Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
  • Users Online:463
  • Home
  • Print this page
  • Email this page


 
 Table of Contents  
REVIEW ARTICLE
Year : 2019  |  Volume : 4  |  Issue : 2  |  Page : 140-147

Platelet refractoriness


Department of Transfusion Medicine, Tata Memorial Hospital, HBNI, Mumbai, Maharashtra, India

Date of Submission02-Aug-2019
Date of Acceptance31-Aug-2019
Date of Web Publication17-Oct-2019

Correspondence Address:
Dr. B Sunil Rajadhyaksha
Department of Transfusion Medicine, Tata Memorial Hospital, HBNI, Mumbai, Maharashtra
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/GJTM.GJTM_45_19

Rights and Permissions
  Abstract 


Platelet transfusion support is extensively required for hemato-oncology patients who are multiply transfused. Platelet refractoriness can represent a significant clinical condition that complicates the platelet transfusion support in such patients. It remains a challenge associated with an increased bleeding risk, longer hospital stays, and increased morbidity and mortality. Causes for refractoriness are broadly divided into nonimmune and immune causes. Approximately two-thirds of refractory episodes are due to nonimmune factors while one-third are due to immune factors. Common formulae to assess platelet refractoriness include corrected count increment (CCI), posttransfusion platelet increment, and percentage platelet recovery. Measurement of CCI is one of the best parameters to differentiate between immune and nonimmune causes. In nonimmune factors which are associated with increased platelet consumption, treating the underlying cause and increasing the frequency of transfusion should be considered. However, in immune factors which are due to increased destruction of platelets owing to alloimmunization, other strategies such as ABO-identical/ABO-compatible fresh platelets, human leukocyte antigen-matched platelets, and crossmatched platelet transfusions should be considered. The newer approach includes epitope-matched platelet transfusion which is still in amateur stage. The strategies in the prevention of alloimmunization include leukoreduction of blood components, reducing donor exposure by providing single-donor platelets, and providing ABO-compatible platelets from the beginning of the treatment. This review will address the causes of platelet refractoriness and practical approach to the diagnosis, management, and its prevention.

Keywords: Alloimmunization, corrected count increment, platelet refractoriness, platelet transfusions


How to cite this article:
Rajadhyaksha B S, Desai D P, Navkudkar A A. Platelet refractoriness. Glob J Transfus Med 2019;4:140-7

How to cite this URL:
Rajadhyaksha B S, Desai D P, Navkudkar A A. Platelet refractoriness. Glob J Transfus Med [serial online] 2019 [cited 2019 Nov 12];4:140-7. Available from: http://www.gjtmonline.com/text.asp?2019/4/2/140/269391




  Introduction Top


Platelets are discoid-shaped cells, anucleate, 3–5 μ in diameter with a normal circulating count of 150–400 × 109 platelets/L. The hemostatic response of platelets at sites of vascular injury involves platelet shape change, adherence to the site, platelet plug formation, scaffolding, and cytokines secretion that are essential for repair.[1] Thus, platelets are a crucial component for maintaining vascular integrity. Thrombocytopenia (low circulating platelets) can lead to bleeding symptoms such as bruising, petechia, nose bleed, bleeding gums, intracranial hemorrhage, and death. The maximum platelet life span of 10.5 days and a fixed requirement for 7.1 platelets per microliter of blood per day or about 18% of the normal rate of platelet turnover is required to maintain vascular integrity.[2] Hence, larger proportion of the platelet pool is required to support vascular integrity for thrombocytopenic patients. Many patients have an adequate platelet count increment after platelet transfusions, but unsatisfactory posttransfusion platelet increment (PPI) can be observed in about 30% of patients.[3],[4],[5] Historically, it has been described in 20%–60% of patients who have received multiple platelet transfusions.[6] This inadequate response to platelet transfusion leads to an increased risk of morbidity and mortality, as well as increased hospital stays.

Data acquisition

Data for the study was obtained by extensively searching for the key words in google and Pubmed databases and the citations in relevant studies.


