correlation between RBCS units received and ferritin levels.

Transfusion-Transmitted Infections (TTI). The prevalence of VHC in SCD-transfused was 1.33% and 1% in non-transfused (p = 0.64). The prevalence of VHB was 2% in SCD-transfused and 3% in non-transfused (p = 0.45). Anti-HIV antibodies were not found neither in SCD-transfused than non-transfused (Table 3).
Risk Factors Occurred Post-Transfusion Complications. The number of RBCs transfused was the only risk factor for RCA (p=0.03) and for iron overload (p=0.023). In this study transmission of infectious agents was not observed after blood transfusions (Table 3).

Table 3 Table 3. Risk factors associated with infectious markers, RCA and iron overload.


BT is an essential treatment in the management of SCD. Its usage is different from one country to another depending on the type of indication.[12,16,17] The objective of BT in SCD is not only correct chronic anemia but also to decrease HBS level and therefore to prevent or treat SCD complications whereas in case, of a simple or a transfusion exchange, either in an acute context or during a transfusion program.[3,6] Iterative transfusions are exposed to RCA, infectious and iron overload which pose a great risk of morbidity and mortality for SCD patients.[4,5]
In this study, simple transfusion was performed in the majority of cases and few patients had a chronic transfusion program. We confirm that our patients are less transfused as compared to other SCD cohort in Africa and in the world.[16,17] The lower severity of the Senegal’s haplotype means that patients have few symptoms with less than 3 VOCs per year and transfusion indications dominated by acute anemia and prolonged VOCs, which are more random than scheduled.[12]
BT is an important treatment for some complications of SCD. On the contrary, transfusion may lead to alloimmunization to red blood cell antigens, with such alloantibodies putting patients at risk for acute or delayed hemolysis and increasing difficulty finding compatible RBCs. In addition, SCD patients are more susceptible to developing RBCs alloantibodies than non-SCD multiply-transfused for not completely understood reasons.[18,19]
The phenotypic and antigenic disparity between blood donors and SCD patients partly explain the appearance of RBCs alloantibodies.[20] In our study, the RCA rate was 16%. RCA frequency has been shown to increase with the BT.[10,15,21] In Africa, where SCD-patients are rarely on a long-term transfusion, RCA rates are lower.[23,24,25] Unlikely in developed countries, in which SCD-patients receive more RBCs, alloimmunization is higher, often reaching half of SCD-patients.[15,26] These high rates of RBCs in developed countries could be explained by genetic differences in blood group antigens distribution between black SCD-patients and Caucasian blood donors.[18,27] Extended phenotyping blood group systems between blood donors and SCD-patients would reduce the risk of RCA.[22,28] Thirty-eight different antibodies were identified in 24 SCD-transfused with positive irregular antibodies detection. These alloantibodies were mainly directed against Rhesus and Kell systems antigens. Anti-Rhesus and anti-Kell specificities were reported by most studies in Africa or developed countries.[21,29] The high immunogenicity of these two systems other than the ABO system could partially explain the high incidence.
