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Journal articles on the topic 'Homozygous sickle cell'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Adhikari, Ram Chandra, T. B. Shrestha, R. B. Shrestha, R. C. Subedi, K. P. Parajuli, and S. Dali. "SICKLE CELL DISEASE - CASE REPORTS." Journal of Nepal Medical Association 42, no. 145 (2003): 36–38. http://dx.doi.org/10.31729/jnma.715.

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ABSTRACTSickle cell diseases are inherited hematological diseases, prevalent in certain parts of the world. We reporttwo cases of sickle cell diseases, first being sickle cell b-thalassaemia and second homozygous sickle celldisease (SS). Our first case was 5 year old boy presenting with hemolytic anaemia & hepatosplenomegalyhaving sickle cell b-thalassaemia disease . Second case was 17 years female presenting with hemolyticanaemia & joint pain having homozygous sickle cell disease.Key Words: Homozygous sickle cell disease, sickle cell b - thalassaemia, hemoglobin electrophoresis.

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2

Pandey, Sanjay, Sweta Pandey, Rahasya Mani Mishra та Renu Saxena. "MODULATING EFFECT OF THE −158 GΓ (C→T) XMN-1 POLYMORPHISM IN INDIAN SICKLE CELL PATIENTS". Mediterranean Journal of Hematology and Infectious Diseases 4, № 1 (2012): e2012001. http://dx.doi.org/10.4084/mjhid.2012.001.

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Xmn-1 polymorphism is a known factor, which increases fetal haemoglobin production. Among the inherited disorders of blood, thalassaemia and SCD constitutes a major bulk of genetic diseases in India. Our aim was to verify the role of the Xmn I polymorphism as a modulating factor in sickle cell patients and frequency of the polymorphism in Indian sickle cell patients. Subjects were 60 sickles homozygous and 75 sickle beta thalassemia patients. 5 ml blood samples collected from patients. Screening of sickle patients done by HPLC. An automated cell analyzer SYSMEX (K-4500 Model) used to analyze t

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3

Parrish, James M., Paul A. Page, David Cohen, et al. "Prebypass Pheresis and Red Blood Cell Exchange in a Patient with Homozygous SS Sickle Cell Disease Undergoing Cardiopulmonary Bypass: A Case Report." Journal of ExtraCorporeal Technology 26, no. 3 (1994): 143–51. http://dx.doi.org/10.1051/ject/1994263143.

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Sickle cell disease was first described by Herrick in 1910. This disease involves an abnormality of the hemoglobin molecule which, under certain conditions, causes the red cell to take on a sickle shape. This abnormal shape and hemoglobin prevent the red cell from performing the normal respiratory functions and interfere with the normal flow through the circulatory system. Individuals demonstrate either a homozygous (dominant) SS or a heterozygous Ss state. Clinical symptoms for patients with SS disease are most often characterized by recurrent painful crises, sequestration of sickled cells, c

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4

Verma, Ashish, Basant Maheshwari, and Debapriya Rath. "Hematological profile of sickle cell disease in Chhattisgarh." International Journal of Basic & Clinical Pharmacology 9, no. 4 (2020): 552. http://dx.doi.org/10.18203/2319-2003.ijbcp20201175.

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Background: Sickle cell disease hemoglobinopathy gets inherited in autosomal recessive pattern. In sickle cell disease substitution of amino acid valine for glutamic acid at the sixth position on beta globin chain takes place resulting in sickled hemoglobin which is a hemoglobin tetramer.Methods: A prospective observational study was conducted in the Sickle Cell Institute, Raipur, India, and Department of Pharmacology in collaboration with Department of Biochemistry, Pt. J.N.M. Medical College, Raipur, Chhattisgarh, India, from February 2018 to June 2018. Patients included were in the steady s

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5

Green, GA, MM Rehn, and VK Kalra. "Cell-bound autologous immunoglobulin in erythrocyte subpopulations from patients with sickle cell disease." Blood 65, no. 5 (1985): 1127–33. http://dx.doi.org/10.1182/blood.v65.5.1127.1127.