  Definition Top


Platelet refractoriness is simply defined as less than expected posttransfusion platelet count increment and is due to the shortened survival of the transfused platelets in the recipient's circulation. It is also defined as a lack of adequate response in PPIs after two or more consecutive platelet transfusions of an adequate dose of allogeneic platelets.[7]

[Table 1] mentions the different formulae used to assess platelet refractoriness; however, the 1-h corrected count increment (CCI) is predominantly used as the objective measure of whether a patient is refractory to platelet transfusion.[8]
Table 1: Formulae used in determination of platelet refractoriness

Click here to view


The pattern of response to PPI is shown in [Figure 1].[13]
Figure 1: Pattern of response to platelet increment posttransfusion[13]

Click here to view


Two patterns can be seen in refractory patients. A normal increment at 1 h following transfusion with return to the baseline count within 24 h is typical of the shortening of platelet survival seen with nonimmune causes. The second pattern consists of little or no increment in platelet count, even within 1 h of transfusion; this pattern is seen with immune cause of platelet refractoriness, i.e., alloimmunization.


  Etiology Top


The causes of platelet refractoriness are often multifactorial and can be grouped into nonimmune and immune causes[10],[12],[14] [Figure 2].
Figure 2: Causes of platelet refractoriness[7],[14]

Click here to view


Nonimmune causes

Approximately two-thirds of refractory episodes are due to nonimmune causes which include:

Clinical conditions

Sepsis

Association of sepsis with thrombocytopenia is well known.[15] Few of the following reasons are contributory to refractoriness in sepsis:

  1. Up to 30% of critically ill thrombocytopenic patients have nonspecific platelet-associated antibodies causing thrombocytopenia[16]
  2. Hemophagocytosis is common in bone marrow of septic patients which can cause thrombocytopenia[17]
  3. Platelets can be sequestered at the level of activated endothelium, playing an important role in response of a recipient to sepsis.[18],[19]


Fever

In hematological malignancy cases, the triad of fever, infections, and medications is the most common cause of refractoriness.[20]

Disseminated intravascular coagulation

It is characterized by consumptive coagulopathy leading to fibrin deposition in small vessels.[1] In patients with acute promyelocytic leukemia, due to chemotherapy-induced or spontaneous release of tissue factor from granules of leukemic cells, patients may present with disseminated intravascular coagulation.[21] Consumptive coagulopathy activates and immobilizes platelets leading to poor CCIs following platelet transfusion.[22]

Bleeding

Persistent external or internal bleeding after platelet transfusions can be considered as a potential indicator of platelet refractoriness.[23]

Splenomegaly

As spleen is the major site of platelet destruction, it is the major factor affecting platelet count increment.[5] Spleen sequesters a large proportion of platelet pool, and larger spleens are associated with more sequestration. Furthermore, hypersplenism is associated with reduced time interval until next transfusion.

Hematopoietic stem cell transplantation, graft-versus-host disease, and veno-occlusive disease

Patients undergoing hematopoietic stem cell transplantation (HSCT) receive multiple platelet transfusions, and hence, they are prone to alloimmunization. HSCT may or may not be an independent risk factor for the development of platelet refractoriness.[24] A study by Jones et al. found that patients undergoing HSCT found no difference in the incidence of refractoriness between patients with and without veno-occlusive disease (56% and 60%, respectively).[25] Graft-versus-host disease (GVHD) is a risk factor in HSCT patients, and there is an increased incidence of autoantibodies to platelets in patients with acute or chronic GVHD.[26],[27]

Drugs

Thrombocytopenia caused by drugs is relatively common, with many drugs implicated in this process [Table 2].[28],[29]
Table 2: Drugs causing thrombocytopenia

Click here to view


Platelet characteristics

Platelet dose/platelet quality

Some patients require proportionally more platelets to achieve adequate increments, and hence, it must be adjusted to the patient's blood volume. Other factors that may adversely affect the quality of the platelets during storage include incorrect storage temperature, improper mode of agitation, and pH (lower than 6.2).[7]

Platelet age

The possible advantage of fresher platelets (<48–72 h) in improving platelet transfusion response in patients with nonimmune refractoriness has been attributed to activation of platelets during storage.[30] An analysis observed in the TRAP study found that platelets stored ≤ 48 hours were associated with significantly higher increments and longer intervals between transfusions.[31]

Leukocyte reduction

The incidence of platelet refractoriness has been decreased with the use of leukocyte-reduced blood components. A significant decrease in the alloimmunization rate leukocyte-reduced platelets was transfused as compared to nonleukocyte-reduced platelet components, which was noted by TRAP study (7%–8% vs. 16%).[11] Leukoreduction does not appear to affect the rate of alloimmunization to platelet-specific antigens.