Given the importance of polymorphism in blood group systems, the number of epitopes defining an erythrocyte antigen, BT may only be one of many RCA risk factors.[18] BT remains a critical component of care for acute and chronic SCD complications. Randomized clinical trials demonstrated the benefits of transfusion therapy to prevent primary and secondary strokes and post-operative acute chest syndrome. Despite overall improvements in blood inventory safety, adverse effects of BT are prevalent among SCD-patients and include RCA, acute and delayed hemolytic BT reactions.[9]
BT plays a prominent role in the management of SCD-patients but causes significant iron overload. As transfusions are used to treat severe complications in SCD, it remains difficult to distinguish whether organ damage is a consequence of iron overload or is due to the complications treated by BT. Better BT management has resulted in increased survival, but prolonged exposure to iron puts SCD-patients at greater risk for iron-related complications that should be treated.[13,30] Post-transfusion iron overload causes serious organ damage. Excess iron accumulates in the parenchymal tissues of different organs and causes degenerative lesions due to its toxicity.[31,34,35] Less than 10% of SCD-transfused received more than twenty RBCs units during follow-up. All these patients had a very high ferritin level (> 1000 ng/ml). Literature data show that organs’ iron overload risk appears when ferritin level is greater than 1000 ng/ml,[32] confirming our hypothesis that iron overload is correlated with the frequency of RBCs transfused.[33] However, it should be noted that serum ferritin assay is a good sensitivity marker but of poorer specificity for detecting iron overload in SCD-polytransfused patients because the inflammatory phenomena are more frequent in SCD.[35] The choice of serum ferritin assay as iron overload evaluation method in our study is guided by the fact that this method is more accessible and less costly than others. However, it can have drawbacks because hyperferritinemia can be related not only to organs’ iron overload but also to pathologies frequent in SCD like liver disease, inflammation or VOCs.[36] Another alternative would be the measurement of unbound plasma iron which evaluates toxic iron fraction, but unfortunately, this test is not available in current practice.[37] Direct methods such as the determination of the intrahepatic iron concentration by hepatic biopsy, magnetic susceptometry or nuclear magnetic resonance imaging (MRI), and myocardial iron overload by MRI make it possible to accurately assess the organs iron overload.[30] Direct methods are more reliable but rarely accessible, so serum ferritin assay is more widely used in Africa.[32,38]
SCD-patients often require RBCs transfusion for clinical complications and then may be exposed to transfusion-transmitted infections.[14] The prevalence of VHB and VHC was low in SCD-transfused in Senegal, and no HIV antibodies were found in any patient. This prevalence is much lower than those found in other countries in Africa.[43,44] This low prevalence is explained by the progress in the medical selection of blood donors and the strengthening of infectious transfusion safety through the systematic screening of these infectious agents.[11] Comparing the prevalence of infections in the Senegalese population, we find that HBsAg was lower (11%) and anti-HCV (2.2%)  and anti-HIV antibodies (0.7%)  were slightly higher than in other African countries.[45] We confirm that TTI is more frequent in Africa.[46] VHB is more common, affecting more than 20% of SCD-polytransfused in some countries,[47,48] followed by VHC.[49] HIV antibodies were not found in this study but were present in studies carried out in several Africa countries with sometimes very high rates.[48,50] This infectious risk in multi-transfused patients is lower in developed countries.[51,52] Establishing infectious blood safety by the genomic screening of infectious markers is the real goal. In Africa, infectious tests which are used do not make it possible to cover the serological period resulting in a persistent residual risk of TTI.[46,52]
Risk factors of RBCs transfused were age, gender, chronic complications, mean baseline hemoglobin level, and number of RBCs-transfused. The only risk factor associated with RCA and iron overload was the number of RBCs transfused. No factors were associated with TTI occurrence by comparing SCD-transfused and non-transfused.
The pathogenesis of alloimmunization is not well understood, and initiatives that aim to reduce the incidence of alloimmunization are generally expensive and either ineffective or unproven. Future reductions in the costs associated with genotype matching could make a largescale program economically feasible. Novel techniques to identify patients at the highest risk for alloimmunization could improve the cost-effectiveness of antigen matching programs.[39] Judicious use of BT, optimization of red cell antigen matching, and the use of erythrocytapheresis and iron chelation can minimize adverse effects. Early recognition and management of hemolytic transfusion reactions can avert poor clinical outcomes.[9] Identifying genetic markers may help predict which patients are at risk of forming alloantibodies. This study found 19 moderately associated SNPs, among others, SNPs in TLR1/TANK and MALT1 were associated with a higher alloimmunization risk, while SNPs in STAM/IFNAR1 and STAT4 conferred a lower alloimmunization risk.[40]
The strong correlation between ferritin level and RBCs received is confirmed in some studies,[32] while others emphasized a lack of relationship between the two parameters.[16,38] Therefore, ferritin assay must be serially performed, and the screening must be made in the basal state without VOCs. The prevention of post-transfusion iron overload is based on the optimization and regulation of BT in managing chronic anemia.[41] In addition, Erythrocytapheresis reduces iron overload and allows a longer interval between procedures without a higher RBCs requirement from the second year on automated RBCs exchange.[42]


Post-transfusion iron overload and RCA strongly correlate with BT frequency, which is not the case with infectious agents (HIV, HBV, HCV). So, we recommend optimization of transfusion practices, extensive phenotyping blood groups, serial ferritin screening after twenty RBCs-transfused, and TTI screening before and after transfusion for improved blood safety in SCD-patients.


