Objective:Platelet transfusion thresholds for very low birth weight (VLBW, <1500g) infants vary widely, and the role of bleeding on platelet transfusion thresholds is unknown. Study Design:This observational birth cohort study of VLBW infants born in 7 hospitals across the US examined pre-transfusion platelet counts in infants with and without bleeding who received at least 1 platelet transfusion in the first 3 weeks of life using mixed effect linear regression models. Results:Of the 210 transfused infants, most (76%) had bleeding; intraventricular hemorrhage (IVH) was the most common (61%) bleeding type. Pre-transfusion platelet counts were not different among infants with or without bleeding diagnoses (56.3 vs 58.5×103/μL, respectively; P=0.7). However, infants with severe IVH had higher platelet counts (68.9×103/μL) compared to the entire cohort (53.5×103/μL, P=0.01). Conclusion:Infants with or without bleeding diagnoses had similar pre-transfusion platelet counts; infants with severe IVH had higher pre-transfusion platelet counts.

Importance:Few studies have evaluated whether modifiable aspects of red blood cell (RBC) transfusions are associated with recipient outcomes in very-low-birth-weight (VLBW) infants. Objective:To determine whether blood donor, RBC modifications and storage, or transfusion thresholds and characteristics are associated with serious adverse outcomes in VLBW infants undergoing transfusion. Design, Setting, and Participants:Transfusion in Preterm Infants was a prospective birth cohort study that recruited VLBW infants (<1500 g at birth) between April 1, 2019, and December 31, 2023, at 5 university-affiliated and 3 community birth hospitals in the US. Electronic medical record data linking blood donor and component data to infants were obtained and linked with Vermont Oxford Network outcome data, with additional outcome review by site. The analysis was completed in January 2026. Exposures:RBC transfusion and transfusion characteristics, evaluated up to the first outcome event. Main Outcomes and Measures:The primary outcome was a composite outcome of severe intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), late-onset sepsis, severe bronchopulmonary dysplasia (BPD), retinopathy of prematurity, or death (and secondary individual outcomes), with follow-up through 90 days or death. Blood donor characteristics (sex, age, and hemoglobin), anticoagulant preservative solution and/or unit characteristics, transfused volumes, transfusion number, and infants' pretransfusion hemoglobin values were evaluated using multivariable generalized estimating equation regression models to account for correlation within hospital, adjusted for illness severity. Results:The study enrolled 2605 VLBW infants, and 1283 (586 [45.7%] female; 713 [55.6%] <27 weeks' gestational age) received RBC transfusion. Median pretransfusion hemoglobin level was associated with higher odds of the composite outcome (odds ratio [OR] per 1 g/dL increase, 1.15; 95% CI, 1.07-1.25; P < .001). In contrast, use of additive solution (AS)-1 or AS-5 vs the reference of citrate phosphate dextrose adenine or citrate phosphate dextrose as the anticoagulant preservative solution was associated with lower odds of the composite outcome (OR, 0.72; 95% CI, 0.53-0.97; P = .03). There were no significant associations with other examined modifiable factors and the composite outcome. Among secondary outcomes, anticoagulant preservative solution was associated with lower risk of BPD (AS-1 and AS-5, OR, 0.48; 95% CI, 0.33-0.69; AS-3, OR, 0.65; 95% CI, 0.56-0.77) and higher risk of NEC (AS-3, hazard ratio [HR], 5.33; 95% CI, 1.22-23.29). Transfusion dose was associated with higher risk of mortality (HR per 5 mL/kg, 1.25; 95% CI, 1.17-1.35), and donor age was associated with a lower risk of mortality (HR for age ≥60 years, 0.63; 95% CI, 0.44-0.92). Shorter postirradiation storage duration (<1 day) was associated with lower risk of NEC (HR, 0.44; 95% CI, 0.22-0.89). Female donor sex was associated with lower risk of IVH (HR, 0.60; 95% CI, 0.36-0.99). Conclusions and Relevance:In this cohort study of VLBW infants, pretransfusion hemoglobin and anticoagulant preservative solution were associated with a composite of morbidities and mortality, unlike other modifiable blood banking practices. For individual outcomes, select donor and blood banking factors were identified that may be modifiable targets for further evaluation.