ABO compatibility

It is a common and acceptable practice to transfuse ABO-nonidentical platelets to patients, especially when ABO-identical platelets are not available. Platelet increments following transfusion of ABO-nonidentical platelets demonstrate a weak response compared with transfusion of ABO-identical platelets with decreased recovery but adequate survival.[32],[33],[34],[35],[36]

Leukocyte content of platelet unit and ABO blood group are platelet unit related factors. However, both these can affect platelet response through the immune mechanism and hence can also be considered an immune cause of platelet refractoriness.

Immune causes

Approximately one-third of refractory episodes are due to immune causes. Immune causes include human leukocyte antigen (HLA) alloimmunization and/or human platelet antigen (HPA) alloimmunization due to prior exposure from pregnancy, transfusion, or transplantation. Other causes include ABO incompatibility, platelet autoantibodies (e.g., autoantibody to platelet glycoprotein), and drug-related platelet antibodies.

Human leukocyte antigen alloimmunization

It is a major risk factor for refractoriness to platelet transfusions. HLA alloimmunization is more common than HPA antibodies and is believed to be the primary cause of immune refractoriness.[37],[38] Although platelets express only HLA Class I antigens, HLA Class II antigens present on leukocytes may be essential for the development of alloimmunization to HLA Class I antigens which may occur through prior transfusion or pregnancy. HLA-A and HLA-B antigens are the predominant HLA antigens expressed on platelets. The risk of HLA antibody formation may be increased in patients who are multiply transfused. Primary HLA alloimmunization occurs at a median of 3–4 weeks (2–56 weeks) after the first transfusion in a recipient of multiple transfusions.[39] Patients with previous HLA antigenic exposure are at high risk to develop alloimmunization and platelet refractoriness.[40] The frequency of HLA alloimmunization also varies with a patient's underlying diagnosis, previous history of pregnancy, and transfusion. The majority of clinically relevant HLA antibodies are directed against epitopes of Class I HLA and are shown to be immunoglobulin G (IgG).[41] The process of indirect allorecognition in the spleen involves host's ability to generate an IgG response to transfused platelets.[14] Thus, HLA antibodies account for the majority of cases of immune platelet refractoriness, with platelet-specific antibodies being much less common.

Human platelet antigen alloimmunization

While alloimmune platelet refractoriness almost always results from the production of antibodies to HLA Class I antigens on the platelet surface, antibodies to platelet-specific antigens (HPA) have also been discussed as a cause for refractoriness to platelet transfusion. In various studies of multitransfused hematology patients, specific HPA antibodies occur at a frequency of 8% to 25%.[11],[20] Usually, they are found in combination with HLA antibodies, but they may also occur in isolation.[14],[42]

ABO incompatibility

Platelets express ABH antigens but not Rhesus antigens on its surface. The ABH antigens expressed are a result of intrinsic molecules due to endogenous synthesis and extrinsic molecules, as a result of adsorption of soluble antigens found in plasma.[43] Earlier, it was common to transfuse ABO-mismatched platelets; however, it became obvious that ABO incompatibility in platelet transfusion affects the efficacy of transfusion.[44] Different studies mention that the patients receiving platelet transfusions with major ABO incompatibility require transfusions at smaller intervals compared to ABO-identical platelets.[45],[46],[47]

Other causes

Other immune causes include platelet autoantibodies (e.g., platelet refractoriness related to an autoantibody to platelet glycoprotein) and drug-related platelet antibodies.[42]


  Diagnostic Approach Top


  1. Measuring response to platelet transfusion with the help of formulae given in [Table 1]. One of the best parameters is a measurement of CCI, and platelet refractoriness due to immune cause is defined as a CCI <7500/μL for at least two sequential platelet transfusions[10]
  2. Determining the cause of refractoriness, i.e., immune or nonimmune cause of platelet refractoriness and treating the underlying condition accordingly
  3. Panel reactive antibody (PRA): It determines the percentage of recipient antibodies directed against the HLA antigens. PRA of >20%–30% suggests probable HLA alloimmunization[42],[48]
  4. Platelet antibody screening assay: Antibody screen to HLA Class I and platelet-specific antibodies can be detected by solid-phase red cell adherence assay (SPRCA) and enzyme-linked immunosorbent assay (ELISA), monoclonal antibody-specific immobilization of platelet antigen, platelet immunofluorescence test, flow cytometry, etc.
  5. Platelet crossmatch: Donor platelets with recipient serum/plasma can be tested by SPRCA, ELISA, and flow cytometry crossmatch. Incompatible crossmatch indicates the presence of antibodies and hence platelet refractoriness.