The authors thank all the staff of the hematology department of Cheikh Anta Diop University and the clinical hematology department and the National Blood Transfusion Center laboratory in Dakar, Senegal.


  1. Diop S, Pirenne F. Transfusion and sickle cell anemia in Africa. Transfus Clin Biol. 2021 May;28(2):143-145 PMid:33515732
  2. Samir KB. Sickle cell disease: Classification of clinical complications and approaches to preventive and therapeutic management. Clin Hemorheol Microcirc. 2018;68(2-3):105-128 PMid:29614627
  3. Stella TC, Ross MF. Management of Patients with Sickle Cell Disease Using Transfusion Therapy. Guidelines and Complications. Hematol Oncol Clin N Am 30 (2016) 591-608. PMid:27112998
  4. Stella TC, Mouaz A, Ross MF, Joshua JF, Jeanne EH, Jo H, Kameka M, Kwiatkowski JL, Pirenne F, Shi PA, Stowell SR, Thein SL, Westhoff CM, Wong TE, Akl EA. American Society of Hematology 2020 guidelines for sickle cell disease: transfusion support. Blood Advances 2019:4(2): 327-355. Blood Adv. 2020 Jan 28;4(2):327-355 PMid:31985807 PMCid:PMC6988392
  5. Sharma D, Ogbenna AA, Kassim A, Andrews J. Transfusion support in patients with sickle cell disease. Semin Hematol. 2020 Apr;57(2):39-50 PMid:32892842
  6. Faye BF, Sow D, Seck M, Dieng N, Touré SA, Gadji M, Senghor AB, Gueye YB, Sy D, Sall A, Dieye TN, Toure AO, Diop S . Efficacy and Safety of Manual Partial Red Cell Exchange in the Management of Severe Complications of Sickle Cell Disease in a Developing Country. Adv Hematol. 2017;2017:3518402. PMid:28584527 PMCid:PMC5443989
  7. Mabien AP, Brown B, Herbert DE, Haynes J. Iron overload in adults with sickle cell disease who have received intermittent red blood cell transfusions. J Am Assoc Nurse Pract. 2015; 27(10):591-6. PMid:25711464
  8. Pirenne F. The cause and pathogenesis of hemolytic transfusion reactions in sickle-cell disease. Curr Opin Hematol. 2019 Nov;26(6):488-494. PMid:31589171
  9. Grace EL and Stella TC. Red cell transfusion and alloimmunization in sickle cell disease. Haematologica. 2021 Jul 1;106(7):1805-1815 PMid:33792218 PMCid:PMC8252926
  10. Allali S, Peyrard T, Amiranoff D, Jérémie FC, Chalumeau M, Brousse V, Montalembert M. Prevalence and risk factors for red blood cell alloimmunization in 175 children with sickle cell disease in a French university hospital reference centre. Br J Haematol.2017 May;177(4):641-647. PMid:28402005
  11. Seck M, Diéye B, Guéye YB, Faye BF, Senghor AB, Toure SA, Dieng N, Sall A, Touré AO, Diéye TN, Diop S. Evaluation of the efficacy of medical screening of blood donors on preventing blood transfusion-transmitted infectious agents. Transfus Clin Biol. 2016;23(2):98-102 PMid:26681660
  12. Seck M, Tall A, Faye BF, Bah DS, Guéye Y, Sall A, Touré AO, Diop S. Evaluation of transfusion practices in sickle cell disease in Senegal: cohort study of 1078 patients with sickle cell disease. Med Sante Trop. 2017 Nov 1;27(4):402-406 PMid:29313508