Importance:Pediatric hemovigilance is a nascent field in transfusion medicine. The lack of standardized hemovigilance reporting in the US makes it difficult to determine age-specific transfusion reaction rates and risks. Objective:To evaluate the rates and epidemiology of transfusion reactions reported to transfusion services in neonatal and pediatric populations. Design, Setting, and Participants:This cohort study analyzed transfusion reactions occurring in children younger than 18 years reported to 8 hospitals' transfusion services during April 1, 2019, through December 31, 2023. Data were evaluated from March 2024 to June 2025 using standardized data collection forms and associated electronic health records. Exposure:Patients who received transfused blood products (red blood cells [RBCs], platelets, plasma, or cryoprecipitate) with at least 1 transfusion reaction reported to the transfusion service. Main Outcomes and Measures:Reaction rates per 100 000 products transfused were calculated. Pediatric transfusion reactions were characterized in detail, including reported severity and imputability; product type; patient age, sex, race, and ethnicity; and reported symptoms, premedication, and clinical management. Results:The sample included 228 886 products transfused to 22 628 patients (median [IQR] age, 4.2 [0.3-12.4] years; 127 903 males [55.9%]). The products were transfused to patients of Asian (18 649 [8.2%]), Black (37 673 [16.5%]), White (93 824 [41.0%]), multiracial (3680 [1.6%]), other (68 857 [30.1%]), or unknown race (6203 [2.7%]) and Hispanic or Latinx (52 398 [22.9%]), non-Hispanic and non-Latinx (144 017 [62.9%]), and unknown ethnicity (32 471 [14.2%]). A total of 1165 imputable transfusion reactions were reported, with an overall reaction rate of 0.52% (95% CI, 0.49%-0.55%). Patients aged 5 to 11 years had the highest reported transfusion reaction rate (891.11 [95% CI, 799.81-989.11] per 100 000 products transfused). Platelet transfusions had the highest transfusion reaction rates (821.75 [95% CI, 754.14-893.80] per 100 000 products transfused), with allergic reactions being most common (506.04 [95% CI 453.30, 563.24] per 100 000 products transfused), whereas RBC transfusions had more reported febrile nonhemolytic transfusion reactions (FNHTRs; 296.20 [267.06, 327.67] per 100 000 products transfused) than other types of reactions. The most common symptoms were urticaria (69.6% [368 of 529 patients]) in allergic reactions, fever (96.5% [559 of 579 patients]) in FNHTRs, and acute respiratory distress (87.5% [21 of 24 patients]) in transfusion-associated circulatory overload (TACO); the most common treatments were antihistamines (80.3% [425 of 529 patients]) for allergic reactions, antipyretics (67.9% [393 of 579 patients]) for FNHTRs, and diuretics (83.3% [20 of 24 patients]) for TACO. Many patients (35.8% [107 of 299]) did not receive premedication after the first reaction in subsequent transfusions, regardless of reaction type. When transfusion reactions recurred, they were often of the same type (77.9% of reactions [120 of 154] after allergic reactions were allergic; 72.1% of reactions [98 of 136] after FNHTRs were FNHTRs). Conclusions and Relevance:In this cohort study of pediatric transfusion reactions, reactions appeared to be age dependent, and rates of allergic reactions and FNHTRs were higher than rates from previously published, possibly underreported, predominantly adult data. These findings underscore the importance of pediatric-specific hemovigilance to improve recognition, reporting, and safety monitoring of transfusion reactions.

