Uric Acid Concentration in Patients with Sickle Cell Anaemia Presenting with Vaso-Occlusive Crises in Uch, Ibadan
American Journal of Laboratory Medicine
Volume 5, Issue 6, November 2020, Pages: 155-161
Received: Oct. 6, 2020;
Accepted: Oct. 21, 2020;
Published: Oct. 30, 2020
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Odebiyi Hassan Abiola, Department of Haematology, University College Hospital, Ibadan, Nigeria
Fasola Foluke Atinuke, Department of Haematology, University College Hospital, Ibadan, Nigeria; Department of Haematology, Faculty of Basic Medical Sciences, College of Medicine, University of Ibadan, University College Hospital, Ibadan, Nigeria
Sickle cell anaemia is a point mutation characterized by homozygous inheritance of HbS, the commonest presenting symptoms in patients with sickle cell anaemia is vaso-occlusive bone pain crisis; this is an acute exacerbation of chronic inflammatory state in them. Elevated serum uric acid is associated with increased oxidative state, inflammation, hyperhaemolysis and sickle cell nephropathy in adult patients with sickle cell disease. There are inconsistence findings on uric acid concentration during vaso-occlusive pain crisis in patients with sickle cell disease. This study compares uric acid concentration in sickle cell disease patients with bone pain crisis, steady state and HbA individuals. It also correlates uric acid concentration with the severity of vaso-occlusive crisis in patients with sickle cell disease using bone pain crisis as a prototype of a vaso-occlusive crisis. Thirty each of sex and age-matched adult patients with sickle cell anaemia in a bone pain crisis, steady state and HbA were recruited in this study. Total summary pain score was used for assessment of bone pain crisis severity, 23 parameters automated haematology analyzer was used to measure haematological parameters. Plasma uric acid concentration was determined by Uricase method using the Landwind LWC 100 plus automated analyzer machine. Data obtained were analyzed using the Statistical Package for the Social Science (SPSS) version 20. Results were considered statistically significant if p<0.05. Biochemical parameters were correlated with the severity of bone pain crisis. Plasma uric acid concentration of mild BPC, moderate BPC and severe BPC were not significantly different from those of steady state group (p=0.523, 0.543 and 1.000 respectively) There was also no significant correlation in the mean plasma uric acid concentration in mild BPC, moderate BPC and severe BPC (Correlation coefficient (r)=0.212, p-value=0.372). In conclusion, this study established that though the uric acid concentration was higher in patients with SCA presenting with severe bone pains crisis than those with mild bone pain crisis and moderate bone pain crisis. However, there was no significant correlation between uric acid concentration and severity of bone pain crisis.
Odebiyi Hassan Abiola,
Fasola Foluke Atinuke,
Uric Acid Concentration in Patients with Sickle Cell Anaemia Presenting with Vaso-Occlusive Crises in Uch, Ibadan, American Journal of Laboratory Medicine.
Vol. 5, No. 6,
2020, pp. 155-161.
Adekile A. What’s new in the pathophysiology of sickle cell disease? Med Princ Pr. 2013; 22 (4): 311–2.
Piel FB, Patil AP, Howes RE, Nyangiri OA, Gething PW, Dewi M, et al. Global epidemiology of Sickle haemoglobin in neonates: A contemporary geostatistical model-based map and population estimates. Lancet [Internet]. 2013; 381 (9861): 142–51. Available from: http://dx.doi.org/10.1016/S0140-6736(12)61229-X.
Luz JA da, Sans M, Kimura EM, Albuquerque DM, Sonati M de F, Costa FF. alpha-thalassemia, HbS, and beta-globin gene cluster haplotypes in two Afro-Uruguayan sub-populations from northern and southern Uruguay. Genet Mol Biol [Internet]. 2006 [cited 2020 Mar 1]; 29 (4): 595–600. Available from: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572006000400002&lng=en&tlng=en.
Kutlar F, Mirmow D. Postmortem molecular diagnosis of sickle cell beta thalassaemia. J Clin Pathol. 2005; 58 (5): 548–9.
