Oxidative Modification of Lipids and Lipoproteins in Steady State Sickle Cell Anemic Patients from South-Eastern Nigeria
American Journal of Pediatrics
Volume 4, Issue 4, December 2018, Pages: 84-88
Received: Aug. 6, 2018;
Accepted: Oct. 12, 2018;
Published: Nov. 7, 2018
Views 1033 Downloads 100
Sylvester Ogbonna Ogbodo, Department of Medical Biochemistry, Faculty of Basic Medical Sciences, College of Medicine, Enugu State University of Science and Technology, Enugu, Nigeria
Christopher Bismarck Eke, Department of Pediatrics, College of Medicine, University of Nigeria Teaching Hospital, University of Nigeria, Enugu Campus, Enugu, Nigeria
Emmanuel Ikechukwu Nwobodo, Department of Biochemistry, Chukwuemeka Odumegwu Ojukwu University, Uli, Nigeria
Ejike Felix Chukwurah, Department of Hematology/Immunology, Faculty of Clinical Medicine, College of Health Sciences, Ebonyi State University, Abakaliki, Nigeria
Vitus Obinna Agama, Department of Applied Biochemistry, Faculty of Natural Sciences, Ebonyi State University, Abakaliki, Nigeria
Sickle cell anemia is a genetic disease associated with constant medical crises. These crises are due to many biochemical and hematological changes arising from multi-organ damages. This study was aimed to assess changes in the plasma levels of lipids and specific lipoproteins in sickle cell anemia patients who were in their steady states. The study is a cross-sectional one involving 75 patients with sickle cell anemia, who were in their stable states while attending their routine check-up at the sickle cell clinic of University of Nigeria Teaching Hospital, Enugu, Nigeria and 72 age and sex-matched apparently healthy school children with normal blood genotypes. The patients were made up of 40 males and 35 females while the controls were 36 males and 36 females. The results of the study showed that patients have the following; total cholesterol 135 ± 38.6mg/dL, HDL-cholesterol 22.7 ± 8.1mg/dL, LDL-cholesterol 91.4 ± 41.2mg/dL, VLDL-cholesterol 20.5 ± 5.0mg/dL and triglycerides 102.7 ± 25.2mg/dL, while the results from the controls were; total cholesterol 162.2 ± 27.4mg/dL, HDL-cholesterol 36.6 ± 7.9mg/dL, LDL-cholesterol 100.2 ± 23.9mg/dL, VLDL-cholesterol 25.4 ± 3.7mg/dL and triglycerides 127.0 ± 18.4mg/dL. These results showed that there were significant decreases (p<0.001 in all) in these parameters in sickle cell anemia except LDL-cholesterol (p=0.28), indicating oxidative modifications of the lipids and the lipoproteins. However, there were no significant differences (p>0.05) between the parameters obtained in males and females in both patients and controls. Lipids and lipoproteins were significantly reduced in steady state sickle cell anemia, causing the patients to depend mainly on limited carbohydrates and proteins for the provision of energy. This may account for constant lack of energy as well as the frail and fragile appearances of these patients.
Sylvester Ogbonna Ogbodo,
Christopher Bismarck Eke,
Emmanuel Ikechukwu Nwobodo,
Ejike Felix Chukwurah,
Vitus Obinna Agama,
Oxidative Modification of Lipids and Lipoproteins in Steady State Sickle Cell Anemic Patients from South-Eastern Nigeria, American Journal of Pediatrics.
Vol. 4, No. 4,
2018, pp. 84-88.
Ohene-Frempong K, Steinberg MH. Clinical Aspects of sickle cell anemia in adults and children. Disorders of Hemoglobin: Genetics. In: Steinberg MH, Forget BG, Higgs DR, Nagel RLedsPathophysiology and Clinical Management. Cambridge University Press, New York, 2001; 611-70.
Stuart MJ, Nagel RL. Sickle cell disease. Lancet. 2004; 364: 1343-60. 10.1016/S0140-6736(04)17192-4.
Okpala I. The intriguing contribution of white blood cells to sickle cell disease- a red cell disorder. Blood Reviews. 2004; 18: 65-73. 10.1016/S0268-960X(03)00037-7.
Telen MJ. Role of adhesion molecules and vascular endothelium in the pathogenesis of sickle cell disease. Hematology Am Soc of Hematol Educ Program, 2007; 84-90. 10.1182/asheducation-2007.1.84.
Villagra J, Shiva S, Hunter LA, Machado RF, Gladwin MT, Kato GJ. Platelet activation in patients with sickle cell disease, hemolysis-associated pulmonary hypertension, and nitric oxide scavenging by cell-free hemoglobin. Blood. 2007; 110: 2166-2172. 10.1182/blood-2006-12-061697.