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Abstract Previously, we have demonstrated a parallel between most-dense (bouyant density) sickle erythrocyte subpopulations and most-dense aged normal red cells in the organization of membrane components in the intact cell. The present study has addressed the possibility that a corresponding similarity may exist between most-dense sickled red cell subpopulations and aged normal erythrocytes in the development of membrane protein components that function as receptors for autologous immunoglobulin (Ig). Autologous IgG retained by density-fractionated erythrocytes has been estimated by a nonequil

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6

Green, GA, MM Rehn, and VK Kalra. "Cell-bound autologous immunoglobulin in erythrocyte subpopulations from patients with sickle cell disease." Blood 65, no. 5 (1985): 1127–33. http://dx.doi.org/10.1182/blood.v65.5.1127.bloodjournal6551127.

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Previously, we have demonstrated a parallel between most-dense (bouyant density) sickle erythrocyte subpopulations and most-dense aged normal red cells in the organization of membrane components in the intact cell. The present study has addressed the possibility that a corresponding similarity may exist between most-dense sickled red cell subpopulations and aged normal erythrocytes in the development of membrane protein components that function as receptors for autologous immunoglobulin (Ig). Autologous IgG retained by density-fractionated erythrocytes has been estimated by a nonequilibrium 12

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7

Abdurrahman, Nurat O., Ninuola I. Akinwande, Samuel A. Somma, and Jamiu Omotola Ibrahim. "STABILITY ANALYSIS OF THE MODELS FOR MALARIA'S EFFECTS ON HUMANS BASED ON THE GENETIC STRUCTURE." FUDMA JOURNAL OF SCIENCES 9 (April 29, 2025): 183–88. https://doi.org/10.33003/fjs-2025-09(ahbsi)-3468.

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Malaria, according to encyclopedia Britannica, is a relapsing infection caused by plasmodium, transmitted to humans through the bite of an anopheles mosquito. The composition of the genes in humans can either be homozygous (AA, SS) or heterozygous (AS), the homozygous are usually prone to the infection of malaria. The homozygous sickle cell genes (SS) encounter serious problems with blood shortage due to the sickle cell, this makes the malaria infection in them more complicated. The heterozygous sickle cell, however, develops a resistance to the infection through the immunity offered by the si

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8

Mohan, J. S., J. M. Marshall, H. L. Reid, P. W. Thomas, and G. R. Serjeant. "Postural Vasoconstriction and Leg Ulceration in Homozygous Sickle Cell Disease." Clinical Science 92, no. 2 (1997): 153–58. http://dx.doi.org/10.1042/cs0920153.

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1. Chronic leg ulceration is a major cause of morbidity in patients with homozygous sickle cell disease; the ulcers commonly resolve on bed rest. We have therefore compared the cutaneous vascular response to dependency in three groups of eight patients with sickle cell disease (those with an active ulcer, with an ulcer scar and with no history of ulceration) and in eight subjects with normal haemoglobin and no history of leg ulceration. 2. We monitored, with a laser Doppler flowmeter, the change in red cell (erythrocyte) flux induced in the skin of the leg, at two sites proximal to the malleol

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9

Vayá, Amparo, Susana Collado, Rafael Alis, and Maria-Angeles Dasí. "Erythrocyte aggregation in homozygous sickle cell disease." Clinical Hemorheology and Microcirculation 58, no. 3 (2014): 475–77. http://dx.doi.org/10.3233/ch-141869.

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10

Magnus, S. A., I. R. Hambleton, F. Moosdeen, and G. R. Serjeant. "Recurrent infections in homozygous sickle cell disease." Archives of Disease in Childhood 80, no. 6 (1999): 537–41. http://dx.doi.org/10.1136/adc.80.6.537.

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11

Adedeji, M. O. "Lymphocyte Subpopulations in Homozygous Sickle Cell Anaemia." Acta Haematologica 74, no. 1 (1985): 10–13. http://dx.doi.org/10.1159/000206155.

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12

Webb, D. K., D. T. Dunn, and G. R. Serjeant. "Gall stones in homozygous sickle cell disease." Archives of Disease in Childhood 64, no. 9 (1989): 1342. http://dx.doi.org/10.1136/adc.64.9.1342.

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13

De Ceulaer, K., M. A. Khamashta, E. N. Harris, G. R. Serjeant, and G. R. Hughes. "Antiphospholipid antibodies in homozygous sickle cell disease." Annals of the Rheumatic Diseases 51, no. 5 (1992): 671–72. http://dx.doi.org/10.1136/ard.51.5.671.

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14

Wright, J. G., I. R. Hambleton, P. W. Thomas, N. D. Duncan, S. Venugopal, and G. R. Serjeant. "Postsplenectomy course in homozygous sickle cell disease." Journal of Pediatrics 134, no. 3 (1999): 304–9. http://dx.doi.org/10.1016/s0022-3476(99)70454-3.

