Evaluation of Biochemical Parameters for Sickle Cell Anemic Children at Kassala City, Eastern Sudan
Background: Sickle cell disease (SCD) is an inherited disease caused by gene mutation. Many investigators reported that Eastern Sudan has rich SCD and also an association with biochemical parameters such as liver and renal function tests.
Objective: The present study was to assess the plasma biochemical parameters such as urea, creatinine and sodium (Na) and potassium (K) total protein, albumin, Bilirubin, Aspartate Transaminase (AST), Alanine Transaminase (ALT) and Alkaline Phosphatase (ALP) in SCD as case group and apparently healthy persons as control group.
Materials and Methods:The study was conducted at Kassala Teaching Hospital, Kassala city, Eastern Sudan. This study was carried during December 2019 to January 2020. A total of 100 subjects enrolled in this study, 50 patients with SCD as case group and 50 apparently healthy as control group. The plasma biochemical parameters were estimated using Biosystem-350(Semi automated chemistry analyzer), and plasma Na and K were estimated using Easylyte. The data was analyzed using SPSS version (23).
Results:Study populations were matched age and sex, the age ranged from 5 to 15 years with their average age 8years. The plasma Na was insignificance difference in case compared to control group. The plasma K, urea and creatinine (p=0.039) were significantly increase compared to control group. Also the plasma total protein, albumin, Bilirubin, creatinine, AST, ALT and ALP were significantly increase in case group compared to control group. The age was strong association into plasma urea(r=0.583, p=.000) and plasma crearinine (r=0.759, p=.000). The negative correlation between plasma Na and plasma urea (r= -.335, p=0.017). There was positive correlation between plasma urea and creatinine (r=0.332, p=0.018). Their strong association between plasma Bilirubin and ALP activity (r= .563, P=.000), and also their strongly association between liver enzymes plasma level among SCD patients (r=.873, 381, 563, P= .000, .006, 000).
Conclusion:The study concluded that, significance increased in plasma K, urea creatinine, plasma total protein, and albumin, Bilirubin, AST, ALT and ALP. Strong association between age and plasma urea, creatinine, and the negative correlation between plasma Na and plasma urea and also positive correlation between plasma urea and creatinine. There were positive correlation between plasma urea and creatinine. Their strong association between plasma bilirubin and ALP levels and also their strongly association between liver enzymes levels among SCD patients. Observation of the study concludes the biochemical abnormality play a significant role in sickle cell patient’s physiopathology and can be used to management of the disease.
2. Muhammed S, Addae S, Suleiman S, Adzaku F, AnnobilS, Kaddoumi, et al. Serum calcium, parathyroid hormone,and vitamin D status in children and young adults with sickle cell disease. Ann Clin Biochem 1993; 30:45-5 1.
3. Michael R, Dc Duan and Elliott vichinsky. Heamoglobinopathies. Kliemgman.Behrman, Jenson. Stanton Nelson text of pediatrics.19th. (2011.) Chapter 462.
4. Awasthy N, Aggarwal KC, Goyal PC, Prasad MS, Saluja S, Sharma M. "Sickle cell disease: Experience of a tertiary care center in a nonendemicarea". Annals of Tropical Medicine and Public Health. 2008. 1 (1): 1–4.
5. Meshikhes AW, al-Faraj AA. Sickle cell disease and the general surgeon. J R Coll Surg Edinb; 1998.43(2):73-79.
6. Rosenblate HJ, Eisenstein R, Holmes AW. The liver in sickle cell anemia. A clinical- pathologic study. Arch Pathol 1970;90:235-45.
7. Banerjee S, Owen C, Chopra S. Sickle cell Hepatopathy. Hepathology 2001; 33: 1021-28.
8. Brody JI, Ryan WN, Haidar MA. Serum alkaline phosphataseisoenzymes in sickle cell anaemia. JAMA 1975; 232: 738-41.
9. Derebail VK. Sickle cell nephropathy. Natl. Kidney Found. Prim. Kidney Dis. Sixth Ed. 2013. p. 357–61.
10. Nath KA, Hebbel RP. Sickle cell disease: renal manifestations and mechanisms. Nat. Rev. Nephrol. Nature Publishing Group; 2015; 11:161–71.
11. Pandey S, Sharma A, Dahia S, Shah V, Sharma V, R. M. Mishra R.M, Pandey Sw, Saxena R. Biochemical Indicator of Sickle Cell Disease: Preliminary Report from India. Indian Journal of Clinical Biochemistry 2012. Volume 27, pages191–195.
12. Schubert IT. Hepatobiliary system in sickle cell disease. Gastroenterology 1986;90: 2013-21.
13. Nduka N, Maxwell-Owhochuku S, Odike P. Current ob-servations on sickle cell genotype in Nigeria. E Afr Med Jf1993;70:646-9.
14. Isichei. U P . Liver function and the diagnostic significance of biochemical changes in the blood of African children with sickle cell disease. JCP. 1980; 33:626-630.
15. Mahera, C Amany H. Mansourb Maha M. Studyof chronic hepatopathy in patients with sickle cell disease. Gastro enterology Research. 2009. 2(6): 338-343.
16. Kotila Taiwo, Kayode Adedapo, Aduragbenro Adedapo,Olayiwola Olluwasola, Eyitayo Fakunle, BiobeleBrown. Liver dysfunction in steady statesickle cell disease. Hepatology.2005; 4(4): 261-263.
17. Nsiah K.V.P. Dzogbefia D. AnsongA. Osei Akotoh. Boateng and D. Ocloo. AST and ALT changes in sickle cell disease. Clinical Medicine Insights: Blood Disorders 2011:4.
18. Akuyam SA, Abubakar A, Lawal N, Yusuf R,Aminu SM, Hassan A, et al. Assessment of biochemical liver function tests in relation to age among steady state sickle cell anemia patients.Niger J Clin Pract 2017;20:1428-33.
19. Airhomwanbor KO, Idehen IC, Okparaku SO, Dic-Ijewere EO, Ehimare RI, Osarobo E, Omolumen LE,Edetanlen GE. Renal Function of Sickle Cell Subjects in Edo State-Nigeria. Archives of Nephrology and Urology 1(2018): 001-008.