Etiology of platelet transfusion refractoriness.
| Immune factors (<20%) | Non-immune factors (>80%) |
|---|---|
| Antibodies to HLA class I (80–90%) | Accerlerated platelet consumption (MAHA, DIC) |
| Antibodies to HPA (10–20%) | Active bleeding |
| ABO-mismatched platelets | Medications (Infectious disease agents; ampicillin, amoxicillin, cephalosporins, penicillin, piperacillin/tazobactam, rifampin, sulfonamides and vancomycinHistamin-receptor antagonists: cimetidine, famotidine etc., Analgesic; acetaminophen, fentanyl, ibuprofen, and naproxen chemotherpeutics and immunosuppressants: rituximab, and cyclosporin antithrombotics; heparin and GPIIb/IIIa antagonists) |
| Antibodies to drug-platelet glycoprotein complex | Graft-versus-host disease |
| Autoimmune (unknown) | Splenic sequestration |
| Poor platelet quality |
Abbreviations: DIC, diffuse intravascular coagulation; GPIIb/IIIa, glycoproteinIIb/IIIa; HLA, human leukocyte antigen; HPA, human platelet antigen; MAHA, microangiopathic hemolytic anemia.
Blood Res 2022;57:S6~S10 https://doi.org/10.5045/br.2022.2021229
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