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Abstract #1641

Cerebral perfusion and oxygen extraction are similar in sickle cell disease patients with hemoglobin SS and hemoglobin S-thalassemia phenotypes  

Spencer L. Waddle1, Ifeanyi Ikwuanusi1, Lori C. Jordan1,2,3, Chelsea A. Lee1,2, Niral J. Patel1,2, Sumit Pruthi1, L. Taylor Davis1, Allison Griffin1, Michael R. Debaun4,5, Adetola A. Kassim5, and Manus J. Donahue1,3,6
1Department of Radiology, Vanderbilt University Medical Center, Nashville, TN, United States, 2Department of Pediatrics, Division of Pediatric Neurology, Vanderbilt University Medical Center, Nashville, TN, United States, 3Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, United States, 4Department of Pediatrics, Vanderbilt-Meharry Center for Excellence in Sickle Cell Disease, Vanderbilt University Medical Center, Nashville, TN, United States, 5Department of Internal Medicine, Division of Hematology/Oncology, Vanderbilt University Medical Center, Nashville, TN, United States, 6Department of Psychiatry, Vanderbilt University Medical Center, Nashville, TN, United States

Sickle cell disease (SCD) comprises multiple sickle phenotypes, yet it is assumed that most phenotypes have similar cerebral hemo-metabolic impact, despite differing hematological characteristics. Here, patients (n=120) with the two most common phenotypes, hemoglobin (Hb)-SS and HbSβ0-thalassemia, were evaluated using anatomical, cerebral blood flow (CBF)-weighted, and oxygen extraction fraction (OEF)-weighted 3T MRI. Results suggest that while CBF depends closely on hematocrit, SCD phenotype does not discriminate either CBF or OEF and anatomical findings of prior infarct and vasculopathy were not significantly different between groups. These findings are consistent with HbSβ0 and HbSS phenotypes having similar impact on cerebral hemo-metabolic dysfunction.

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