Studies on the hepatic and renal status of patients with sickle cell disease from western zone of Maharashtra, India

Authors

  • Deepa Garg School of Biotechnology and Bioinformatics, D. Y. Patil University, Navi Mumbai, Maharashtra, India
  • Neha Satam School of Biotechnology and Bioinformatics, D. Y. Patil University, Navi Mumbai, Maharashtra, India
  • Nimisha N. School of Biotechnology and Bioinformatics, D. Y. Patil University, Navi Mumbai, Maharashtra, India
  • T. Marar School of Biotechnology and Bioinformatics, D. Y. Patil University, Navi Mumbai, Maharashtra, India
  • V. W. Patil Department of Department of Biochemistry, Grant Government Medical College and Sir J. J. Groups of Hospital, Mumbai, Maharashtra, India

DOI:

https://doi.org/10.18203/2320-6012.ijrms20181272

Keywords:

Hemolytic events, Liver function, Pathogenesis, Renal function, Sickle cell disease

Abstract

Background: Sickle cell disease (SCD) is the most common inherited monogenic genetic disorder in Indian tribal and non-tribal population. This condition is caused by mutations in the hemoglobin gene and inherited in an autosomal recessive pattern. Pathogenesis in SCD varies widely from patient to patient. Most of the infections affect SCD pathogenesis, so early diagnosis of the same is important.

Methods: The present study was designed to evaluate the biochemical parameters to assess the hepatic and renal status in SCD subjects from west zone of Maharashtra, India. Patients with sickle cell disease (n=50) from primary health centres of Palghar were included in this study and age and sex matched healthy persons (n=50) were controls. Informed written consent was obtained from all the study subjects.

Results: Our findings showed that Aspartate trasaminase (AST), Alanine transaminase (ALT), bilirubin and creatinine increased significantly above normal level in SCD subjects. Albumin and urea levels in SCD were found to have decreased in the SCD subjects. There is a slight increase in uric acid and creatinine levels; this indicates an adverse effect on hepatic function and moderate effect on renal function in sickle cell anemia patients. Most common events of SCD pathogenesis, can be categorized into hemolytic events and vaso-occlusive crisis-based events. Adverse effect on hepatic function can lead to further hemolytic events.

Conclusions: Although specific biomarkers related to these different events needs to understand for assessment of pathogenesis, the ones we have studied can be useful to assess the status of hepatic and renal function to follow the effectiveness of therapeutic interventions. 

References

Herrick JB. Peculiar elongated and sickle-shaped red blood corpuscles in a case of severe anemia. Archives Inter Med.1910;6:517-21.

Serjeant GR. The sickle cell trait, In: Sickle cell disease. Searjeant GR, editor. New York city, Oxford university press;1992:415-425.

Seth T, Gupta P, Paul VK. Hematological Disorder, In Textbook of Pediatrics. Ghai OP, editor. CBS Publishers New Delhi; 7th Edition; 2009.

Sears DA. The morbidity of sickle cell trait: a review of literature. Ame J Med. 1978;6496:1021-36

Berthelot MP. Violet d'aniline. Report, chimie appliquee. 1859;1:284.

Bonsnes RW, Taussky HH. On the colorimetric determination of creatinine by the Jaffe reaction. J Biol Chem. 1945;158:581-91.

Gochman N, Schmitz JM. Automated determination of uric acid with use of a Uricase-Peroxidase system. Clin Chem. 1971;17:1154-9.

King J. The transferases-alanine and aspartate transaminases. In: King J (Ed.), Practical Clinical Enzymology. Van Nostrand Company Ltd, London. 1965c:121-38.

Kind PR, King EJ. Estimation of plasma phosphatase by determination of hydrolysed phenol with amino-antipyrine. J Clin Pathol. 1954;7(4):322-6.

Mathieu M, Artur Y, Aubry A, Bailly M, Braun JP, Bretaudiere JP. Recommendations for determining the catalytic concentration of lactate dehydrogenase in human serum at +30°C. Ann Biol Clin. 1982;40:87-164.

Zilva JF, Pannall PR. Plasma protein and immunoglobulins in clinical chemistry in diagnosis and treatment. 1979:305-16.

Jendrassik L, Grof P. Colorimetric method of determination of bilirubin. Biochem Z. 1938;297:81-2.

Banerjee S, Owen C, Chopra S. Sickle cell hepatopathy. Hepathology. 2001;33:1021-28.

Stephan JL, Merpit-Gonon E, Richard O, Raynaud-Ravni C, Freycon F. Fulminant liver failure in a 12-year-old girl with sickle cell anaemia: favourable outcome after exchange transfusions. Euro J Pediatr. 1995;154:469-71.

Gürkan E, Ergun Y, Zorludem RS, Bafilamifili F, Koçak R. Liver involvement in sickle cell disease. Turk J Gastroenterol. 2005;16(4):194-8.

Maske MM, Meher S, Dora P, Dehury S, Kullu BK, Patel DK, et al. Nephrotic syndrome in sickle cell disease of Western Odisha, India: a case report of five cases. Int J Pharma Sci Inven. 2015;2319-6718.

Kumar A, Tripathi S. Study of certain biochemical parameters in patients of sickle cell anemia. Advan Bio. 2011;(2):79-81.

Arquhar MG, Vernier RL, Good RA. An electron microscope study of the glomerulus in nephrosis, glomerulonephritis, and lupus erythematosus. J Experimental Med. 1957;106:649-58.

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Published

2018-03-28

How to Cite

Garg, D., Satam, N., N., N., Marar, T., & Patil, V. W. (2018). Studies on the hepatic and renal status of patients with sickle cell disease from western zone of Maharashtra, India. International Journal of Research in Medical Sciences, 6(4), 1224–1227. https://doi.org/10.18203/2320-6012.ijrms20181272

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Original Research Articles