Abstract:
Background: Foetal haemoglobin has been implicated
in the modulation of sickle cell crisis. Its level is generally
inversely proportional to the severity of sickle cell
disease (SCD) for a given sickle cell phenotypes. The
main aim of therapy for vaso-occlusive crisis (VOC),
which is the hallmark of SCD, is to reduce the chances
of sickling through the prevention of polymerization of
HbS. One way of preventing this polymerization is by
increasing foetal haemoglobin levels.