An anonymised dataset of 199 pediatric patients aged 3-18 years of age, enrolled in the prospective Muhimbili Sickle Cohort (MSC), (Makani et al. PloS ONE 2011), whose parent or guardian consented to participate, which included having blood and DNA samples archived for studies relating to understanding the pathophysiology of sickle cell disease in Tanzanian patients. The dataset contains variables on age, sex, sickle phenotype (derived from electrophoresis and high performance liquid chromatography), history of previous blood transfusion and averaged steady state hemoglobin concentrations over the previous year prior to the samples included in this analysis. Samples included in this analysis were collected at scheduled routine clinic visits at which children were assessed by the attending physician as “clinically well” with no current pain, no fever and were malaria test (smear and or rapid test) negative, and had no reported or recorded hospitalization in the previous month. Laboratory data from the analysed samples include complete blood count data, clinical chemistry values, inflammatory markers, iron markers, erythropoietin and hepcidin. Alpha thalassaemia 3.7 deletion and glucose-6-phosphate dehydrogenase deficiency as potentially disease modifying genotypes are also included.

Sickle cell disease, Iron metabolism, Children, Hepcidin