OBJECTIVE:To evaluate if hematologic thresholds for red blood cell (RBC) and platelet transfusions changed over time following publication of new evidence from randomized trials in a multicenter cohort of extremely low birth weight (ELBW) infants. STUDY DESIGN:We analyzed data from the National Heart Lung and Blood Institute Recipient Epidemiology and Donor Evaluation Study-IV-Pediatrics study from April 2019 through December 2023. We compared pretransfusion hemoglobin and platelet counts closest to each transfusion within 24 hours by year using linear mixed models and used model interaction terms to determine if trends over time differed by postnatal weeks. RESULTS:We evaluated 981 ELBW infants. For trends in RBC transfusion thresholds, 785 infants (80%) received 5182 RBC transfusions, of which 4835 (93%) had a pretransfusion hemoglobin value. Pretransfusion hemoglobin declined over time (P < .0001), with trends differing by postnatal week (interaction P = .005). The greatest year-over-year decline in pretransfusion hemoglobin was in the third postnatal week or later. For platelet transfusions, 221 infants (23%) received 934 platelet transfusions, of which 900 (96%) had a corresponding pretransfusion platelet count. There was no change in pretransfusion platelet count over time (P = .24). These trends did not differ by postnatal week (interaction P = .14), although pretransfusion platelet counts were lower after the first postnatal week (P < .001). CONCLUSIONS:In this cohort of US centers, we observed declines in pretransfusion hemoglobin but not pretransfusion platelet counts from 2019 to 2023. These findings suggest evidence from recent RBC and platelet transfusion threshold trials may have been differentially translated into clinical practice for ELBW infants.

BACKGROUND:Major ABO-incompatible platelet transfusions are associated with poor intracerebral hemorrhage (ICH) outcomes, yet drivers for this relationship remain unclear. Brain magnetic resonance imaging (MRI) ischemic lesions after ICH are neuroimaging biomarkers of secondary brain injury and are associated with poor outcomes. Given that ABO-incompatible platelet transfusions can induce immune complex formation, thrombo-inflammation, and endothelial barrier disruption, factors that could exacerbate cerebral ischemia, we explored whether major ABO-incompatible platelet transfusions are risk factors for ischemic lesions on brain MRI after ICH. METHODS:Adult patients admitted to a tertiary-care academic center between 2009 and 2016 who received a single-platelet transfusion within 24 hours of admission after an ICH, had available donor/recipient ABO data, and brain MRI during the hospitalization were analyzed. Adjusted regression models evaluated relationships between major ABO-incompatible platelet units and MRI ischemic lesions. RESULTS:A total of 40 patients were included in the study. The mean age was 67.1 (SD, 14.1), and 37.5% were female. Twenty percent of patients received a major ABO-incompatible platelet unit. Major ABO-incompatible platelet transfusions were associated with increased odds of MRI ischemic lesions after adjusting for ICH severity (adjusted odds ratio, 9.2 [95% CI, 1.3-62.7]). CONCLUSIONS:Our exploratory findings suggest that major ABO-incompatible platelet transfusions may contribute to secondary brain injury after ICH. Further work is needed to assess whether avoiding major ABO-incompatible platelet transfusions can prevent secondary brain injury burden and improve ICH outcomes.

BACKGROUNDBlood donation increases the risk of iron deficiency, but its effect on brain iron, myelination, and neurocognition remains unclear.METHODSThis ancillary study enrolled 67 iron-deficient blood donors, 19-73 years of age, participating in a double-blind, randomized trial. After donating blood, positive and negative susceptibility were measured using quantitative susceptibility mapping (QSM) MRI to estimate brain iron and myelin levels, respectively. Furthermore, neurocognitive function was evaluated using the NIH Toolbox, and neural network activation patterns were assessed during neurocognitive tasks using functional MRI (fMRI). Donors were randomized to i.v. iron repletion (1 g iron) or placebo, and outcome measures repeated approximately 4 months later.RESULTSIron repletion corrected systemic iron deficiency and led to trends toward increased whole brain iron (P = 0.04) and myelination (P = 0.02), with no change in the placebo group. Although overall cognitive performance did not differ significantly between groups, iron-treated participants showed improved engagement of functional neural networks (e.g., memory pattern activation during speed tasks, P < 0.001). Brain region-specific changes in iron and myelin correlated with cognitive performance: iron in the putamen correlated with working memory scores (P < 0.01), and thalamic myelination correlated with attention and inhibitory control (P < 0.01).CONCLUSIONIron repletion in iron-deficient blood donors may influence brain iron, myelination, and function, with region-specific changes in iron and myelination linked to distinct cognitive domains.REGISTRATIONClinicalTrials.gov NCT02990559FUNDINGThis work was funded by the NIH.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymopathy in humans. G6PD is an essential enzyme in the pentose phosphate pathway (PPP), generating NADPH needed for cellular biosynthesis and reactive oxygen species (ROS) homeostasis, the latter especially key in red blood cells (RBCs). Beyond the RBC, there is emerging evidence that G6PD exerts an immunologic role by virtue of its functions in leukocyte oxidative metabolism and anabolic synthesis necessary for immune effector function. We review these here, and consider the global immunometabolic role of G6PD activity and G6PD deficiency in modulating inflammation and immunopathology.