  Management of the Alloimmunized Patient Top


In cases of nonimmune platelet refractoriness, the underlying illness must be treated. In cases of immune-mediated refractoriness, there are several strategies to consider when selecting platelets for these patients: provision of HLA-matched platelets or HLA “compatible” (antigen-negative) platelets, platelets selected by crossmatch tests, and methods to reduce alloimmunization.

Furthermore, given the transient nature of antibody production, patients diagnosed with refractoriness need to be regularly reassessed (approximately monthly) for the presence/specificity of antibodies in order to assure the provision of compatible platelet units and avoid unnecessary use of more expensive and difficult to obtain compatible units.

Platelet selection

Once antibodies to HLA or HPA are identified, compatible platelet products need to be made available.

ABO-matched platelets

The initial approach of managing platelet refractory patients should be to select ABO-identical/ABO-compatible fresher platelet units.[49],[50]

Human leukocyte antigen-matched platelets

The traditional management of patients with HLA antibodies is to provide platelets from donors HLA matched for the HLA-A and HLA-B loci. HLA-matched donors can be found either among family members or via a registry of HLA-typed unrelated individuals if available.[51],[52],[53] The degree of match, based on the traditional classification system, can predict the success of posttransfusion platelet count increments. Grade A and BU (B1U or B2U) HLA-matched platelets are associated with the best increases in platelet count.[54]

Cross-reactive group-matched platelets

Selection of platelet donors with antigens in the same “cross-reactive groups” (CREGs) as the patient's antigens has been demonstrated to be nearly as successful in supporting alloimmune platelet refractoriness as HLA-matched transfusions. Expanding the available number of units with the use of CREGs can significantly increase the pool of potential “compatible” donors. HLA-matched donors are frequently unavailable for many patients, particularly those who are highly alloimmunized. Under these circumstances, transfusion of platelets from partially mismatched donors may provide adequate responses.[49],[55]

Crossmatch-compatible platelets

Another possible approach is to identify aphaeresis platelet units compatible by crossmatching with the patient's plasma. The SPRCA test is the most widely used method for platelet crossmatching.[50] Compared with HLA matching strategies, crossmatching can be both more convenient and economical. Crossmatching allows for a quick and effective selection of units from the available inventory and can be performed in a few hours as opposed to the days it may take to perform patient testing and to identify, recruit, collect, and test an appropriate HLA-matched donor. It is also of benefit to patients with uncommon HLA types where it would be very difficult to find an HLA-matched donor.[56] In addition, it avoids the exclusion of HLA mismatched but otherwise compatible donors, thereby increasing the number of potentially compatible units. This method is feasible in resource-limited nations.

Epitope-matched platelets

Alternative computerized matching techniques are now emerging; for example, the HLA matchmaker is a software algorithm that predicts HLA compatibility including acceptable mismatched options. Eplets are considered as essential components of HLA epitopes recognized by antibodies. Therefore, the eplet version of HLA matchmaker represents a more complete collection of HLA epitopes and provides an elaborate assessment of HLA compatibility. HLA epitope matching approach in immune refractory patients can have impressive 1-h CCI results.[57] This technique requires HLA-typed voluntary platelet donor registry to make the eplet-matched platelets available whenever required and hence not feasible in resource constraint countries.

[Table 3] mentions the advantages and disadvantages of different methods to support platelet transfusions in refractory patients. [Figure 3] mentions the algorithm for the diagnosis and management of platelet refractoriness.
Table 3: Advantages and disadvantages of different methods to support platelet transfusions in refractory patients

Click here to view
Figure 3: Algorithm for diagnosis and management of platelet refractoriness

Click here to view


Other treatment aspects in platelet refractoriness include immunosuppression, rituximab, intravenous immunoglobulin, plasma exchange, antifibrinolytic agents, and recombinant factor VIIa.