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15

Serjeant, Graham R., Douglas R. Higgs, and Ian R. Hambleton. "Elderly Survivors with Homozygous Sickle Cell Disease." New England Journal of Medicine 356, no. 6 (2007): 642–43. http://dx.doi.org/10.1056/nejmc066547.

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16

Bainbridge, R., D. R. Higgs, G. H. Maude, and G. R. Serjeant. "Clinical presentation of homozygous sickle cell disease." Journal of Pediatrics 106, no. 6 (1985): 881–85. http://dx.doi.org/10.1016/s0022-3476(85)80230-4.

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17

Simms-Stewart, Donnette, Minerva Thame, Aleith Hemans-Keen, Ian Hambleton, and Graham R. Serjeant. "Retained Placenta in Homozygous Sickle Cell Disease." Obstetrics & Gynecology 114, no. 4 (2009): 825–28. http://dx.doi.org/10.1097/aog.0b013e3181b6f762.

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18

Austin, Publishing Group. "How Do Sickle Cell Genes Protect Tribal People from Deadly Malaria? Is This a Type of Natural Selection?" Annals of Hematology & Oncology 10, no. 5 (2023): 1437. https://doi.org/10.26420/annhematoloncol.2023.1437.

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Abstract In humans, genetic mutations have led to the formation of several haemoglobin (Hb) variants during human evolution. These mutations usually occur in the genes for a and Β- polypeptide or globin chains of haemoglobin located on chromosomes 11 and 16, respectively. Among these haemoglobin variants, sickle cell haemoglobin (Hb-S) is highly significant in the humans. In fact, this abnormal or mutant haemoglobin is the resultant of a point mutation in the gene for Β-globin, located on chromosome 11. No doubt, this sickle cell gene is relatively more prevalent among tribal people

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19

Campbell, Andrew, Osamu Tanabe, Rebekah Urbonya, et al. "Analysis of Fetal Hemoglobin Expression within Humanized Sickle Cell Disease Mice Overexpressing the TR2/4 Transgene." Blood 116, no. 21 (2010): 1619. http://dx.doi.org/10.1182/blood.v116.21.1619.1619.

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Abstract Abstract 1619 Background: Sickle Cell Disease (SCD) is a chronic debilitating hematologic condition caused by a missense mutation within the adult beta globin gene leading to significant morbidity and mortality. Increased Fetal Hemoglobin production has been shown to significantly ameliorate SCD symptoms and improve survival. A novel specific DNA-binding factor DRED (direct repeat erythroid definitive) was recently identified that regulated epsilon and gamma globin gene expression (Tanimoto et al Genes Dev 2000). Purification of DRED revealed that it harbored the nuclear orphan hormon

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20

Onyegeme-Okerenta, B. M., and E. B. Essien. "In Vitro Antisickling Potentials of Ethanol Extract of Annona Muricata, Delonix Regia and Senna Alata." Recent Trends in Pharmaceutical Sciences and Research 2, no. 1 (2019): 7–18. https://doi.org/10.5281/zenodo.3458736.

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<em>Sickle cell anemia (SCA) is a genetic condition caused by defective hemoglobin molecules. The in vitro antisickling effects of different concentrations of ethanol extracts of Annona muricata, Senna alata and Delonix Regia on homozygous sickle cell erythrocyte was investigated. Standard antisickling tests evaluated include: Osmotic fragility, antioxidants (Superoxide dismutase, catalase and Glutathione), and polymerization of the sickled red blood cell. The experiment was in five groups Group 1 (Normal RBC), Group 2 (Sickle RBC – experimental control group), Group 3 (Sickle RBC +&nbsp

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21

Gangwe, Anil B., Abhishek Singh, Swapnil M. Parchand, Deepshikha Agrawal, Chibuzo B. Ekumankama, and Raj Vardhan Azad. "Asymmetric sickle cell retinopathy in a patient with sickle cell hemoglobin D disease: A case report." Indian Journal of Ophthalmology - Case Reports 3, no. 3 (2023): 760–61. http://dx.doi.org/10.4103/ijo.ijo_981_23.