Johnson C, Telen MJ. Adhesion molecule and hydroxyurea in the pathophysiology of sickle cell disease. Hematologica. 2008; 93: 481-486. 10.3324/haematol.12734.
Kato GJ, McGowan V, Machado RF, Little JA, Taylor J, Morris CR, Nichols JS, Wang X, Poljakovic M, Morris SM, Gladwin MT. 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: 2279-2285. 10.1182/blood-2005-06-2373.
O'Driscoll S, Height SE, Dick MC, Rees DC. Serum lactate dehydrogenase activity as a biomarker in children with sickle cell disease. Br J Haematol. 2007, 140: 206-209. 10.1111/j.1365-2141.2007.06894.x.
Ogbodo SO, Ogah O, Obu HA, Shu E. N, Afiukwa C. Lipid and lipoprotein levels in children with malaria parasitaemia. Curr Pediatric Res. 2008; 12 (1 & 2): 12-17.
Hennekens CH. Alcohol and risk of coronary event. In: Zakhari S and Wussef M eds Alcohol and the CV system. MMAA research monograph. Washington, 1996; 15-24.
Musselman NL, Evans DL, Nermorott CB. The relationship of depression to cardiovascular disease; epidemiology, biology and treatment. Arch Gen Psychiatr 1998; 55: 580-595. PMID 9672043.
Leonarduzzi G, Arkan MC, Basaga H, Chiarpotto E, Sevonian A, Poli G. Lipid peroxidation products in cell signaling. Free RadicBiol Med 2000; 28: 1370-1378. 10.1016/S0891-5849(00)00216-1.
Navab M, Berliner JA, Subbanago under G, Hama S, Lusis AJ, Castellani LW, Reddy S, Shih D, Shi W, Watson AD, Van Lenten BJ, Vora D, Fogelman AM. HDL and inflammatory response induced by LDL-derived oxidized phospholipids. Arterioscler Thromb Vasc Biol. 2001; 21: 481-488. PMID: 11304461.
Navab M, Ananthramaiah GM, Reddy ST. The oxidation hypothesis hypothesis of atherogenesis: the role of oxidized phospholipids and HDL. J Lipid Res. 2004; 45: 9932-1007. 10.1194/jlr.R400001-JLR200.
Minniti CP, Sable C, Campbell A, Rana S, Ensing G, Dham N, Onyekwere O, Nouraie M, Kato GJ, Gladwin MT, Castro OL, Gordeuk VR. Elevated tricuspid regurgitant jet velocity in children and adolescents with sickle cell disease: association with hemolysis and hemoglobin oxygen desaturation. Haematologica. 2009; 94: 340-347. 10.3324/haematol.13812.
Daniels SR, Greer FR. Lipid screening and cardiovascular health in childhood. Clinical Report. Pediatrics 2008; 122(1):198-208. PMID 18596007.
Friedwald TW, Fredrickson DS, Levy RJ. LDL – Cholesterol estimation. ClinChem 1972;18:499-501.
Rahimi Z, Merat A, Haghshenass M, Madani H, Nagel RL. Plasma lipids in Iranians with sickle cell disease: Hypocholesterolemia in sickle cell anemia and increase of HDL-cholesterol in sickle cell trait. Clinica Chimica Acta. 2006;365(1–2): 217-220.
Zorca S, Freeman L, Hildesheim M, Allen D, Remaley AT, Taylor JG, Kato GJ. Lipid levels in sickle-cell disease associated with haemolytic severity, vascular dysfunction and pulmonary hypertension. Br J Haematol. 2010; 149: 436-45. 10.1111/j.1365-2141.2010.08109.
Seixas MO, Rocha LC, Carvalho MB, Menezes JF, Lyra IM, Nascimento VML, Couto RD, Atta AM, Reis MG, Goncalves MS. Levels of high-density lipoprotein cholesterol (HDL-C) among children with steady-state sickle cell disease. Lipids in Health and Disease. 2010; 9:91. doi:10.1186/1476-511X-9-91.
Bhatkulkar P, Khare R, Meshram AW, Dhok A. Status of Oxidative Stress and Lipid Profile in Patients of Sickle Cell Anemia. Intern J Health Sci Res.2015; 5(3): 189 – 193.
Akinlade KS, Adewale CO, Rahamon SK, Fasola FA, Olaniyi JA, Atere AD. Defective lipid metabolism in sickle cell anaemia subjects in vaso-occlusive crisis. Niger Med J. 2014; 55(5): 428–431.