Reversible cerebral vasoconstriction syndrome (RCVS) is a rare and understudied transfusion reaction most commonly seen in adult females after correction of chronic, severe anemia. Transfusion-associated RCVS (TA-RCVS) typically presents with thunderclap headaches and one or more systemic (hypertension, nausea/vomiting) or neurologic (seizure, stroke, visual changes) symptoms within a week after red blood cell transfusion. Treatment of RCVS is based on blood pressure control; a recent study suggested that early use of nimodipine could shorten the disease course.

Immune checkpoint inhibitors (ICPi) have revolutionized cancer immunotherapy but also can induce autoimmune hemolytic anemia (AIHA), a severe disease with high mortality. However, the cellular and molecular mechanism(s) of ICPi-AIHA are unclear, other than being initiated through decreased checkpoint inhibition. Herein, we report ICPi-AIHA in a novel mouse model that shows similar characteristics of known human ICPi-AIHA (e.g., autoantibodies, hemolysis, increased mortality). During ICPi-AIHA, there is the simultaneous reduction of two regulatory T cell populations (FoxP3+ and Tr1 Tregs) and an increase in inflammatory TH17 T cells. Moreover, a novel CD39+CD73-FoxP3-CD25- CD4+ T cell subset (i.e., CD39 single positive [CD39SP]) emerges, and early increases in CD39SP predict AIHA development; CD39 is an ectonuclease that breaks down ATP. Additionally, we found that boosting ATPase activity by injecting recombinant apyrase mitigates AIHA development and significant CD39SP reductions, both suggesting a functional role for CD39 and demonstrating a novel therapeutic approach. Importantly, CD39SP are detectable in multiple mouse models developing AIHA and in patients with AIHA, demonstrating applicability to idiopathic and secondary AIHA. Highlighting broader autoimmunity relevance, ICPi-treated NZB mice experienced accelerated onset and severity of lupus, including AIHA. Moreover, ICPi treatment of healthy B6 animals led to detectable CD39SP and development of autoantibodies against multiple autoantigens including those on red blood cells and platelets. Together, our findings elucidate cellular and molecular mechanisms of ICPi-AIHA, leading to novel diagnostic and therapeutic approaches with translational potential for use in humans being treated with ICPi.

BACKGROUND:Platelet transfusions are increasing with advances in medical care. Based on FDA criteria, platelet units are assessed by in vitro measures; however, it is not known how platelet processing and storage duration affect function in vivo. To address this, we developed a novel platelet transfusion model that meets FDA criteria adapted to mice, and transfused fresh and stored platelets are detected in clots in vivo. STUDY DESIGN AND METHODS:Platelet units stored in mouse plasma were prepared using a modified platelet rich plasma collection protocol. Characteristics of fresh and stored units, including pH, cell count, in vitro measures of activity, including activation and aggregation, and post-transfusion recovery (PTR), were determined. Lastly, a tail transection assay was conducted using mice transfused with fresh or stored units, and transfused platelets were identified by confocal imaging. RESULTS:Platelet units had acceptable platelet and white cell counts and were negative for bacterial contamination. Fresh and 1-day stored units had acceptable pH; the platelets were activatable by thrombin and ADP, aggregable with thrombin, had acceptable PTR, and were present in vivo in clots of recipients after tail transection. In contrast, 2-day stored units had clinically unacceptable quality. DISCUSSION:We developed mouse platelets for transfusion analogous to human platelet units using a modified platelet rich plasma collection protocol with maximum storage of 1 day for an "old" unit. This provides a powerful tool to test how process modifications and storage conditions affect transfused platelet function in vivo.