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Sickle cell disease (SCD), the most commonly inherited hemoglobinopathy, can result in vision loss due to sickle cell retinopathy (SCR), vascular occlusions, and retinal atrophy. SCR is more common in heterozygous (HbSc) than homozygous (HbSS) patients. HbD (Punjab) is a less commonly reported form of hemoglobin in SCD, seen in northwestern states of India. Patients with sickle cell hemoglobin D disease (HbSD) can clinically behave like HbSS. We report a case of asymmetric SCR and multiple branch retinal artery occlusions in a patient with sickle cell hemoglobin D disease in central India.

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22

Matimbo, Jean Jacques Koyondele, Aliocha Natuhoyila Nkodila, Christophe Duvoux, Francky Mubenga, and Antoine Wola Yaba Tshimpi. "Evaluation of survival of sickle cell patients after liver transplantation at the Henri Mondor Hospital in Créteil (HHM) in France: A Retrospective cohort study." Gastroenterology & Hepatology: Open access 13, no. 3 (2022): 115–19. http://dx.doi.org/10.15406/ghoa.2022.13.00509.

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Background: Hepatic cholestasis is very common in sickle cell disease, thus requiring liver transplantation; but this technique is not practiced in the developing world. The objective of this study was to evaluate the survival of sickle cell patients after liver transplantation followed at the Henri Mondor Hospital in Créteil (HHM) in France. Methods: Historical cohort study conducted in 24 sickle cell patients followed at the Henri Mondor hospital in Créteil in France during the period from 1991 to 2019. The clinical, biological and evolutionary parameters were studied. Patient survival was d

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23

Singhal, A., P. Davies, A. Sahota, P. W. Thomas, and G. R. Serjeant. "Resting metabolic rate in homozygous sickle cell disease." American Journal of Clinical Nutrition 57, no. 1 (1993): 32–34. http://dx.doi.org/10.1093/ajcn/57.1.32.

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24

Kim, Yu-Sok, Erfan Nur, Eduard J. van Beers, et al. "Dynamic Cerebral Autoregulation in Homozygous Sickle Cell Disease." Stroke 40, no. 3 (2009): 808–14. http://dx.doi.org/10.1161/strokeaha.108.531996.

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25

Serjeant, G. R., B. E. Serjeant, P. W. Thomas, M. J. Anderson, G. Patou, and J. R. Pattison. "Human parvovirus infection in homozygous sickle cell disease." Lancet 341, no. 8855 (1993): 1237–40. http://dx.doi.org/10.1016/0140-6736(93)91145-c.

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26

Condon, P. I., R. A. Whitelocke, A. C. Bird, J. F. Talbot, and G. R. Serjeant. "Recurrent visual loss in homozygous sickle cell disease." British Journal of Ophthalmology 69, no. 9 (1985): 700–706. http://dx.doi.org/10.1136/bjo.69.9.700.

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27

Walker, T. M., D. T. Dunn, and G. R. Serjeant. "The metacarpal index in homozygous sickle-cell disease." British Journal of Radiology 61, no. 724 (1988): 280–81. http://dx.doi.org/10.1259/0007-1285-61-724-280.

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28

Calder, John F. "The metacarpal index in homozygous sickle-cell anaemia." British Journal of Radiology 61, no. 731 (1988): 1089. http://dx.doi.org/10.1259/0007-1285-61-731-1089-b.

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29

Walker, T. M. "The metacarpal index in homozygous sickle-cell anaemia." British Journal of Radiology 61, no. 731 (1988): 1089. http://dx.doi.org/10.1259/0007-1285-61-731-1089-c.

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30

Levin, Stuart. "HUMAN PARVOVIRUS INFECTION IN HOMOZYGOUS SICKLE CELL DISEASE." Infectious Diseases in Clinical Practice 2, no. 5 (1993): 373. http://dx.doi.org/10.1097/00019048-199309000-00020.

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31

Serjeant, Graham R., Luana Look Loy, Mark Crowther, Ian R. Hambleton, and Minerva Thame. "Outcome of Pregnancy in Homozygous Sickle Cell Disease." Obstetrics & Gynecology 103, no. 6 (2004): 1278–85. http://dx.doi.org/10.1097/01.aog.0000127433.23611.54.

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32

Singhal, A., P. Thomas, R. Cook, K. Wierenga, and G. Serjeant. "Delayed adolescent growth in homozygous sickle cell disease." Archives of Disease in Childhood 71, no. 5 (1994): 404–8. http://dx.doi.org/10.1136/adc.71.5.404.

