📖 ABSTRACT/OVERVIEW
Transfusional iron overload is a significant complication of chronic blood transfusion therapy in sickle cell disease, leading to progressive organ damage if inadequately monitored. This study biochemically characterises iron overload in frequently transfused sickle cell disease patients at a sickle cell centre in Abuja, North Central Nigeria. A cross-sectional analytical design was employed, recruiting 100 HbSS patients who had received 10 or more transfusions. Serum ferritin, serum iron, transferrin saturation, and non-transferrin-bound iron were measured using standard immunoassay and colorimetric methods. Liver function tests, cardiac troponin, and creatinine were also assessed to identify end-organ consequences of iron deposition. Serum hepcidin, the master regulator of iron homeostasis, was measured by ELISA to characterise its response in the transfusional iron overload context. The number of transfusions received and duration of chelation therapy were documented and correlated with iron marker severity. The study tests whether ferritin alone is sufficient to predict non-transferrin-bound iron and organ iron burden in this population. Findings will support biochemically informed transfusion and chelation protocols for sickle cell patients in Nigerian haematology centres. Keywords: transfusional iron overload, sickle cell disease, serum ferritin, hepcidin, Abuja.
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