International Journal of Science and Healthcare Research Vol.4; Issue: 4; Oct.-Dec. 2019 Website: www.ijshr.com Original Research Article ISSN: 2455-7587 International Journal of Science and Healthcare Research (www.ijshr.com) 70 Vol.4; Issue: 4; October-December 2019 Assessment of Cormic Index in Sickle Cell Disease Subjects and Its Association with Clinical Severity Dr. Mainak Bardhan 1 , Ipsita Das 2 , Romesh Tiwari 3 , Dr Dnyanesh Amle 4 , Dr Debapriya Rath 5 1 House Surgeon, Pt JNM Medical College, Raipur (CG) 2 Research Scholar, Department of Biochemistry, Pt JNM Medical College, Raipur (CG) 3 MBBS Final Year, Pt JNM Medical College, Raipur (CG) 4 Assistant Professor, Department of Biochemistry, AIIMS, Nagpur 5 Assistant Professor, Department of Biochemistry, Pt JNM Medical College, Raipur (CG) Corresponding Author: Dr Debapriya Rath ABSTRACT Sickle cell anemia is a complex pathophysiologic single gene defect genetic disorder with a wide spectrum in the severity of the disease. Decomposing stature into its major components is a useful strategy to assess antecedents of disease, morbidity, and death in adulthood. CORMIC INDEX is calculated as (Sitting Height / Height) × 100. Leg length relative to total body proportions is a good indicator of overall growth reserve capacity of a person or a group of people. Previous studies in sickle cell patients have shown evidence of growth failure and are associated with delayed puberty. There is no study correlating growth pattern in sickle cell disease patients with the CORMIC index, in our study we tried to do this. The main conclusion in which we arrived is that “there is no significant correlation between the severity of sickle cell anemia and Cormic index”, however, sickle cell affects many growth parameters i.e. height, weight, and sitting height. Keywords: Cormic index, Sickle cell Anemia, Hydroxyurea, Chhattisgarh INTRODUCTION Sickle cell disease, one of the world’s commonest single-gene disorders, was first described by Herrick in 1910, who linked his patients’ symptoms to abnormally shaped erythrocytes in the blood. [1,2] Sickle cell disease (SCD) is a highly variable condition. [3] It is caused by a mutation in the β-globin gene. An Adenine (A) to Thymine (T) substitution (GAG to GTG transversion) in the 6th codon of the β- globin gene specifies the insertion of Valine in place of Glutamic acid. [4] India is known to be home of over 50 % of global sickle cell disease patients. [5] The World Health Organization (WHO) estimates that hemoglobinopathies cause 3.4% of deaths worldwide in children younger than five years old (2008). In addition to the close geographic correlation between the frequency of the Haemoglobin S gene in populations and the historic incidence of malaria, evidence for the partial resistance of carriers to all forms of Plasmodium falciparum malaria has been reported in many populations. [6,7] Bone marrow infarction is a well- recognized complication of sickle cell disease. [8-10] Sickle cell disease is also associated with an impaired oxygen delivery system to skeletal muscle that could alter the ATP production process. Exercise induces intramuscular necrosis more in sickle cell disease patients as compared to those not having sickle cell disease. [11] SCD also results in impaired muscle force production and resistance to fatigue, independent of muscle mass. SCD is also associated with high fatigability when exercise intensity is high. [12] There is also the presence of persistent red marrow in the axial and appendicular skeleton, avascular necrosis of femur head, bone infarcts, septic arthritis and tubercular infection of bone in SCD. [13] SCD is associated with microvessel rarefaction, decrease in