  Prevention of Platelet Refractoriness Top


Leukocyte depletion

Studies observed that leukocyte depletion below 5 × 106 per transfusion is effective in the prevention of primary HLA alloimmunization and results in <5% HLA antibody formation.[40],[58]

Reduction of donor exposure

Primary HLA alloimmunization occurs at a median of 3–4 weeks after the first transfusion in a recipient of multiple transfusions.[39] Reduction of donor exposure by the use of apheresis single-donor platelets showed that alloimmunization was postponed.[59]

Providing ABO-identical or ABO-compatible platelets

A reduction in posttransfusion platelet count increments has been demonstrated with transfusion of ABO-nonidentical platelets as compared to transfusion of ABO-identical platelets.[60] The transfusion of only ABO-identical platelets to patients requiring ongoing platelet support yields better increments, a reduction of overall platelet requirement, and a decrease in platelet refractoriness.[61],[62]


  Summary Top


Major advances have occurred in the management of patients with hemato-oncological disorders. Platelet transfusion support plays a vital role in its management as these patients are multiply transfused. Moreover, platelet refractoriness once developed poses a challenge to cater to the platelet transfusion needs of such patients. Hence, understanding the etiology, treating the underlying conditions and prevention of development of refractoriness forms the pillars of its management.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Hoffman R. Hematology: Basic Principles and Practice. Philadelphia, PA: Churchill Livingstone/Elsevier; 2005.  Back to cited text no. 1
    
2.
Hanson SR, Slichter SJ. Platelet kinetics in patients with bone marrow hypoplasia: Evidence for a fixed platelet requirement. Blood 1985;66:1105-9.  Back to cited text no. 2
    
3.
Legler TJ, Fischer I, Dittmann J, Simson G, Lynen R, Humpe A, et al. Frequency and causes of refractoriness in multiply transfused patients. Ann Hematol 1997;74:185-9.  Back to cited text no. 3
    
4.
Novotny VM. Prevention and management of platelet transfusion refractoriness. Vox Sang 1999;76:1-3.  Back to cited text no. 4
    
5.
Slichter SJ, Davis K, Enright H, Braine H, Gernsheimer T, Kao KJ, et al. Factors affecting posttransfusion platelet increments, platelet refractoriness, and platelet transfusion intervals in thrombocytopenic patients. Blood 2005;105:4106-14.  Back to cited text no. 5
    
6.
Slichter SJ. Mechanisms and management of platelet refractoriness. In: Nance SJ, editor. Transfusion Medicine in the 1990's. Arlington, VA: American Association of Blood Banks; 1990. p. 95-179.  Back to cited text no. 6
    
7.
Delaflor-Weiss E, Mintz PD. The evaluation and management of platelet refractoriness and alloimmunization. Transfus Med Rev 2000;14:180-96.  Back to cited text no. 7
    
8.
Rebulla P. Formulae for the definition of refractoriness to platelet transfusion. Transfus Med 1993;3:91-3.  Back to cited text no. 8
    
9.
Hod E, Schwartz J. Platelet transfusion refractoriness. Br J Haematol 2008;142:348-60.  Back to cited text no. 9
    
10.
Fung MK, Grossman BJ, Hillyer CD, Westhoff CM. Technical Manual. 18th ed. Bethesda MD: AABB Press; 2014.  Back to cited text no. 10
    
11.
Slichter SJ. Leukocyte reduction and ultraviolet B irradiation of platelets to prevent alloimmunization and refractoriness to platelet transfusions. The Trial to Reduce Alloimmunization to Platelets Study Group. N Engl J Med 1997;337:1861-9.  Back to cited text no. 11
    
12.
Simon TL, Snyder EL, Solheim BG, Stowell CP, Strauss RG, Petrides M. Rossi's Principles of Transfusion Medicine. 5th ed. UK: Blackwell Publishing Limited; 2016. p. 206-64.  Back to cited text no. 12
    
