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SCD PathophysiologySCD PathophysiologyHbS PolymerizationHemolysisAnemiaVaso-occlusionChronic SCD ComplicationsChronic SCD ComplicationsSilent DamageOrgan DamageSCD MortalityResourcesResourcesSCD StatisticsSCD is UnderservedSCD ResourcesContact
SCD pathophysiology may be associated with long-term organ damage1-5Hallmarks of SCD pathophysiology include anemia, hemolysis, inflammation, vaso-occlusion, and endothelial dysfunction. These, in turn, may be associated with further complications, including long-term organ damage.1-5

The degree to which SCD pathophysiology may be associated with end-organ damage is not known, as multiple factors—including age, sex, genotype/genogroup, treatment status, and other patient-specific variables—may also affect its etiology.7

Learn how SCD pathophysiology may be associated with organ damage.Learn moreLoadingSCD is characterized by a mutation in HBB and polymerization of HbS1,2SCD is characterized by a mutation in HBB, the gene that encodes
hemoglobin subunit β (beta-globin), leading to the expression and
polymerization of hemoglobin S (HbS), which can distort RBCs into a characteristic crescent or sickled shape. Sickled RBCs can, in turn, impact hematologic and vascular function.5,8,9

Discover hematologic and vascular changes in SCD.Discover moreLoadingSee the impact that a mutation in HBB and polymerizartion of HbS have on RBC functionWatch videoLoadingA medical expert discusses SCDListen to an expert discuss the impact of SCD on patients and describe some of the underlying pathophysiology of SCD.Watch the presentationLoadingSIGN UP FOR SCD INSIGHTSStay informed about sickle cell disease.Sign UpLoadingReferences:Telen MJ, Malik P, Vercellotti GM. Therapeutic strategies for sickle cell disease: towards a multi‐agent approach. Nat Rev Drug Discov. 2019;18(2):139-158.Kato GJ, Piel FB, Reid CD. Sickle cell disease. Nat Rev Dis Primers. 2018;4:(article 18010). doi:10.1038/nrdp.2018.10Kato GJ, McGowan V, Machado RF, et al. Lactate dehydrogenase as a biomarker of hemolysis-associated nitric oxide resistance, priapism, leg ulceration, pulmonary hypertension, and death in patients with sickle cell disease. Blood. 2006;107(6):2279-2285.Damanhouri GA, Jarullah J, Marouf S, Hindawi SI, Mustaq G, Kamal MA. Clinical biomarkers in sickle cell disease. Saudi J Biol Sci. 2015;22(1):24-31. doi:10.1016/j.sjbs.2014.09.005Kato GJ, Steinberg MH, Gladwin MT. Intravascular hemolysis and the pathophysiology of sickle cell disease. J Clin Invest. 2017;127(3):750-760.van Tuijn CFJ, Schimmel M, van Beers EJ, Nur E, Biemond BJ. Prospective evaluation of chronic organ damage in adult sickle cell patients: a seven-year follow-up study. Am J Hematol. 2017;92(10):E584-E590. doi:10.1002/ajh.24855Buchanan G, Vichinsky E, Krishnamurti L, Shenoy S. Severe sickle cell disease—pathophysiology and therapy. Biol Blood Marrow Transplant. 2010;16(1 suppl):S64-S67. doi:10.1016/j.bbmt.2009.10.001Stuart MJ, Nagel RL. Sickle-cell disease. Lancet. 2004;364(9442):1343-1360.Gordeuk VR, Castro OL, Machado RF. Pathophysiology and treatment of pulmonary hypertension in sickle cell disease. Blood. 2016;127(7):820‐828.References

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