Prevention and Management of Platelet Transfusion Refractoriness

Abstract

Platelet transfusion refractoriness is a major complication of long–term platelet supportive care. Refractoriness may lead to fatal bleeding complications in thrombocytopenic patients. Major factors involved are factors related to the clinical condition of the patient as well as HLA alloimmunisation. Non–alloimmune factors may occur in up to 80% of the patients. However, platelet transfusion outcome is impaired in only 50% of the patients having these conditions. HLA alloimmunisation has been convincingly reduced by the use of leucocyte–depleted transfusions. UV–B irradiation of platelet transfusions may be alternatively used to reduce HLA alloimmunisation. Despite these measures, patients with a history of pregnancy or non–leucocyte–depleted transfusions form HLA antibodies in a high proportion (up to 50%). HPA antibodies play a minor but relatively important role in patients with HLA antibodies. ABO antibodies may play a role in refractoriness, which can be abolished by transfusion of ABO–identical platelets. Screening for the presence of HLA and/or HPA antibodies is indicated in case of transfusion failure after ABO–identical or HLA–matched platelets. If no alloantibodies are detected, further analysis to define a role of drug– related or autoantibodies is required. In case of HLA and/or HPA alloimmunisation associated with refractoriness, matched platelet transfusions are indicated. In case of non–alloimmune factors associated with increased platelet consumption, increasing the transfusion frequency can be considered. Additional investigations are still necessary to define risk factors for secondary HLA alloimmunisation and refractoriness due to non–immune factors to further decrease the incidence of refractoriness.

Platelet activation during plasma‐reduced multicomponent PLT collection: a comparison between COBE Trima and Spectra LRS turbo cell separators

“…All plateletpheresis (20 from Group A and 21 from Group B) were infused within 36 hours from collection as a prophylactic treatment in hematologic patients with a pretransfusion PLT count below 10 ¥ 10 3 per m L, according to the patient's weight. CCI at 1 hour was 13 (5-22) and 19 (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22) for patients receiving plateletpheresis from Group A and B, respectively (p = 0.25). Platelet increment at 24 hours was 14 (3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) in patients who received plateletpheresis units from Group A donors and 18 in those who received plateletpheresis units from Group B donors (p = 0.22).…”

Selecting donors of platelets for refractory patientson the basis of HLA antibody specificity

“…Our study did not determine the incidence or specificity of antibodies to human platelet antigens (HPAs), and their relevance to platelet transfusion practice is not well defined. 15,17,[65][66][67][68] Although there are a few well-documented cases of transfusion failures due to the presence of platelet-specific antibodies, most examples of platelet-specific reactivity detected in tests in vitro do not appear to affect transfusion responses. 15 Antibodies to HPAs are generally found in patients who are highly immunized to HLA, as indicated by a high PRA level, 66,67 which makes their significance difficult to assess.…”

Differential Immunogenicity of HLA Class I Alloantigens for the Humoral versus the Cellular Immune Response: “Towards Tailor-Made HLA Mismatching”

“…Both in transplantation [7,8] and in platelet transfusion [9], the use of HLA-matched donors leads to the best clinical results, although HLA matching does not preclude the induction of alloimmune responses directed against minor transplantation antigens [10] or platelet-specific alloantigens [11].…”