Transfusion · 2026
Clinical application of a modified platelet desialylation test for mechanistic characterization of platelet transfusion refractoriness.
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Ziza Karen, Silva Thamy, Domentino Mateus, Conrado Marina, Oliveira João, Moritz Elyse, Chiba Akemi, Rocha Vanderson, Mendrone-Junior Alfredo, Bordin José, Dante Langhi, Dinardo Carla
Аннотация
BACKGROUND: Platelet transfusion refractoriness (PTR) is a major challenge in transfusion medicine and may result from both immune and non-immune mechanisms. Although alloantibodies are well-established contributors, Fc-independent pathways such as platelet desialylation have emerged as alternative mechanisms of clearance.
STUDY DESIGN AND METHODS: In this prospective diagnostic study, 81 patients with suspected PTR were evaluated using an integrated approach combining the platelet immunofluorescence test (PIFT) to detect antibody-mediated refractoriness and a modified platelet desialylation test (PDT) to assess Fc-independent clearance. Demographic, clinical, and laboratory variables were analyzed using non-parametric tests, including Mann-Whitney U, Kruskal-Wallis, and binomial tests.
RESULTS: The cohort exhibited severe thrombocytopenia and diverse clinical profiles. PIFT detected platelet-bound antibodies in 63/81 cases (78%), while PDT identified desialylation in 41/81 patients (50%). PIFT positivity was similar between PDT-positive (80.5%) and PDT-negative (76.9%) groups, with no significant association (χ2 = 0.15, p = .69). Although mean fluorescence intensity (MFI) varied across diagnostic categories, no significant differences were observed (p = .3095). Fever was the only clinical variable significantly associated with reduced desialylation (median MFI 401 vs. 1328.3; p = .0109), while splenomegaly, infection, antifungal use, and bleeding had no significant effects. PDT status was not significantly associated with the number of pooled platelet transfusions (p = .391) or apheresis procedures (p = .515), indicating that desialylation alone does not predict transfusion demand.
DISCUSSION: PTR occurs both independently and in parallel with antibody-mediated pathways. The combined PIFT-modified PDT approach improves mechanistic characterization and enhances diagnostic accuracy, in cases of platelet refractoriness of immune and non-immune etiology.
STUDY DESIGN AND METHODS: In this prospective diagnostic study, 81 patients with suspected PTR were evaluated using an integrated approach combining the platelet immunofluorescence test (PIFT) to detect antibody-mediated refractoriness and a modified platelet desialylation test (PDT) to assess Fc-independent clearance. Demographic, clinical, and laboratory variables were analyzed using non-parametric tests, including Mann-Whitney U, Kruskal-Wallis, and binomial tests.
RESULTS: The cohort exhibited severe thrombocytopenia and diverse clinical profiles. PIFT detected platelet-bound antibodies in 63/81 cases (78%), while PDT identified desialylation in 41/81 patients (50%). PIFT positivity was similar between PDT-positive (80.5%) and PDT-negative (76.9%) groups, with no significant association (χ2 = 0.15, p = .69). Although mean fluorescence intensity (MFI) varied across diagnostic categories, no significant differences were observed (p = .3095). Fever was the only clinical variable significantly associated with reduced desialylation (median MFI 401 vs. 1328.3; p = .0109), while splenomegaly, infection, antifungal use, and bleeding had no significant effects. PDT status was not significantly associated with the number of pooled platelet transfusions (p = .391) or apheresis procedures (p = .515), indicating that desialylation alone does not predict transfusion demand.
DISCUSSION: PTR occurs both independently and in parallel with antibody-mediated pathways. The combined PIFT-modified PDT approach improves mechanistic characterization and enhances diagnostic accuracy, in cases of platelet refractoriness of immune and non-immune etiology.