  13. Thomas DC, John CW. How we manage iron overload in sickle cell patients. Br J Haematol.2020. PMid:28295188 PMCid:PMC5444974
  14. Blatyta PF, Kelly S, Sabino E, Preiss L, Mendes F, Carneiro-Proietti AB. Prevalence of serological markers of transfusion and sexually transmitted infections and their correlation with clinical features in a large cohort of Brazilian sickle cell disease patients. Transfusion. 2020; 60(2): 343-350. PMid:31804727 PMCid:PMC8010912
  15. Sally ACL, Kristina G, Mia CK, Yi-Fan C, Santosh LS, Lewis LH, Gordeuk VR, Ronald G Strauss RG, Triulzi DJ. Red blood cell alloimmunization in sickle cell disease: assessment of transfusion protocols during two time periods. Transfusion. 2018 Jul;58(7):1588-1596 PMid:29570817 PMCid:PMC7193458
  16. Boulat C. La transfusion du drépanocytaire. Transfus. Clin. Biol. 2013 ; 20 :68-71 PMid:23597585
  17. Elira Dokekias A, Ngolet Ossini L, Atipo Tsiba FO. Blood transfusion assessment to 112 homozygous sickle-cell disease patients in university hospital of Brazzaville. Transfus Clin Biol. Nov-Dec 2009;16(5-6):464-70. PMid:19369104
  18. Krystalyn EH, Ross MF, Matthew SK, Jeanne EH, Richard OF. Mechanisms of alloimmunization in sickle cell disease. Curr Opin Hematol 2019, 26:434-441 PMid:31483335
  19. Ross MF, Erin KM, Jane B, Mia SW, Robert WG, James RE. Impact of Red Blood Cell Antigen Matching on Alloimmunization and Transfusion Complications in Patients with Sickle Cell Disease: A Systematic Review. Ytmrv (2018), doi:10.1016/j.tmrv.2018.07.003. PMid:30122266
  20. Ben AI, Louati N, Khemekhem H, Dhieb A, Rekik H, Mdhaffar M, Gargouri J. Red blood cell immunization in haemoglobinopathie: about 84 cases. Transfus Clin Biol. 2012 Dec;19(6):345-52 PMid:23103424
  21. Zalpuri S, Zwaginga JJ, le Cessie S, Elshuis J, Schonewille H, Van der bom JG. Red-blood-cell allo-immunization and number of red-blood-cell transfusions. Vox Sang. 2012 Feb;102(2):144-9. PMid:21729098
  22. Balbuena-Merle R, Hendrickson JE. Red blood cell alloimmunization and delayed hemolytic transfusion reactions in patients with sickle cell disease. Transfus Clin Biol, 2019 ;26 : 112-115 PMid:30857806
  23. Noizat-Pirenne F. Immunohematologic characteristics in the Afro-caribbean population. Consequences for transfusion safety. Transfus Clin Biol. 2003 Jun;10(3):185-91.
  24. Kangiwa U, Ibegbulam O, Ocheni S, Madu A, Mohammed N. Pattern and prevelence of alloimmunization in multiply transfused patients with sickle cell disease in Nigeria. Biomark Res. 2015 Oct 13; 3: 26. PMid:26464798 PMCid:PMC4603770
  25. Dias Zanette AM, de Souza Goncalves M, Vilasboas Schettini L, Magalhaes Agguiar L, Santos Bahia RC, Vasconcelos Nogueira LA, de Freitas Brandão CJ, Neves de Azevedo AC, Ramos de Aragao L, Marcos Arruda S. Alloimmunisation and clinical profile of sickle cell disease patients from Salvador-Brazil. Ethn Dis. Spring 2010;20(2):136-41.
