Volume : 08, Issue : 12, December – 2021

Title:

09.AN OVERVIEW OF SICKLE CELL DISEASE VASO-OCCLUSIVE CRISIS AND APPROACHES TO MANAGEMENT

Authors :

Mohammad hamid Ahmed alabdali,Ashraf Faisal Fahad Alharbi,Mishal Abdullah Faisal Alharbi,Mohammed Mhwes Abdullah Almalki,Saud Abdulaziz R ALOTAIBI,Majed Saleh Jaza Al-Otaibi,Abdurahman Hizab jaber Alsulami,Fatmah HMEDIN oja Al EJEFI,Muslih Mohammed Ahmed Aljahdaly,Ali Saeed Ali Alzahrani

 

Abstract :

Early diagnosis, treatment, and prevention of a vaso-occlusive crisis (VOC) are critical to the management of patients with sickle cell disease. Literature search conducted through electronic databases, such as PUBMED, EMBASE. We aimed to discuss the proper management of VOC, after emphasizing the mechanism and complications of VOC in SCD. Vaso-occlusive crisis in people with SCD is a multifactorial process identified by inflammation, attachment, and multicellular aggregation of sickled RBCs, endothelial cells, platelets, and also other blood cells, resulting in vaso-occlusion and acute extreme pain.

Cite This Article:

Please cite this article in press Mohammad hamid Ahmed alabdali et al, An Overview Of Sickle Cell Disease Vaso-Occlusive Crisis And Approaches To Management., Indo Am. J. P. Sci, 2021; 08(12)

Number of Downloads : 10

References:

1. Darbari DS, Sheehan VA, Ballas SK. The vaso-occlusive pain crisis in sickle cell disease: Definition, pathophysiology, and management. Eur J Haematol. 2020 Sep;105(3):237-246.
2. Okpala I. The management of crisis in sickle cell disease. Eur J Haematol. 1998 Jan;60(1):1-6.
3. Jang, T., Poplawska, M., Cimpeanu, E. et al. Vaso-occlusive crisis in sickle cell disease: a vicious cycle of secondary events. J Transl Med 19, 397 (2021).
4. Anyaegbu CC, Okpala IE, Akren’Ova YA, Salimonu LS. Peripheral blood neutrophil count and candidacidal activity correlate with the clinical severity of sickle cell anaemia (SCA). Eur J Haematol. 1998;60:267–8.
5. Dutta D, Methe B, Amar S, Morris A, Lim SH. Intestinal injury and gut permeability in sickle cell disease. J Transl Med. 2019;17:183.
6. Lard LR, Mul FP, de Haas M, Roos D, Duits AJ. Neutrophil activation in sickle cell disease. J Leukoc Biol. 1999;66:411–5.
7. Lum AF, Wun T, Staunton D, Simon SI. Inflammatory potential of neutrophils detected in sickle cell disease. Am J Hematol. 2004;76:126–33.
8. Belcher JD, Marker PH, Weber JP, Hebbel RP, Vercellotti GM. Activated monocytes in sickle cell disease: potential role in the activation of vascular endothelium and vaso-occlusion. Blood. 2000;96:2451–9.
9. Hebbel RP, Boogaerts MA, Eaton JW, Steinberg MH. Erythrocyte adherence to endothelium in sickle-cell anemia: a possible determinant of disease severity. N Engl J Med. 1980;302:992-995.
10. Kaul DK, Hebbel RP. Hypoxia/reoxygenation causes inflammatory response in transgenic sickle mice but not in normal mice. J Clin Invest. 2000;106:411-420.
11. Rees DC, Williams TN, Gladwin MT. Sickle-cell disease. Lancet. 2010;376:2018-2031.
12. Schlaeger JM, Molokie RE, Yao Y, et al. Management of sickle cell pain using pregabalin: a pilot study. Pain Manag Nurs. 2017;18:391-400.
13. Manwani D, Frenette PS. Vaso-occlusion in sickle cell disease: pathophysiology and novel targeted therapies. Blood. 2013;122:3892-3898.
14. Connes P, Alexy T, Detterich J, et al. The role of blood rheology in sickle cell disease. Blood Rev. 2016;30:111-118.
15. Hebbel RP. Adhesive interactions of sickle erythrocytes with endothelium. J Clin Invest. 1997;99:2561-2564.
16. Wick TM, Eckman JR. Molecular basis of sickle cell-endothelial cell interactions. Curr Opin Hematol. 1996;3:118-124.
17. Schimmel M, Luken BM, Nur E, et al. Inflammatory and endothelial markers during vaso-occlusive crisis and acute chest syndrome in sickle cell disease. Am J Hematol. 2017;92:E634-E636.
18. Turhan A, Weiss LA, Mohandas N, Coller BS, Frenette PS. Primary role for adherent leukocytes in sickle cell vascular occlusion: a new paradigm. Proc Natl Acad Sci USA. 2002;99:3047-3051.
19. Madigan C, Malik P. Pathophysiology and therapy for haemoglobinopathies. Part I: sickle cell disease. Expert Rev Mol Med. 2006;8:1-23.
20. Keikhaei B, Mohseni AR, Norouzirad R, et al. Altered levels of pro-inflammatory cytokines in sickle cell disease patients during vaso-occlusive crises and the steady state condition. Eur Cytokine Netw. 2013;24:45-52.
21. Mousa SA, Al Momen A, Al Sayegh F, et al. Management of painful vaso-occlusive crisis of sickle-cell anemia: consensus opinion. Clin Appl Thromb Hemost. 2010;16:365-376.
22. Coates TD, Chalacheva P, Zeltzer L, Khoo MCK. Autonomic nervous system involvement in sickle cell disease. Clin Hemorheol Microcirc. 2018;68:251-262.
23. Chalacheva P, Khaleel M, Sunwoo J, et al. Biophysical markers of the peripheral vasoconstriction response to pain in sickle cell disease. PLoS One. 2017;12:e0178353.
24. Evidence-Based Management of Sickle Cell Disease: Expert Panel Report, 2014. US Department of Health and Human Services. National Heart, Lung, and Blood Institute; 2014.
25. Steinberg MH, Barton F, Castro O, et al. Effect of hydroxyurea on mortality and morbidity in adult sickle cell anemia: risks and benefits up to 9 years of treatment. JAMA. 2003;289:1645-1651.
26. Vichinsky E, Hoppe CC, Ataga KI, et al. A phase 3 randomized trial of voxelotor in sickle cell disease. N Engl J Med. 2019;381:509-519.
27. Gupta K, Jahagirdar O, Gupta K. Targeting pain at its source in sickle cell disease. Am J Physiol Regul Integr Comp Physiol. 2018;315:R104-R112.