13.
Miller D. Platelet Refractoriness in HemOnc Patients – A Retrospective Analysis. Thrombolux Quality Reassurance; May, 2018. Available from: https://thrombolux.com/platelet-refractoriness-in-hemonc-patients. [Last accessed on 19 July 20].  Back to cited text no. 13
    
14.
Pavenski K, Freedman J, Semple JW. HLA alloimmunization against platelet transfusions: Pathophysiology, significance, prevention and management. Tissue Antigens 2012;79:237-45.  Back to cited text no. 14
    
15.
Davis RB, Meeker WR, Mcquarrie DG. Immediate effects of intravenous endotoxin on serotonin concentrations and blood platelets. Circ Res 1960;8:234-9.  Back to cited text no. 15
    
16.
Stéphan F, Cheffi MA, Kaplan C, Maillet J, Novara A, Fagon J. Autoantibodies against platelet glycoproteins in critically ill patients with thrombocytopenia. Am J Med 2000;108:554-60.  Back to cited text no. 16
    
17.
François B, Trimoreau F, Vignon P, Fixe P, Praloran V, Gastinne H. Thrombocytopenia in the sepsis syndrome: Role of hemophagocytosis and macrophage colony-stimulating factor. Am J Med 1997;103:114-20.  Back to cited text no. 17
    
18.
Warkentin TE, Aird WC, Rand JH. Platelet-endothelial interactions: Sepsis, HIT, and antiphospholipid syndrome. Hematology Am Soc Hematol Educ Program 2003;1:497-519.  Back to cited text no. 18
    
19.
Heffner JE. Platelet-neutrophil interactions in sepsis – Platelet guilt by association? Intensive Care Med 1997;23:366-8.  Back to cited text no. 19
    
20.
Doughty HA, Murphy MF, Metcalfe P, Rohatiner AZ, Lister TA, Waters AH. Relative importance of immune and non-immune causes of platelet refractoriness. Vox Sang 1994;66:200-5.  Back to cited text no. 20
    
21.
Bayer WL, Bodensteiner DC, Tilzer LL, Adams ME. Use of platelets and other transfusion products in patients with malignancy. Semin Thromb Hemost 1992;18:380-91.  Back to cited text no. 21
    
22.
Bishop JF, McGrath K, Wolf MM, Matthews JP, De Luise T, Holdsworth R, et al. Clinical factors influencing the efficacy of pooled platelet transfusions. Blood 1988;71:383-7.  Back to cited text no. 22
    
23.
Chitlur M, Rajpurkar M, Recht M, Tarantino MD, Yee DL, Cooper DL, et al. Recognition and management of platelet-refractory bleeding in patients with Glanzmann's thrombasthenia and other severe platelet function disorders. Int J Gen Med 2017;10:95-9.  Back to cited text no. 23
    
24.
Friedberg RC, Donnelly SF, Boyd JC, Gray LS, Mintz PD. Clinical and blood bank factors in the management of platelet refractoriness and alloimmunization. Blood 1993;81:3428-34.  Back to cited text no. 24
    
25.
Jones RJ, Lee KS, Beschorner WE, Vogel VG, Grochow LB, Braine HG, et al. Venoocclusive disease of the liver following bone marrow transplantation. Transplantation 1987;44:778-83.  Back to cited text no. 25
    
26.
Ishida A, Handa M, Wakui M, Okamoto S, Kamakura M, Ikeda Y. Clinical factors influencing posttransfusion platelet increment in patients undergoing hematopoietic progenitor cell transplantation – A prospective analysis. Transfusion 1998;38:839-47.  Back to cited text no. 26
    
27.
Anasetti C, Doney KC, Storb R, Meyers JD, Farewell VT, Buckner CD, et al. Marrow transplantation for severe aplastic anemia. Long-term outcome in fifty “untransfused” patients. Ann Intern Med 1986;104:461-6.  Back to cited text no. 27
    
28.
Ferreira AA, Zulli R, Soares S, Castro VD, Moraes-Souza H. Identification of platelet refractoriness in oncohematologic patients. Clinics (Sao Paulo) 2011;66:35-40.  Back to cited text no. 28
    
29.
Aster RH, Bougie DW. Drug-induced immune thrombocytopenia. N Engl J Med 2007;357:580-7.  Back to cited text no. 29
    
30.
Fijnheer R, Modderman PW, Veldman H, Ouwehand WH, Nieuwenhuis HK, Roos D, et al. Detection of platelet activation with monoclonal antibodies and flow cytometry. Changes during platelet storage. Transfusion 1990;30:20-5.  Back to cited text no. 30
    