  26. Aygun B, Padmanabhan S, Paley C, Chandrasekaran V. Clinical significance of RBCS alloantibodies and autoantibodies in sickle cell patients who received transfusions. Transfusion 2002; 42:37-43. PMid:11896310
  27. Higgins JM, Sloan SR. Stochastic modeling of human RBCS alloimmunization: evidence for a distinct population of immunologic responders. Blood. 2008; 112:2546-53. PMid:18535200
  28. Lilian AB, Andrew DC, Robertson DD, Alex OA, Sheri HA, Henk S. Red blood cell alloimmunization and minor red blood cell antigen phenotypes in transfused Ghanaian patients with sickle cell disease. Transfusion. 2019;9999;1-7
  29. Boateng LA, Ngoma AM, Bates I, Schonewille H. Red Blood Cell Alloimmunization in Transfused Patients With Sickle Cell Disease in Sub-Saharan Africa; a Systematic Review and Meta-Analysis. Transfus Med Rev. 2019 Jul;33(3):162-169 PMid:31345590
  30. Stanley HM, Friedman DF, Webb J, Kwiatkowski JL. Transfusional Iron Overload in a Cohort of Children with Sickle Cell Disease: Impact of Magnetic Resonance Imaging, Transfusion Method, and Chelation. Pediatr Blood Cancer 2016;63:1414-1418 PMid:27100139 PMCid:PMC5132054
  31. Oduor H, Minniti CP, Brofferio A, Gharib AM, Abd-Elmoniem KZ, Hsieh MM, Tisdale JF, Fitzhugh CD. Severe cardiac iron toxicity in two adults with sickle cell disease. Transfusion. 2017 Mar;57(3):700-704. PMid:28019032 PMCid:PMC5352507
  32. Hafsia R, Belakhal F, Ben Salah N, Gouider E, Elborji W. Iron overload in sickle cell anemia : a study of 94 patients. Tunis Med. 2011 Jun;89(6):548-52.
  33. Leo-Kodeli S, Renaudier P, Lassale B. Evaluation of transfusion hemochromatosis prevalence, SFVTT-01 study: preliminary results of the SFVTT working group. Transfus Clin Biol. 2014 Nov;21(4-5):182-8. PMid:25277422
  34. Ginwalla M, AlMasoud A, Tofovic D, Alin T, Al-Kindi S, Oliveira G, Rajagopalan S, Schilz R, Little J. Cardiovascular Evaluation and Management of Iron Overload Cardiomyopathy in Sickle Cell Disease. Am J Hematol. 2018 Jan;93(1):E7-E9. doi: 10.1002/ajh.24924. Epub 2017 Oct 23. PMid:28971490
  35. Yassin M, Soliman A, De Sanctis V, Nashwan A, Abusamaan S, Moustafa A, Samah K, Soliman D. Liver iron content (LIC) in adults with sickle cell disease (SCD): correlation with serum ferritin and liver enzymes concentrations in trasfusion dependent (TD-SCD) and non-transfusion dependent (NT-SCD) patients. Mediterr J Hematol Infect Dis. 2017 Jun 20;9(1):e2017037. PMid:28698780 PMCid:PMC5499497
  36. Thuret I, Barlogis V, Michel G. Current concepts in the management of transfusional iron overload. Arch Pediatr. 2009 Jun;16(6):559-61.
