Algorithm for managing the platelet refractory patient

Slichter, Sherrill J.

doi:10.1002/(sici)1098-1101(1997)12:1<4::aid-jca2>3.0.co;2-e

Cited by 15 publications

(9 citation statements)

References 37 publications

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“…This would result in a posttransfusion increment of 30,000 to 40,000 platelets/mL 1 hour after platelet transfusion. 49 Platelet refractoriness describes a clinical condition in which patients do not achieve the anticipated platelet count increment from repeated platelet transfusions. It is possible to be alloimmunized to platelet antigens without being refractory to platelet transfusions and also to be refractory to platelet transfusions without being alloimmunized.…”

Section: Multiplatelet Transfusion Refractorinessmentioning

confidence: 99%

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Genotyping for Human Platelet Alloantigen Polymorphisms: Applications in the Diagnosis of Alloimmune Platelet Disorders

Curtis

2008

Semin Thromb Hemost

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Molecular typing for platelet allelic polymorphisms was first made possible by discovery of the HPA-1a/1b single nucleotide polymorphism in 1989. Since then, six other biallelic human platelet antigen (HPA) systems have been determined and can be typed using genomic DNA. The introduction of polymerase chain reaction enabled development of several different assays including polymerase chain reaction-sequence-specific primer, melting curve analysis by LightCycler, and 5'-nuclease assays. More recently, multiplex polymerase chain reaction has allowed for the development of high-throughput assays for genotyping large numbers of patients and blood donors for not only platelet gene polymorphisms but also for those of other blood cell genes. Platelet genotyping is a valuable tool in confirming platelet antigen specificities of alloantibodies detected in patient sera to complement the clinical history in the diagnosis of alloimmune platelet disorders such as fetal and neonatal alloimmune thrombocytopenia (FNAIT), posttransfusion purpura, and multiplatelet transfusion refractoriness. In addition, it has made possible prenatal platelet typing of the fetus in suspected cases of FNAIT and large-scale blood donor typing for provision of antigen-negative platelets to transfuse highly alloimmunized patients. Platelet genotyping may also someday prove important as an aid in determining the relative risk of patients for various thrombotic disorders.

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Section: Multiplatelet Transfusion Refractorinessmentioning

confidence: 99%

“…MPTR occurs when the level of alloimmunization as measured by the breadth of antibody response to platelet antigens is sufficient to impact the majority of randomly selected platelet products. 49,50 MPTR is most often seen in oncology patients after receiving a bone marrow transplant or high-dose chemotherapy.…”

Section: Multiplatelet Transfusion Refractorinessmentioning

confidence: 99%

Genotyping for Human Platelet Alloantigen Polymorphisms: Applications in the Diagnosis of Alloimmune Platelet Disorders

Curtis

2008

Semin Thromb Hemost

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“…18 If no incremental response to platelet therapy occurs, nonstored ABO-identical platelets should be transfused to exclude a role of ABO antibodies or impaired quality of the platelets transfused. 21 In the presence of factors associated with increased platelet consumption, such as fever, sepsis, or DIC, frequent transfusion of platelets rather than increased dosages per transfusion is recommended because of the impaired platelet survival. In case of splenomegaly, when recovery of transfused platelets is very low but platelet survival is normal, one can consider increasing the platelet transfusion dose to increase post-transfusion platelet counts.…”

