Iron deficiency is associated with reduced levels of inflammation and haemolysis in patients with <scp>HbSS</scp> and <scp>HbSC</scp> and reduced clinical admissions in those with <scp>HbSC</scp>

Evidence suggests that iron deficiency may reduce sickle cell disease (SCD) complications by decreasing sickle haemoglobin polymerization through reduced red cell haemoglobin concentration. The aim is to investigate the effects of iron deficiency in SCD patients. We reviewed clinical and laboratory data from 512 patients (408 HbSS, 104 HbSC) at King's College Hospital (2008-2020). Outpatient data were collected from patients with no blood transfusions or hydroxyurea (hydroxycarbamide) use in the prior 90 days. Patients were categorized as hypoferritinaemic (<45 μg/L), normoferritinaemic (45-800 μg/L) or hyperferritinaemic (>800 μg/L) and analysed for laboratory markers and clinical complications. In HbSC patients, hypoferritinaemia was associated with significantly fewer hospital admissions and inpatient days per year compared to normoferritinaemia. Although this was not seen in HbSS patients, hypoferritinaemia correlates with lower haemolysis and inflammation markers, with no differences in total haemoglobin or erythropoietin in both groups. In HbSS patients, haemoglobin F was significantly lower in hypoferritinaemic compared to normoferritinaemic patients. Iron deficiency may reduce inflammation and haemolysis in both HbSS and HbSC, with clinical benefits demonstrable in HbSC. Low ferritin levels were not associated with increased anaemia, suggesting improved red cell survival. Iron-restricted erythropoiesis may benefit SCD patients in certain circumstances.