The Biophysics and Flow Haemodynamics in Sickle Cell Patients: A Mathematical Model That Takes into Account Electochemical and Vascular Factors in the Genesis of Vaso-Occlusion

Abstract

Sickle Cell Disease is inherited genetic disease. An autosomal recessive gene is responsible for the synthesis of Haemoglobin S. The disease manifests usually in Homozygous SS state. Synthesis of the Haemoglobin S is courtesy of beta globin gene mutation in chromosome number 11 within the nucleus of Erythroblast. Valine replaces Glutamic acid in position 6 of beta polypeptide chain of haemoglobin. But deoxygenation of Haemoglobin S results in polymerization of the Haemoglobin and the deformable discoid red cell changes to stiff sickle cell, and this is the hallmark of vaso-occlusion and crises. Intracellular concentration of both Magnesium ions and Potassium ions in red cells correlate positively with lower risk of sickling and crises in SCD according to studies. Introducing a hypothetical equation that determines Vaso-occlusion risk, shortened and christen VASOcclusity, a product of biochemical and biophysical considerations in SCD haemodynamics where the radius of the blood vessel and the Body Mass Index by extension are also considered strong factors and variables.

Keywords:  Haemoglobin S, Polymerization, ions, Magnesium, Potassium, radius,