Clinical application of a modified platelet desialylation test for mechanistic characterization of platelet transfusion refractoriness.

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.