Zolaly M, Al-Mohammadi G, Al-Saadi G, Qasim D. Vaso-occlusive crises in patients with sickle cell disease: Parents’ perspectives and association with disease outcomes. J Taibah Univ Med Sci [Internet]. 2019 Dec 1 [cited 2020 Mar 1]; 14 (6): 515–22. Available from: https://www.sciencedirect.com/science/article/pii/S165836121930109X.
Kiefmann R, Rifkind JM, Nagababu E, Bhattacharya J. Red blood cells induce hypoxic lung inflammation. 2016; 111 (10): 5205–15.
Ramos C, Pou S, Britigan B, Cohen M, Rosen G. Spin trapping evidence for myeloperoxidase-dependent hydroxyl radical formation by human neutrophils and monocytes. J Biol Chem. 1992; 267: 8307–8312.
Corry DB, Eslami P, Yamamoto K, Nyby MD, Makino H, Tuck ML. Uric acid stimulates vascular smooth muscle cell proliferation and oxidative stress via the vascular renin–angiotensin system. J Hypertens [Internet]. 2008; 26 (2). Available from: https://journals.lww.com/jhypertension/Fulltext/2008/02000/Uric_acid_stimulates_vascular_smooth_muscle_cell.19.aspx.
Battelli MG, Polito L, Bortolotti M, Bolognesi A. Xanthine Oxidoreductase-Derived Reactive Species: Physiological and Pathological Effects. Reed TT, editor. Oxid Med Cell Longev [Internet]. 2016; 2016: 3527579. Available from: https://doi.org/10.1155/2016/3527579.
Nduka N, Kazeem Y, Saleh B. Variation in serum electrolytes and enzyme concentration in patient with sickle cell disease. J Clin Pharmacol. 1995; 48 (7): 648–651.
Gupta S, Yui JC, Xu D, Fitzhugh CD, Clark C, Siddiqui S, et al. Gout and sickle cell disease: Not all pain is sickle cell pain. Br J Haematol. 2015; 171 (5): 872–5.
Al-Naama LM, al-Sadoon EA al-Sadoon T. Levels of uric acid, urea and creatinine in Iraqi children with sickle cell disease. J Pak Med Assoc. 2000; 50: 98–102.
Obeagu E, Okoroiwu I, Gloria A, Queen B, Ogwuegbu V. Uric acid concentration in sickle cell disease patients in Owerri metropolis. Int J Adv Multidiscip Res. 2015; 2 (12): 31–34.
El-Hazmi, M. A. F., A. M. Al-Hazmi and ASW. Sickle cell disease in Middle East Arab countries. Indian J Med Res. 2011; 134 (5): 597–610.
Rasheed Y, Abdulaziz H, Ibrahim I, Babadoko A, Ibinaiye P. Assessment of kidney function in sickle cell anaemia patients in Zaria, Nigeria. Sahel Med J. 2017; 20 (1): 21–5.
Platt O. Pain in Sickle Cell disease. N Engl J Med. 1991; 325 (1): Platt, O. S., et al., Pain in Sickle Cell Disease.
Adekunle E, Olaniyi J, Oladapo W. Adult Sickle CellAnaemia Patients in Bone Pain Crisis have elevated Pro-Inflammatory Cytokines. Mediterr J Hematol Infect Dis. 2018; 10 (1): 1–9.
Herbert SD, Allen D, Dorothy H. The Natural History of Urate Overproduction in Sickle. Cell Anemia Ann Intern Med. 1979; 90 (5): 752–7.
Pandey S, Sharma A, Dahia S, Shah V, Sharma V, Mishra R. Biochemical indicator of sickle cell disease: Preliminary report from India. Biochem. Indian J Clin. 2012; 27: 191-195.
Steinberg MH. Pathophysiology of sickle cell disease. Baillieres Clin Haematol [Internet]. 1998 Mar; 11 (1): 163–84. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10872477.