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33

Malek, Y., T. Abdellaoui, M. Khmamouche, R. Zerrouk, K. Reda, and A. Oubaaz. "Angioid streaks secondary to homozygous sickle cell disease." Journal Français d'Ophtalmologie 43, no. 8 (2020): 813–15. http://dx.doi.org/10.1016/j.jfo.2019.11.030.

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34

Baum, Kenneth F. "The Painful Crisis of Homozygous Sickle Cell Disease." Archives of Internal Medicine 147, no. 7 (1987): 1231. http://dx.doi.org/10.1001/archinte.1987.00370070045007.

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35

Khan, Almas, Saima Siddiqui, Haya ul Batool Abbasi, Danish Zahid, Arpna Nihal, and Sumaira Sharif. "Association of Xmn-1 Polymorphism with HbF Levels in Patients Presenting with Sickle Cell Disease at Tertiary Care Hospital, Karachi." National Journal of Health Sciences 10, no. 1 (2025): 8–14. https://doi.org/10.21089/njhs.101.0008.

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Abstract: Background: Sickle cell anemia is a common hereditary disease in Pakistan, which still maintains significant inter patient variation in disease manifestations and the reasons behind such variations remain uncertain. Among other genetic modifiers the XmnI polymorphism has been noted to influence HbF levels, response to HbF augmenting drugs and milder phenotype of disease as observed in studies conducted in various parts of world and subcontinent. XmnI polymorphism frequency and its association with HbF levels have not been investigated in Pakistani patients of sickle cell disorder. Th

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36

Byrd, Kendra A., Thomas N. Williams, Audrie Lin та ін. "Sickle Cell and α+-Thalassemia Traits Influence the Association between Ferritin and Hepcidin in Rural Kenyan Children Aged 14–26 Months". Journal of Nutrition 148, № 12 (2018): 1903–10. http://dx.doi.org/10.1093/jn/nxy229.

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ABSTRACTBackgroundThe relation between subclinical hemoglobinopathies and concentrations of the iron-regulatory hormone hepcidin is not well characterized.ObjectiveWe investigated the relation of hepcidin concentration with hemoglobinopathies among young children in Kenya.MethodsWe quantified serum hepcidin and ferritin in 435 Kenyan children aged 14–20 mo in a subsample of the Water, Sanitation, and Handwashing (WASH) Benefits Trial. Blood samples were genotyped for α+-thalassemia and for sickle cell disorder. Hepcidin was compared across sickle cell and α+-thalassemia genotypes separately by

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37

Javazon, Elisabeth H., Leslie S. Kean, Jennifer Perry, Jessica Butler, and David R. Archer. "Effects of Sickle Cell Disease on Hematopoietic Stem Cell Function and the Bone Marrow Microenvironment." Blood 108, no. 11 (2006): 1227. http://dx.doi.org/10.1182/blood.v108.11.1227.1227.

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Abstract Gene therapy and stem cell transplantation are attractive potential therapies for sickle cell disease (SCD). Previous studies have shown that the sickle environment is highly enriched for reactive oxygen species (ROS), but have not addressed whether or not the increased ROS may alter the bone marrow (BM) microenvironment or affect stem cell function. Using the Berkeley sickle mouse model, we examined the effects of sickle cell disease on hematopoietic stem cell function and the bone marrow microenvironment. We transplanted C57BL/6 (control) BM into C57BL/6 and homozygous sickle mice.

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38

Kamble, Milind B., and Vidhya S. Totewad. "Renal manifestations of sickle cell disease in children." International Journal of Contemporary Pediatrics 7, no. 7 (2020): 1524. http://dx.doi.org/10.18203/2349-3291.ijcp20202609.

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Background: Sickle cell disease prevalence is more in central part of India. This study tries to find extent of renal involvement, risk factors and screening tests in sickle cell disease.Methods: Study was Cross sectional observational study. Demographic and clinical findings were recorded. Renal function tests like serum creatinine, blood urea nitrogen, eGFR were studied. Presence of microalbuminuria was checkeed. Ultrasonography abdomen was done to see the texture and corticomedullary differentiation of kidney.Results: Total 143 patients were studied. Out of which, 117 homozygous (SS type),

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39

Behera, Samira K., Sonali Kar, and Monali Kar. "Haematological profile of sickle cell patients attending tertiary health care centre of southern Odisha: a cross sectional study." International Journal of Research in Medical Sciences 8, no. 1 (2019): 170. http://dx.doi.org/10.18203/2320-6012.ijrms20195902.