Abstract Platelets play a crucial role in hemostasis. For cardiovascular and stroke prophylaxis, patients are commonly placed on either single or dual antiplatelet drugs, such as aspirin and/or clopidogrel. Here we outline a mouse model examining antiplatelet therapy and the resulting changes in platelet activation and aggregation. Using commercially available transgenic mice with platelets expressing green fluorescent protein (GFP) or red fluorescent protein (RFP), endogenous platelets were inhibited with a single, dual, or control antiplatelet treatment. We used 100µg aspirin/g mouse or 50µg clopidogrel/g mouse for a single dose; dual antiplatelet therapy was a combined dose of 100µg aspirin/g mouse and 50µg clopidogrel/g; control treatment was DMSO alone. One hour after treatment, whole blood (WB) was collected by aseptic cardiac puncture and mixed in the following groups: aspirin treated RFP and GFP WB, clopidogrel treated RFP and GFP WB, aspirin and clopidogrel treated RFP and GFP WB, control treated RFP and GFP WB. Each combined sample was then treated with a panel of agonists: no agonist, 0.5U/mL thrombin, 20µM ADP, and 500µg/mL arachidonic acid. Thrombin samples were activated for 2 minutes at room temperature while ADP and arachidonic acid samples were activated for 10 minutes at 37°C. Platelets were labeled with anti-CD41a to label all platelets and anti-CD62P to label activated platelets. Aggregation is measured as double-colored GFP and RFP platelet events. Compared to control mice, mice treated with antiplatelet agents demonstrated statistically significant decreases in activation following thrombin administration (ranging from 90% to 83% activated); there was no significant difference in platelet aggregation following thrombin among the samples from different antiplatelet therapies. Following ADP activation, clopidogrel treatment decreased platelet activation (1% activation) compared to control (3% activation) and aspirin-treated (5% activation) mice with no additional decrease in dual treatment (1% activation); unexpectedly, aspirin treatment alone or dual therapy decreased platelet aggregation with ADP (15% and 17% aggregated, respectively) compared to control and clopidogrel (23% and 27% aggregated, respectively). Finally, after arachidonic acid activation, aspirin treatment significantly decreased activation (7% activated) compared to control (20% activated), while clopidogrel decreased activation more than that of aspirin (3% activated), with no additional decrease from dual therapy (3% activated). Though not significant, aspirin treatment (1.4% aggregation) and dual therapy (1.2%) demonstrated a trend with decreased platelet aggregation following arachidonic acid activation compared to control (1.8% aggregation) and clopidogrel-treated platelets (3.2%). These data presented here show a novel application of platelet activation and aggregation of GFP and RFP platelet populations in a mouse model following aspirin and/or clopidogrel treatment. This model can be applied generally to other drugs and disease models for platelet dysfunction using additional markers for platelet activation. Additionally, these experiments can be used to further investigate the function of transfused murine platelets.

Long-chain polyunsaturated fatty acids (LC-PUFAs) are important modulators of red blood cell (RBC) rheology. Dietary LC-PUFAs are readily incorporated into the RBC membrane, improving RBC deformability, fluidity, and hydration. Female C57BL/6J mice consumed diets containing increasing amounts of fish oil (FO) ad libitum for 8 weeks. RBC deformability, filterability, and post-transfusion recovery (PTR) were evaluated before and after cold storage. Lipidomics and lipid peroxidation markers were evaluated in fresh and stored RBCs. High-dose dietary FO (50%, 100%) was associated with a reduction in RBC quality (i.e., in vivo lifespan, deformability, lipid peroxidation) along with a reduced 24 h PTR after cold storage. Low-dose dietary FO (6.25–12.5%) improved the filterability of fresh RBCs and reduced the lipid peroxidation of cold-stored RBCs. Although low doses of FO improved RBC deformability and reduced oxidative stress, no improvement was observed for the PTR of stored RBCs. The improvement in RBC deformability observed with low-dose FO supplementation could potentially benefit endurance athletes and patients with conditions resulting from reduced perfusion, such as peripheral vascular disease.

