Evaluation and management of platelet transfusion refractoriness

Hee-Jeong Youk; Sang-Hyun Hwang; Heung-Bum Oh; Dae-Hyun Ko

doi:10.5045/br.2022.2021229

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Blood Res 2022; 57(S1):

Published online April 30, 2022

https://doi.org/10.5045/br.2022.2021229

Evaluation and management of platelet transfusion refractoriness

Hee-Jeong Youk, Sang-Hyun Hwang, Heung-Bum Oh, Dae-Hyun Ko

Author Info. +

Department of Laboratory Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea

Correspondence to : Dae-Hyun Ko, M.D., Ph.D.
Department of Laboratory Medicine, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-Ro 43-Gil, Songpa-gu, Seoul 05505, Korea
E-mail: daehyuni1118@amc.seoul.kr

Received: December 29, 2021; Accepted: January 13, 2022

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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Abstract

Platelet transfusion refractoriness (PTR), in which platelet counts do not increase after transfusion, occurs in many patients receiving platelet transfusions. PTR is a clinical condition that can harm patients. The causes of PTR can be divided into two types: immune and non-immune. Most cases of PTR are non-immune. Among immune causes, the most common is human leukocyte antigen (HLA) class I molecules. PTR caused by anti-HLA antibodies is usually managed by transfusing HLA-matched platelets. Therefore, it is important, especially for hemato-oncologists who frequently perform transfusion, to accurately diagnose whether the cause of platelet transfusion failure is alloimmune or non-immunological when determining the treatment direction for the patient. In this review, we discuss the definitions, causes, countermeasures, and prevention methods of PTR.

Keywords Platelet transfusion refractoriness, Platelet transfusion, Human leukocyte antigen, HLA-matched, Platelet count

Article

Review Article

Blood Res 2022; 57(S1): S6-S10

Published online April 30, 2022 https://doi.org/10.5045/br.2022.2021229

Evaluation and management of platelet transfusion refractoriness

Hee-Jeong Youk, Sang-Hyun Hwang, Heung-Bum Oh, Dae-Hyun Ko

Department of Laboratory Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea

Correspondence to:Dae-Hyun Ko, M.D., Ph.D.
Department of Laboratory Medicine, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-Ro 43-Gil, Songpa-gu, Seoul 05505, Korea
E-mail: daehyuni1118@amc.seoul.kr

Received: December 29, 2021; Accepted: January 13, 2022

Abstract

Keywords: Platelet transfusion refractoriness, Platelet transfusion, Human leukocyte antigen, HLA-matched, Platelet count

Abstract

Table 1 . Various formula to assess platelet transfusion refractoriness (modified from Rebulla,1993)..

Post-transfusion platelet increment (PPI)=(post-transfusion platelet count)-(pre-transfusion platelet count)

Corrected count increment (CCI)=PPL(/μL)×BSA(m2)Number of Platelets transfused(1011)

Percentage platelet recovery (PPR)=PPL(/μL)×TBV×100%Number of Platelets transfused(1011)

Percentage platelet increment (PPI)=PPR/0.67 (0.67 accounts for splenic pooling)

Abbreviations: BSA, body surface area; TBV, total blood volume..

Table 2 . 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..