  37. Walter PB, Fung EB, Killilea DW, Jiang Q, Hudes M, Madden J, Porter J, Patricia E, Vichinsky E, Harmatz P. Oxidative stress and inflammation in iron-overloaded patients with beta-thalassaemia or sickle cell disease. Br J Haematol. 2006 Oct;135(2):254-63. PMid:17010049 PMCid:PMC2185791
  38. Akinbami AA, Dosunmu AO, Adediran AA, Oshinaike OO, Osunkalu VO, Ajibola SO, Arogundade OM. Serum ferritin levels in adults with sickle cell disease in Lagos, Nigeria. J Blood Med. 2013 May 22;4:59-63 PMid:23723723 PMCid:PMC3666661
  39. Gehrie EA, Ness PM, Bloch EM, Kacker S, Tobian AA. Medical and economic implications of strategies to prevent alloimmunization in sickle cell disease. Transfusion. 2017 Sep;57(9):2267-2276. PMid:28653325 PMCid:PMC5695925
  40. Meinderts SM, Gerritsma JJ, Sins JW, de Boer M, van Leeuwen K, Biemond BJ, Rijneveld AW, Kerkhoffs Jean-Louis H, Habibi A, Bruggen RV, Kuijpers TW, Schoot EVD, Pirenne F, Fijnvandraat K, Tanck MW, Van den Berg TK. Identification of genetic biomarkers for alloimmunization in sickle cell disease. Br J Haematol. 2019 Sep;186(6):887-899. PMid:31168801
  41. Noizat-Pirenne F. Transfusion and sickle cell disease: axes of transfusion safety optimization. Transfus Clin Biol. 2014 May;21(2):77-84. PMid:24811565
  42. Dedeken L, Quoc LP, Rozen L, El Kenz H, Huybrechts S, Devalck C, Diallo S, Heijmans C, Ferster A. Automated RBCs exchange compared to manual exchange transfusion for children with sickle cell disease is cost-effective and reduces iron overload. Transfusion. 2018 Jun;58(6):1356-1362. PMid:29574950
  43. Diarra AB, Guindo A, Kouriba B, Dorie A. Sickle cell anemia and transfusion safety in Bamako, Mali. Seroprevalence of HIV, HBV and HCV infections and alloimmunization belonged to Rh and Kell systems in sickle cell anemia patients. Transfus Clin Biol. 2013 Dec;20(5-6):476-81.
  44. Ngo-Sack F, Noah D, Zouhaïratou H, Mbanya D. Prevalence of HBsAg and anti-HCV antibodies in homozygous sickle cell patients at Yaounde Central Hospital. Pan Afr Med J. 2013;14:40.doi: 10.11604/pamj.2013.14.40.2069. Epub 2013 Jan 28. PMid:23560123 PMCid:PMC3612872
  45. Agence National de la Statistique et de la Démographie (ANSD): Rapport sur la prévalence des infections au Sénégal en 2016.
  46. Kissou SA, Koura M, Sawadogo A, Ouédraogo AS, Traoré H, Kamboulé K, Zogona WWF, Nacro B. Serological Markers of Viral Hepatitis B and C in Children with Sickle Cell Disease Monitored in the Pediatrics Department at the University Hospital of Bobo-Dioulasso (Burkina Faso). Bull Soc Pathol Exot. 2017 Aug;110(3):160-164. PMid:28417347
  47. Fasola FA, Odaibo GN, Aken'Ova YA, Olaleye OD. Hepatitis B and C viral markers in patients with sickle cell disease in Ibadan, Nigeria. Afr J Med Sci, 2003; 32: 293 -295.
  48. Séka-séka J, Yapo-Crezoit AC, Dasse-Sery R, Akre-Draga P, Sorho F, Sombo Mambo F. Etude de la séroprévalence de l'hépatite virale C dans la population drépanocytaire en Côte d'Ivoire. Méd Afr N, 1998; 45 (1):102-10
  49. Schreiber GB, Busch MP, Kleinman SH, Korelitz JJ. The risk of transfusion-transmitted viral infections. The Retrovirus Epidemiology Donor Study. N Engl J Med. 1996 Jun 27;334(26):1685-90. PMid:8637512
  50. Uwingabiye J, Zahid H, Unyendie L, Hadef R. Seroprevalence of viral markers among blood donors at the Blood Donor Center of Mohammed V Military Teaching Hospital of Rabat, Morocco. Pan Afr Med J. 2016 Nov 24;25:185. PMid:28292147 PMCid:PMC5326047
  51. Karafina MS, Carpenterb E, Panb A, Simpsonb P, Field JJ. Older red cell units are associated with an increased incidence ofinfection in chronically transfused adults with sickle cell disease. Transfus Apher Sci. 2017 Jun;56(3):345-351 PMid:28279592
  52. Touré-Fall AO, Dièye TND, Sall A, Diop M, Diop S, Thiam D, Diakhate L. Residual risk of transmission of HIV and HBV, in Senegalese national blood bank from 2003 to 2005. Transfus Clin Biol. Nov-Dec 2009;16(5-6):439-43. PMid:19926508