TransfusionVolume 63, Issue S5 p. 45A-45A SUPPLEMENT ARTICLE OA1-AM23-MN-19 | Acute Treadmill Training of FVB Mice Leads to Improved RBC Deformability and Decreased Lipid Peroxidation After Cold Storage V. Laurencin, V. Laurencin Columbia University Irving Medical CenterSearch for more papers by this authorD. Lamb, D. Lamb University of Maryland School of MedicineSearch for more papers by this authorD. Gordy, D. Gordy Columbia University Irving Medical CenterSearch for more papers by this authorE. Stone, E. Stone Columbia University Irving Medical CenterSearch for more papers by this authorK. Hudson, K. Hudson Columbia University Irving Medical CenterSearch for more papers by this authorS. Spitalnik, S. Spitalnik Columbia University Irving Medical CenterSearch for more papers by this authorE. Hod, E. Hod Columbia University Irving Medical CenterSearch for more papers by this authorP. Buehler, P. Buehler University of Maryland School of MedicineSearch for more papers by this authorJ. Kao, J. Kao University Maryland School of MedicineSearch for more papers by this authorT. Thomas, T. Thomas Columbia University Irving Medical CenerSearch for more papers by this author V. Laurencin, V. Laurencin Columbia University Irving Medical CenterSearch for more papers by this authorD. Lamb, D. Lamb University of Maryland School of MedicineSearch for more papers by this authorD. Gordy, D. Gordy Columbia University Irving Medical CenterSearch for more papers by this authorE. Stone, E. Stone Columbia University Irving Medical CenterSearch for more papers by this authorK. Hudson, K. Hudson Columbia University Irving Medical CenterSearch for more papers by this authorS. Spitalnik, S. Spitalnik Columbia University Irving Medical CenterSearch for more papers by this authorE. Hod, E. Hod Columbia University Irving Medical CenterSearch for more papers by this authorP. Buehler, P. Buehler University of Maryland School of MedicineSearch for more papers by this authorJ. Kao, J. Kao University Maryland School of MedicineSearch for more papers by this authorT. Thomas, T. Thomas Columbia University Irving Medical CenerSearch for more papers by this author First published: 12 October 2023 https://doi.org/10.1111/trf.44_17554Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume63, IssueS5October 2023Pages 45A-45A RelatedInformation

Abstract Malaria infection is a major cause of mortality worldwide. According to the 2022 World Health Organization Malaria Report, malaria caused approximately 247 million infections and 619,000 deaths in 2021, with more than 470,000 children dying of malaria. The gold-standard for measuring parasitemia is counting infected red blood cells (RBCs) by eye using Giemsa staining whole blood smears. This method is time consuming and is subject to error by both who is counting, the number of cells counted, and which frames are selected for counting. Automating the process of measuring malaria infection by flow cytometry decreases both the time required to obtain accurate parasitemia counts and the possible error on behalf of the researcher. Hundreds of thousands of cells can be counted by flow cytometry in a shorter period of time. Animal models of malaria infection are widespread and well-characterized. The rodent malaria strain P. berghei has shown preferential infection of reticulocytes over mature RBCs. Here we outline a method of measuring P. berghei blood stage infection in reticulocytes and mature RBCs and comparing the results to Giemsa stained whole blood smears. Using commercially available P. berghei ANKA expressing green-fluorescent protein (GFP), we infected wild type mice with 1x106 parasitized RBCs by intraperitoneal injection. Whole blood samples were collected daily starting day 3 post infection through day 7 by tail vein collection. Random and representative fields of Giemsa stained peripheral smears were selected to measure the percentage of parasitemia in mature RBCs and reticulocytes for a total cell count of approximately 1000. For flow cytometry, whole blood was incubated in 500uL of 1X SYBR Green I Nucleic Acid Gel Stain in PBS at 37°C for 20 minutes in the dark, washed with PBS, and stained with anti-CD71 to label reticulocytes. During the early stages of infection, the reticulocyte percentage of infected animals is not significant from uninfected animals, approximately 1.86%. As parasitemia increases over time, although the percentage of total reticulocytes decreases, the percentage of infected reticulocytes increases. On day 3 through 7 for one experimental replicate, day 3 demonstrated 1.86% total reticulocytes, and of these 2.56% reticulocytes were infected; day 4 had 0.66% total reticulocytes, and of these 32.92% were infected; day 5 showed 0.18% reticulocytes with 71.81% infected reticulocytes; on day 6 there were 0.04% reticulocytes with 75.44% infected reticulocytes; and day 7 had 0.01% reticulocytes with 69.56% infected reticulocytes. There was a strong correlation (R2 = 0.9147) when comparing flow cytometry to measure parasitemia with counting parasitemia by peripheral smear. This flow cytometry panel is an excellent tool to assess malarial infection of reticulocytes compared to mature RBCs and can be applied to other malarial species while decreasing bias, error and time needed to conduct the experiment.

