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Published on: September 6, 2017
Platelet loss during hematopoietic progenitor cell apheresis: Predictive factors and clinical implications in
Yandy Marx Castillo-Aleman1, Shinnette Lumame1, Jay Mary Rose-Roque1
1Abu Dhabi Stem Cells Center (ADSCC), Abu Dhabi, United Arab Emirates; Yas Clinic Khalifa City (YCKC) Hospital, Abu Dhabi, United Arab Emirates.
Platelet loss (PL) is a frequent consequence of G-CSF mobilization and hematopoietic progenitor cell apheresis [HPC(A)] that can impact donor safety during apheresis. This study aims to quantify PL during G-CSF-mobilized collections and identify donor- and procedure-related factors associated with greater PL and post-apheresis thrombocytopenia. We retrospectively analyzed 286 HPC(A) procedures performed in 212 donors between 2023 and 2025. Platelet outcomes were assessed using two predefined endpoints: PL ≥ 30% and post-apheresis platelet count <150 × 103/µL. PL ≥30% and post-collection thrombocytopenia occurred in 66.1% and 67.1% of procedures, respectively. Greater PL was associated in donors with higher pre-apheresis neutrophil, lymphocyte, and platelet counts and in procedures with longer collection times and larger processed blood volumes, accompanied by higher CD34+ cell yield and crude collection efficiency. In contrast, post-collection thrombocytopenia was driven by a distinct biological profile characterized by lower baseline platelet, lymphocyte, and CD34+ cell counts and intensified intra-apheresis mobilization of CD34+ and mononuclear cells. In summary, PL during HPC(A) in G-CSF-mobilized donors is frequent and reflects mobilization biology, including G-CSF-driven hematopoietic reprogramming, and procedural burden related to extracorporeal platelet removal. These findings support risk-adapted collection planning to improve donor safety while preserving apheresis yield and procedural efficiency.
Platelet loss (PL) is a frequent consequence of G-CSF mobilization and hematopoietic progenitor cell apheresis [HPC(A)] that can impact donor safety during apheresis. This study aims to quantify PL during G-CSF-mobilized collections and identify donor- and procedure-related factors associated with greater PL and post-apheresis thrombocytopenia. We retrospectively analyzed 286 HPC(A) procedures performed in 212 donors between 2023 and 2025. Platelet outcomes were assessed using two predefined endpoints: PL ≥ 30% and post-apheresis platelet count <150 × 103/µL. PL ≥30% and post-collection thrombocytopenia occurred in 66.1% and 67.1% of procedures, respectively. Greater PL was associated in donors with higher pre-apheresis neutrophil, lymphocyte, and platelet counts and in procedures with longer collection times and larger processed blood volumes, accompanied by higher CD34+ cell yield and crude collection efficiency. In contrast, post-collection thrombocytopenia was driven by a distinct biological profile characterized by lower baseline platelet, lymphocyte, and CD34+ cell counts and intensified intra-apheresis mobilization of CD34+ and mononuclear cells. In summary, PL during HPC(A) in G-CSF-mobilized donors is frequent and reflects mobilization biology, including G-CSF-driven hematopoietic reprogramming, and procedural burden related to extracorporeal platelet removal. These findings support risk-adapted collection planning to improve donor safety while preserving apheresis yield and procedural efficiency.
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