31.
Slichter SJ, Davis K, Enright H, Braine H, Gernsheimer T, Kao KJ, et al. Factors affecting post-transfusion platelet increments, platelet refractoriness, and platelet transfusion intervals in thrombocytopenic patients. Blood 2005;105:4106-14.  Back to cited text no. 31
    
32.
Lozano M, Cid J. The clinical implications of platelet transfusions associated with ABO or Rh(D) incompatibility. Transfus Med Rev 2003;17:57-68.  Back to cited text no. 32
    
33.
Josephson CD, Mullis NC, Van Demark C, Hillyer CD. Significant numbers of apheresis-derived group O platelet units have “high-titer” anti-A/A, B: Implications for transfusion policy. Transfusion 2004;44:805-8.  Back to cited text no. 33
    
34.
Julmy F, Ammann RA, Taleghani BM, Fontana S, Hirt A, Leibundgut K, et al. Transfusion efficacy of ABO major-mismatched platelets (PLTs) in children is inferior to that of ABO-identical PLTs. Transfusion 2009;49:21-33.  Back to cited text no. 34
    
35.
Kaufman RM. Platelet ABO matters. Transfusion 2009;49:5-7.  Back to cited text no. 35
    
36.
Triulzi DJ, Assmann SF, Strauss RG, Ness PM, Hess JR, Kaufman RM, et al. The impact of platelet transfusion characteristics on posttransfusion platelet increments and clinical bleeding in patients with hypoproliferative thrombocytopenia. Blood 2012;119:5553-62.  Back to cited text no. 36
    
37.
Kickler T, Kennedy SD, Braine HG. Alloimmunization to platelet-specific antigens on glycoproteins IIb-IIIa and Ib/IX in multiply transfused thrombocytopenic patients. Transfusion 1990;30:622-5.  Back to cited text no. 37
    
38.
Laundy GJ, Bradley BA, Rees BM, Younie M, Hows JM. Incidence and specificity of HLA antibodies in multitransfused patients with acquired aplastic anemia. Transfusion 2004;44:814-25.  Back to cited text no. 38
    
39.
Kripke ML. Immunological unresponsiveness induced by ultraviolet radiation. Immunol Rev 1984;80:87-102.  Back to cited text no. 39
    
40.
Novotny VM, van Doorn R, Witvliet MD, Claas FH, Brand A. Occurrence of allogeneic HLA and non-HLA antibodies after transfusion of prestorage filtered platelets and red blood cells: A prospective study. Blood 1995;85:1736-41.  Back to cited text no. 40
    
41.
Yankee RA, Grumet FC, Rogentine GN. Platelet transfusion therapy; the selection of compatible platelet donors for refractory patients by lymphocyte HL-A typing. N Engl J Med 1969;281:1208-12.  Back to cited text no. 41
    
42.
Stanworth SJ, Navarrete C, Estcourt L, Marsh J. Platelet refractoriness – Practical approaches and ongoing dilemmas in patient management. Br J Haematol 2015;171:297-305.  Back to cited text no. 42
    
43.
Dunstan RA, Simpson MB, Knowles RW, Rosse WF. The origin of ABH antigens on human platelets. Blood 1985;65:615-9.  Back to cited text no. 43
    
44.
Djerassi I, Farber S, Evans AE. Transfusions of fresh platelet concentrates to patients with secondary thrombocytopenia. N Engl J Med 1963;268:221-6.  Back to cited text no. 44
    
45.
Lozano M, Heddle N, Williamson LM, Wang G, AuBuchon JP, Dumont LJ, et al. Practices associated with ABO-incompatible platelet transfusions: A BEST collaborative international survey. Transfusion 2010;50:1743-8.  Back to cited text no. 45
    
46.
Shehata N, Tinmouth A, Naglie G, Freedman J, Wilson K. ABO-identical versus nonidentical platelet transfusion: A systematic review. Transfusion 2009;49:2442-53.  Back to cited text no. 46
    