TransfusionVolume 63, Issue S5 p. 291A-292A SUPPLEMENT ARTICLE P-TS-55 | Major ABO-Incompatible Platelet Transfusion is Not Associated with Higher Incidence of Hospital Complications in Patients with Intracerebral Hemorrhage F. Carvalho Poyraz, F. Carvalho Poyraz Columbia University Irving Medical CenterSearch for more papers by this authorJ. Magid-Bernstein, J. Magid-Bernstein Yale School of MedicineSearch for more papers by this authorE. Stone, E. Stone Columbia University Irving Medical CenterSearch for more papers by this authorS. Ghoshal, S. Ghoshal Columbia University Irving Medical CenterSearch for more papers by this authorS. Agarwal, S. Agarwal Columbia University Irving Medical CenterSearch for more papers by this authorS. Park, S. Park Columbia University Irving Medical CenterSearch for more papers by this authorJ. Claassen, J. Claassen Columbia University Irving Medical CenterSearch for more papers by this authorE. Hod, E. Hod Columbia University Irving Medical CenterSearch for more papers by this authorD. Roh, D. Roh Columbia University Irving Medical CenterSearch for more papers by this author F. Carvalho Poyraz, F. Carvalho Poyraz Columbia University Irving Medical CenterSearch for more papers by this authorJ. Magid-Bernstein, J. Magid-Bernstein Yale School of MedicineSearch for more papers by this authorE. Stone, E. Stone Columbia University Irving Medical CenterSearch for more papers by this authorS. Ghoshal, S. Ghoshal Columbia University Irving Medical CenterSearch for more papers by this authorS. Agarwal, S. Agarwal Columbia University Irving Medical CenterSearch for more papers by this authorS. Park, S. Park Columbia University Irving Medical CenterSearch for more papers by this authorJ. Claassen, J. Claassen Columbia University Irving Medical CenterSearch for more papers by this authorE. Hod, E. Hod Columbia University Irving Medical CenterSearch for more papers by this authorD. Roh, D. Roh Columbia University Irving Medical CenterSearch for more papers by this author First published: 12 October 2023 https://doi.org/10.1111/trf.392_17554Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume63, IssueS5October 2023Pages 291A-292A RelatedInformation

