Vitalant Sullivans Island, South Carolina, United States
Background/Case Studies: Normal adult platelet counts (PltCts) range from 150K-450K/μL and the US CFR mandates a PltCt ≥150K/μL to donate apheresis platelets, without an established upper limit. Upper limits may be set by the blood center medical director or separators’ defined upper limits. Thrombocytosis (>450K/μL) may be due to primary myeloproliferative disease (MPD), iron deficiency (ID) or secondary to an inflammatory process. Donors with thrombocytosis require assessment for proper counseling. Historically, donors with intermittent high PltCts continued donating, providing evaluable trends after 1-2 high counts.
Study
Design/Methods: Two physicians performed a chart review of 183 platelet donors with PltCts >575/μL (Trima Accel’s upper limit) on at least 1 presentation from 2019-2022, representing 0.22% of the apheresis donor base. Each donor’s age, sex, and lifetime donation history were reviewed for PltCt & hemoglobin (Hb) trends, and ferritin (F) values, if available. PltCt trends were categorized as slowly rising, stable at high values, or without a discernable trend (incl. stably low PltCts with occasional high values). RBC donation history, Hb trends and low Hb deferrals were considered when assigning a likely or potential ID etiology.
Results/Findings: Of the 183 donors, 66% were female, compared to 52% in our active apheresis donor base. The median(IQR) most recent age was 51(36-54), with a median of 36(9-79) donations. Approximately 1/3rd each had slowly rising PltCts or stable high counts. Decreasing or stable lower counts with only intermittent high counts were seen in 15%. Thirty-one (17%) had 1 or 2 PltCts >575K/μL, and etiology could not be inferred. Of 63 donors with a slow rise, 60% were judged likely ID vs. 30% of those with stable high counts. MPD was suspected (with sudden sustained PltCt elevations. Donors with likely MPD (4 donors) were older with a median age of 61 compared to the median of 51 for all donors. Of 152 evaluable donors, 69 (45%) were classified as likely ID and 46 (30%) as possible ID due to decreasing Hb or F < 15 ng/mL and 66 of the 115 (57%) with likely/possible ID had a history of low Hb deferrals. Conclusions: Identification of the etiology of thrombocytosis is not always possible. Centers should have policies to identify and counsel donors with thrombocytosis. While all might benefit from referral to a healthcare provider (HCP), donors with downward trending Hb values/recent Hb deferrals, particularly with slowly increasing PltCts, may continue to donate with low-dose iron replacement, as ID is a reversible cause of high PltCts. Identification of donors with MPD is important for appropriate donor management and to avoid collection of platelets with abnormal function. HCP referral is indicated for persistent high counts, expeditiously for PltCts >1M/μL.
Importance of research: Blood centers must determine local policies for management of apheresis platelet donors with thrombocytosis. Our data suggest that more than a third of donors can be counseled to mitigate donation-related iron deficiency, while others may need to be referred to their HCP for further evaluation before continuing platelet donation.