47.
Pavenski K, Warkentin TE, Shen H, Liu Y, Heddle NM. Posttransfusion platelet count increments after ABO-compatible versus ABO-incompatible platelet transfusions in noncancer patients: An observational study. Transfusion 2010;50:1552-60.  Back to cited text no. 47
    
48.
Kiefel V, König C, Kroll H, Santoso S. Platelet alloantibodies in transfused patients. Transfusion 2001;41:766-70.  Back to cited text no. 48
    
49.
Schiffer CA, Anderson KC, Bennett CL, Bernstein S, Elting LS, Goldsmith M, et al. Platelet transfusion for patients with cancer: Clinical practice guidelines of the American society of clinical oncology. J Clin Oncol 2001;19:1519-38.  Back to cited text no. 49
    
50.
Kopko PM, Warner P, Kresie L, Pancoska C. Methods for the selection of platelet products for alloimmune-refractory patients. Transfusion 2015;55:235-44.  Back to cited text no. 50
    
51.
McFarland JG, Anderson AJ, Slichter SJ. Factors influencing the transfusion response to HLA-selected apheresis donor platelets in patients refractory to random platelet concentrates. Br J Haematol 1989;73:380-6.  Back to cited text no. 51
    
52.
Heal JM, Blumberg N, Masel D. An evaluation of crossmatching, HLA, and ABO matching for platelet transfusions to refractory patients. Blood 1987;70:23-30.  Back to cited text no. 52
    
53.
Yankee RA, Graff KS, Dowling R, Henderson ES. Selection of unrelated compatible platelet donors by lymphocyte HL-A matching. N Engl J Med 1973;288:760-4.  Back to cited text no. 53
    
54.
Duquesnoy RJ, Filip DJ, Rodey GE, Rimm AA, Aster RH. Successful transfusion of platelets “mismatched” for HLA antigens to alloimmunized thrombocytopenic patients. Am J Hematol 1977;2:219-26.  Back to cited text no. 54
    
55.
Hussein MA, Lee EJ, Fletcher R, Schiffer CA. The effect of lymphocytotoxic antibody reactivity on the results of single antigen mismatched platelet transfusions to alloimmunized patients. Blood 1996;87:3959-62.  Back to cited text no. 55
    
56.
Sacher RA, Kickler TS, Schiffer CA, Sherman LA, Bracey AW, Shulman IA, et al. Management of patients refractory to platelet transfusion. Arch Pathol Lab Med 2003;127:409-14.  Back to cited text no. 56
    
57.
Navkudkar A, Rajak J, Tambe M, Rajadhyaksha S, Singh M. Epitope matched platelets: An effective way to provide platelet transfusion support in platelet refractory patients in a tertiary care oncology centre. J Blood Lymph 2018;8:217.  Back to cited text no. 57
    
58.
van Marwijk Kooy M, van Prooijen HC, Moes M, Bosma-Stants I, Akkerman JW. Use of leukocyte-depleted platelet concentrates for the prevention of refractoriness and primary HLA alloimmunization: A prospective, randomized trial. Blood 1991;77:201-5.  Back to cited text no. 58
    
59.
Gmür J, von Felten A, Osterwalder B, Honegger H, Hörmann A, Sauter C, et al. Delayed alloimmunization using random single donor platelet transfusions: A prospective study in thrombocytopenic patients with acute leukemia. Blood 1983;62:473-9.  Back to cited text no. 59
    
60.
Jiménez TM, Patel SB, Pineda AA, Tefferi A, Owen WG. Factors that influence platelet recovery after transfusion: Resolving donor quality from ABO compatibility. Transfusion 2003;43:328-34.  Back to cited text no. 60
    
61.
Heal JM, Rowe JM, McMican A, Masel D, Finke C, Blumberg N. The role of ABO matching in platelet transfusion. Eur J Haematol 1993;50:110-7.  Back to cited text no. 61
    
62.
Carr R, Hutton JL, Jenkins JA, Lucas GF, Amphlett NW. Transfusion of ABO-mismatched platelets leads to early platelet refractoriness. Br J Haematol 1990;75:408-13.  Back to cited text no. 62
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Definition
Etiology
Diagnostic Approach
Management of th...
Prevention of Pl...
Summary
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed112    
    Printed7    
    Emailed0    
    PDF Downloaded28    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]