International Journal of Science and Healthcare Research Vol.5; Issue: 1; Jan.-March 2020 Website: ijshr.com Original Research Article ISSN: 2455-7587 International Journal of Science and Healthcare Research (www.ijshr.com) 274 Vol.5; Issue: 1; January-March 2020 Association of Biochemical Markers with Cardiovascular Status in Sickle Cell Disease Manish Kumar Sahu 1 , P.K.Khodiar 1 , D.Rath 1 , R.L.Khare 2 , Smit Shrivastava 2 1 Pt J.N.M. Medical College, Raipur. 2 Dr B.R. Ambedkar Memorial Hospital, Raipur. Corresponding Author: Manish Kumar Sahu ABSTRACT Background: Sickle-cell disease is a group of blood disorders caused by single nucleotide polymorphism at the 6th codon of HBB gene. It is well known fact that in sickle cell disease patients many cardiac abnormalities found. So aim of this study is to find out whether these biochemical markers are associated with cardiac diseases in sickle cell patients or not. Materials And Methods: This cross sectional study enrolled 60 subjects positive for sickle cell disease. Serum IRON, LDH, TIBC was measured using I lab 650. Serum FERRITIN, NT-proBNP, was measured by chemiluminescence. Cardiac status of all the patients was assessed by echocardiography. Results: Serum LDH was found to be increase in all the study subjects (mean=938.21). So there is no correlation between high serum LDH and cardiac disease of sickle cell patients. Significant difference was observed between normal and abnormal ECHO findings for iron (p= 0.55). Serum NT Pro BNP was found to be significantly higher in subjects with abnormal ECHO findings (P=<0.0001). Significant difference was observed in ECHO findings for different age groups in study subjects indicating that Normal ECHO findings were significantly frequent in lower age group (p= 0.186). Conclusion: 13 patients out of 70 who were having abnormal echo findings and also they have abnormal serum NT pro BNP level. Most common echo finding was left ventricular hypertrophy, tricuspid regurgitation. Ldh was higher in all the study subjects. Keywords: Sickle Cell Disease, Biochemical Markers, Cardiovascular Status, Blood Disorders INTRODUCTION Sickle hemoglobin (HbS) is the first molecular disease known to human. The mutation causing sickle cell anemia is a single nucleotide substitution (A to T) in the codon for amino acid at 6 th position. This change converts a glutamic acid codon (GAG) to valine codon (GTG). [1] Sickle cell is caused by a single point mutation in the hemoglobin gene, which is called as hemoglobin S. Hb S leads to polymerization of deoxygenated hemoglobin. So the red blood cells of a person with sickle cell anemia tend to be fragile and less flexible or rigid, stiff in nature then normal RBC. [2] When the red blood cells become fragile this leads to cardiac complications in SCD and are known to be an important cause of the morbidity and mortality. [3] To assess the function of heart in sickle cell patients a peptide hormone called Brain natriuretic peptide (BNP) is estimated. The human BNP gene is located on chromosome 1 and encodes the prohormone proBNP. The biologically active BNP and the remaining part of the prohormone, NT‐pro BNP (76 amino acids) can be measured by immunoassay in human blood. Cardiac myocytes constitute the major source of BNP related peptides. The main stimulus for peptide synthesis and secretion is myocyte stretch. [4] Pulmonary hypertension and diastolic dysfunction has been identified as a predictor of death in the adult SCD population. [5]