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Background: Sickle Cell Disorder (SCD) is a major health problem in India. After introduction of High-Performance Liquid Chromatography (HPLC) in MKCG Medical College, this study is first of its kind to describe haemoglobin variants of SCD. The aim of the study was to document haematological profile and pattern of haemoglobin variants in SCD patients.Methods: A Hospital based cross sectional study was conducted in Pathology department, MKCG medical college from October 2018 to May 2019. Sickle cell patients were included and patients in Sickle cell crisis or transfused with blood in last 3 mon

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40

Al-Ebrahim, Khaled E. "Cardiac Surgery and Sickle Cell Disease." Asian Cardiovascular and Thoracic Annals 16, no. 6 (2008): 479–82. http://dx.doi.org/10.1177/021849230801600610.

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Three patients with homozygous sickle cell disease underwent successful open heart surgery for multivalvular lesions. Details of the surgical technique and the necessary precautions are described. Exchange transfusion was implemented in all cases. Crucial issues in cardiac surgical management to avoid or at least minimize vasoocclusive crisis and associated complications are discussed.

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41

Overby, M. Chris, and Allen S. Rothman. "Multiple intracranial aneurysms in sickle cell anemia." Journal of Neurosurgery 62, no. 3 (1985): 430–34. http://dx.doi.org/10.3171/jns.1985.62.3.0430.

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✓ Neurological complications of sickle cell anemia occur in 18% to 29% of patients with homozygous hemoglobin S disease. A review of the literature yielded reports of two cases, both treated conservatively, of multiple intracranial aneurysms occurring in patients with sickle cell anemia. The authors report two cases of subarachnoid hemorrhage secondary to multiple intracranial aneurysms in patients with sickle cell anemia. One of the two patients underwent three craniotomies for ablation of six intracranial aneurysms. The techniques used in the treatment of these patients are presented.

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42

Ogre, Shyama Charan, Priyamvada Shrivastava, and Moyna Chakravarty. "Association of somatic problems with mental health among sickle cell anaemic adolescents of Chhattisgarh, India." International Journal Of Community Medicine And Public Health 5, no. 3 (2018): 1069. http://dx.doi.org/10.18203/2394-6040.ijcmph20180763.

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Background: The sickle cell disease is characterized by various somatic problems and medical complications with psychological problems. Sickle cell patient faces physical, economical and psychological burden. There is paucity of evidences in understanding the bio-psychological aspects of sickle cell anaemic patients especially in India. Therefore, an attempt has been made to know the somatic problems in adolescents and its effects in mental health of the adolescents suffering from sickle cell anaemia. The main aim was to find out association of somatic problems with mental health among adolesc

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43

Omoto, Alloysius Luambo, Duncan Mumbo, Samira Nassir Hussein, Moses Apela, and George Audi. "Analysis of Provider Initiated Sickle Cell Disease Screening in Mathare Slums, Nairobi Kenya: A Case of German Doctors, Baraka Health Centre." Journal of Advances in Medicine and Medical Research 35, no. 24 (2023): 74–80. http://dx.doi.org/10.9734/jammr/2023/v35i245325.

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Sickle cell disease (SCD) results in alteration of both hematological and biochemical parameters of the affected individuals. In Kenya, it is estimated that 4,000 children are born with SCD annually; about 21% of children in Kisumu are born with Sickle cell trait. Study objective was to analyze the screening of SCD using various screening techniques at German Doctors-Baraka Health Center in Mathare, Nairobi. On methodology, purposive sampling and cross sectional study design was employed among patients of all ages with clinical features suggestive of SCD. Data utilization permission was sought

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44

Brahmbhatt, Niravkumar Kamleshbhai, Urja Nagadia, Ghulam Ghous, and Verghese Cherian. "Use of Conventional Transfusion Thresholds Contributes to Ongoing Iron Overload Issues in Patients with Homozygous (SS) Sickle Cell Disease." Blood 142, Supplement 1 (2023): 5322. http://dx.doi.org/10.1182/blood-2023-187224.