Introduction: Intracranial hemorrhage (ICH) patients require rapid treatment to reverse coagulopathy, which can help establish hemorrhage control and improve outcomes. While acute platelet transfusions are given in ICH to reverse platelet dysfunction, delays in administration of hemorrhage control therapies and platelet unit characteristics themselves may impact the efficacy and clinical outcomes in different patient populations. Thus, we sought to evaluate the relationship of platelet transfusion timing and platelet unit characteristics with ICH mortality. Methods: Available data for incident hospitalizations of adult ICH patients between 2019-2022 from 3 of the 5 participating sites within the multicenter REDS-IV-P network were assessed. ICH patients were included if they received ≥ 1 acute platelet transfusion within 48 hours of admission and presented with one of the following ICH etiologies: trauma (tICH), spontaneous intracerebral hemorrhage (sICH), and aneurysmal subarachnoid hemorrhage (aSAH). Patients with early withdrawal of care and death within the first 48 hours were excluded. Separate logistic regression models (each adjusting for age, sex, race/ethnicity, comorbidities, and number of platelet transfusions) assessed the relationship of 30 day ICH mortality outcome with the following: a) time to initial platelet transfusion in hour quartiles: <2.7 hours [reference] vs 2.7-5.6 hours vs 5.7-14.5 hours vs 14.6-48 hours, b) any major ABO incompatible platelet transfusion versus identical or minor mismatch, and c) any donor-recipient sex mismatched platelet transfusion. Separate subgroup analyses were performed by ICH etiologic subgroups. Results: Amongst 619 ICH patients receiving an acute platelet transfusion, 52% were from tICH, 36% from sICH, and 12% from aSAH. Mortality was seen in 17% of the overall cohort. Longer times to platelet transfusion (longest quartile: 14.6-48 hours) were associated with mortality in the overall ICH cohort (adjusted OR 2.12; 95%CI: 1.10-4.12). In sICH, effect size estimates were notably greater with the longest quartile time to platelet transfusion also being associated with mortality (adjusted OR 4.66; 95%CI: 1.58-14.8). Longer times to platelet transfusion were not associated with mortality in tICH (adjusted OR 1.19; 95%CI: 0.45-3.15). Amongst 543 ICH patients with available donor-recipient ABO data, 32% received a major ABO incompatible platelet transfusion. While there was not an association of major ABO incompatible platelet transfusion with mortality in the overall cohort (adjusted OR 1.41; 95%CI 0.82-2.40), there again was a significant association of this exposure with mortality in the sICH subgroup (adjusted OR 3.06; 95%CI: 1.22-7.90). No associations of major ABO incompatible platelet transfusions were identified in tICH subgroup (adjusted OR 1.02; 95%CI: 0.49-2.10). We did not identify a relationship of sex mismatched platelet units with mortality in the overall ICH cohort or in any ICH subgroups. Conclusions: In our analyses of data available from the REDS-IV-P network, we identified a suggestive relationship between longer times to platelet transfusion and mortality, but not of ABO mismatch in our overall ICH cohort. However, sICH may be a specific ICH subgroup more vulnerable to platelet transfusion characteristics and practices, particularly time to platelet transfusion and major ABO incompatible platelet unit exposures. Further work is necessary to assess the generalizability of our data and to clarify whether certain adult ICH patients require specially tailored platelet transfusion approaches.

Background/Case Studies: Manufacturers of Food and Drug Administration-approved chimeric antigen receptor T-cell (CAR-T) therapies specify apheresis collection parameters (ACP) for harvest of mononuclear cells (MNCs). With the growing number of products, the varying requirements for ACP are increasing apheresis unit operations complexity and decreasing efficiency. Given the lack of ACP standardization, we investigated the rationale for the ACPs requested by the manufacturers. We assessed if ACPs were based on the pivotal study protocols or publications and whether physician authors involved in the publications were transfusion medicine (TM) affiliated. Study Design/Methods: Pivotal study protocols and publications for the 6 approved CAR-T products were reviewed to search for ACP. The standard operating procedure (SOP) provided by each company was reviewed to obtain ACP. ACP were compared for alignment between the SOP and protocols or publications. Study author affiliations were identified through PubMed and verified on department websites or LinkedIn if available. Results/Findings: Study results are summarized in Table 1. All (100%) of the products request specific ACP in the collection SOPs. ACP were stated in study protocols for three of six products (50%). When stated in protocols, ACP matched those requested in collection SOPs. Only one of six (16.7%) products specified target ACP in the study publication and this product, which is the most recently approved, required only a target MNC number in the SOP. The minimum target MNC number requested in the SOPs varied from 1 10 to 5 10. Finally, only one of six (16.7%) study publications had a physician author who was clearly affiliated with a TM department or division, but none were found that were trained in TM. Conclusions: Only 50% of approved CAR-T products had specific ACP in their pivotal study protocols, and these parameters likely guided collection SOPs. Target MNC number may be the only required ACP for CAR-T products, providing an opportunity for standardization. The limited TM physician involvement in the protocols and publications may have contributed to the wide variation of ACPs and increased involvement may accelerate standardization.