Sickle Cell Disease Biofluid Chip Technology (SCD BioChip)

'Sickle-shaped' anemia was first clinically described in the US in 1910, and the mutated heritable sickle hemoglobin molecule was identified in 1949. The pathophysiology of SCD is a consequence of abnormal polymerization of sickle hemoglobin (HbS) and its effects on red cell membrane properties, shape, and density, and subsequent critical changes in inflammatory cell and endothelial cell function. Our goal is to understand the impact of CMA abnormalities in SCD, by interrogating a number of recognized interactions in a range of clinical phenotypes. To date, correlative studies in SCD, by us and others, have range between clinical reports, based on tests, interventions, and chart review of individuals or groups of individuals and, at the other extreme, identification of functional gene polymorphisms based on population studies. The investigators wish to augment these studies through a systematic examination of cellular membrane properties and activation status. Of hematologic disorders, SCD may be unusually susceptible to such an examination.

NCT Number	NCT02824471
Lead Sponsor	University Hospitals Cleveland Medical Center Collaborators: Case Western Reserve University
Conditions	Sickle Cell Disease
Enrollment	100 participants
Start Date	2014-10
Primary Completion	2028-05-31 (estimated)
Study Completion	2028-05-31 (estimated)
Updated on ClinicalTrials.gov	2025-08-21