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Introduction: Homozygous sickle cell disease is characterized by chronic anemia which contributes to a clinical course characterized by recurrent pain crisis episodes. These episodes are usually managed with the use of packed red blood cell products. Randomized data is currently available that supports lower transfusion thresholds in non-sickle cell related conditions including but not limited to patients undergoing orthopedic procedures, cardio-vascular interventions and those needing intensive care. Due to lack of similar randomized trials in patients with sickle cell disease, recommendation

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45

Khannouri, Imane El, Mahjouba Baiya, Safia Chellak, and Abderrahmane Boukhira. "Biological Evolution in a Homozygous Adult with Sickle Cell Disease on Hydroxyurea: A Case Report." SAS Journal of Medicine 10, no. 06 (2024): 503–5. http://dx.doi.org/10.36347/sasjm.2024.v10i06.005.

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Sickle cell disease is an autosomal recessive genetic disorder and one of the most common haemoglobinopathies in Morocco. It is characterised by the polymerisation of haemoglobin S, resulting in a change in the spatial conformation of sickle cell haemoglobin, and consequently in its function. Hydroxyurea is the only product with proven efficacy in preventing the complications of sickle cell anaemia and has been approved by the "Food and Drug Administration". The effects of hydroxyurea are essentially linked to the increase in HbF by inhibiting the polymerisation of haemoglobin S, which is the

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Gupta, Dipti, Sarah Sturtevant, Benjamin Vieira, Yukio Nakamura, Sriram Krishnamoorthy, and Melanie Demers. "Characterization of a Genetically Engineered HUDEP2 Cell Line Harboring a Sickle Cell Disease Mutation As a Potential Research Tool for Preclinical Sickle Cell Disease Drug Discovery." Blood 134, Supplement_1 (2019): 3559. http://dx.doi.org/10.1182/blood-2019-127330.

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Sickle cell disease (SCD) is a genetic disorder caused by a missense mutation in the beta-globin gene [Glu6Val] resulting in the formation of HbS (sickle hemoglobin). HbS polymerizes under low oxygen tension causing an array of severe pathophysiological complications, including vaso-occlusion, pain and hemolytic anemia. Traditionally, research efforts toward studying anti-sickling effects of various pathways and compounds in vitro have been made using sickle cell patient derived samples. However, such studies are limited based on sample availability and a large degree of phenotypic variability

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Dosunmu, Adedoyin, Akinsegun Akinbami, Ebele Uche, Adewumi Adediran, and Sarah John-Olabode. "Electrocardiographic Study in Adult Homozygous Sickle Cell Disease Patients in Lagos, Nigeria." Journal of Tropical Medicine 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/4214387.

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Background. This study sought to identify the pattern of electrocardiographic changes in steady state adult sickle cell anaemia.Methods.A case-control, cross-sectional study was conducted amongst sickle cell patients attending the sickle cell clinic of Lagos State University Teaching Hospital, Ikeja, and HbAA controls. All consenting participants had haemoglobin electrophoresis done and were subjected to electrocardiography (ECG). The descriptive data were given as means ± standard deviation (SD). The differences were considered to be statistically significant when thepvalue obtained was <0

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Buchanan, George R., and Christine A. Holtkamp. "Plasma Levels of Platelet and Vascular Prostaglandin Derivatives in Children with Sickle Cell Anaemia." Thrombosis and Haemostasis 54, no. 02 (1985): 394–96. http://dx.doi.org/10.1055/s-0038-1657747.

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SummaryPlatelet and vascular endothelial prostaglandin derivatives were measured by radioimmunoassay in the plasma of 39 children with homozygous sickle cell anaemia and 27 control subjects. The levels of both thromboxane B2 and 6-keto-PGF1α, the stable endproducts of platelet and vascular prostaglandin metabolism, were significantly (p <0.001) greater in sickle cell anaemia plasma than in the plasma of the controls. There were no differences in levels of either 6-keto-PGF1α or thromboxane B2 between steady state and vaso-occlusive crisis in the sickle cell patients. Injury to the endotheli

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Vayá, Amparo, Susana Collado, Ma Angeles Dasí, Ma Luz Pérez, Jose Luis Hernandez, and Eva Barragán. "Erythrocyte deformability and aggregation in homozygous sickle cell disease." Clinical Hemorheology and Microcirculation 58, no. 4 (2014): 497–505. http://dx.doi.org/10.3233/ch-131717.

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Lester, D. A., A. A. Richards, N. O. Younger-Coleman, and D. J. Pepple. "Cilostazol and Blood Viscoelasticity in Homozygous Sickle Cell Disease." British Journal of Biomedical Science 71, no. 4 (2014): 172–75. http://dx.doi.org/10.1080/09674845.2014.11669983.

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