1Professor and HOD, Department of General Medicine, Alluri Sitarama Raju Academy of Medical sciences, Eluru
21st Year Post Graduate, Department of General Medicine, Alluri Sitarama Raju Academy of Medical sciences, Eluru
33rd Year Post Graduate, Department of General Medicine, Alluri Sitarama Raju Academy of Medical sciences, Eluru
4Assistant Professor, Department of Pathology, Alluri Sitarama Raju Academy of Medical sciences, Eluru
5Professor, Department of General Medicine, Alluri Sitarama Raju Academy of Medical sciences, Eluru
6Professor, Department of Pathology, Alluri Sitarama Raju Academy of Medical sciences, Eluru
*Corresponding author: Swarnalatha Devi G, Professor & HOD, General Medicine, Alluri Sita Ramaraju Academy of Medical Sciences, Eluru, West Godavari, A.P.-534005. E-mail: drswarnalathadevi@gmail.com
Online published on 11 March, 2014.
Sickle cell disease occurs when an individual is homozygous for sickle cell mutation (β6-Glutamic acid β Valine) (HbS/A: 100/0; HbF: 2 - 25%). Heterozygous mutation results in sickle cell trait (HbS/HbA: 40/60). Inheritance of sickle cell gene along with mutations of α/β/δ genes in compound heterozygosis results in sickle cell variants. CASE REPORT: A 16year old male patient presented with fever, pain abdomen, anaemia, massive tender splenomegaly, unconjugated hyperbilirubinemia, microcytic hypochromic anaemia with sickle cells and target cells, elevatedHbF, HbS with normal HbA2 and decreased HbA.
Sickle Cell Mutation, Compound Heterozygosity, Fever, Anaemia, Massive Splenomegaly, Unconjugated Hyperbilirubinemia