Section: • Platelet Refractorinessmentioning

confidence: 99%

Management of Patients Refractory to Platelet Transfusion

Chockalingam

Sacher

2007

Journal of Infusion Nursing

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Refractoriness to infused platelets becomes a major clinical problem for many patients with acute myeloid leukemia (AML). Inadequate post-transfusion platelet count increments can be due to a number of host-related factors such as: spleno-megaly, severe infection with high fever, disseminated intrava-scular coagulation, drug-mediated antibodies and/or alloim-munization, and occasionally by administration of platelets damaged or activated during collection or storage. Lymphocy-totoxic antibody directed against HLA-A orB antigens is an excellent serologic marker for alloimmunization. In one large study, the presence of anti-HLA antibodies was correlated with a poor post-transfusion platelet increase in over 90% of such patients, whereas patients lacking antibodies had satisfactory increments after transfusion 85% of the time. 1 Similar predictive information can be obtained using a variety of anti-platelet antibody tests. Post-transfusion counts obtained at the conclusion of transfusion, at a time that the patient must be seen by the physician or nurse to switch infusion bags, are identical to counts obtained 1 h later and it is therefore relatively simple to assess the results of every platelet transfusion to determine if the expected count increment was achieved. 2 The incidence of alloimmunization appears to be unrelated to the number of transfusions that patients receive. In a series of 114 newly diagnosed AML patients receiving 2-10+ transfusions of pooled non-leukocyte-depleted platelet concentrates (PC) from random donors, there was no relationship between the number of transfusions or donor exposures, and the development of new anti-HLA antibody. 3 At the end of induction therapy, 35-40% of patients had developed anti-body. The majority had persistence of the antibody, but 20% had disappearance of antibody over time. After marrow recovery from the induction therapy, 60% of patients remained anti-body-negative and, indeed, never developed antibody or refractoriness to platelet transfusion despite multiple subsequent red blood cell and platelet transfusions, suggesting that they had become immune tolerant to histocompatibility antigens. These patients continued to be easily supported with random donor transfusions and therefore measurement of lym-phocytotoxic antibody at this time in a patient's treatment course is helpful in predicting and arranging for their future transfusion needs. The traditional management of alloimmune-mediated plate-let refractoriness is by HLA typing of donors and recipients. A significant fraction of HLA 'matched' transfusions do not produce satisfactory increments, however, while some 'mismat-ched' transfusions are successful, and a number of studies have evaluated subtleties of HLA serology to attempt to explain these discrepancies. As one example, there is a high

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“…Following infusion of an average 6 U RDP or equivalent apheresis product, one may use another formula (see above for abbreviations) to determine posttransfusion platelet increment to identify refractoriness [33]:(1‐hr post tx plt ct) − (pre tx plt ct) ≥ 30,000 plts/μl.…”

Section: Unresponsiveness To Platelet Transfusionmentioning

confidence: 99%

“…If none of the above factors seem to be of major importance in causing platelet refractoriness, then alloimmune refractoriness is more likely and a platelet alloantibody screening test should be requested. If positive, most institutions would first transfuse crossmatch‐compatible platelets [33,41‐43]. Ongoing controversy exists regarding the benefits of using single‐donor HLA‐matched platelets versus crossmatch‐compatible platelets [43,44].…”

Section: Unresponsiveness To Platelet Transfusionmentioning

confidence: 99%

Thrombocytopenia and Critical Care Medicine

Gelinas¹,

Stoddart²,

Snyder³

2001

J Intensive Care Med

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Platelet transfusions play an important role in the treatment of critically ill patients. Like any blood component, however, there are various aspects of platelet transfusion therapy that need be considered by the intensivist. These include the proper dose and type of platelet component to infuse, as well as the route and method of administration. Methods to reduce the volume of the transfused platelets, for example, must ensure that the infused platelets will be functional and viable, posttransfusion. Treatment and diagnosis of the HLA alloimmunized recipient can pose a serious challenge to the clinician and an obstacle to adequate platelet therapy. An ICU patient for whom an adequate posttransfusion platelet increment cannot be achieved is at great risk of suffering a fatal hemorrhage. The ICU physician should be aware of the techniques used in modern transfusion practice to avoid having to deal with this complication. Adverse reactions to platelet transfusion include not only serologic ones, but those related to febrile and allergic complications, as well as infectious complications. The latter group includes diseases caused by infection with cytomegalovirus, bacteria, and a cadre of viruses including HIV and hepatitis. The clinical approach to thrombocytopenia in the ICU will be covered in some detail in an effort to review many of the conditions associated with recipient thrombocytopenia, including ITP, TTP, dilutional thrombocytopenia, DIC, surgery, HELLP syndrome, and drug‐induced thrombocytopenia. Unfortunately the treatment approaches traditionally used are not always derived from evidence‐based studies. This review covers many of these topics in an attempt to help physicians become better able to manage thrombocytopenia in the ICU and thus provide the best transfusion therapy for their patients.

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Algorithm for managing the platelet refractory patient

Cited by 15 publications

References 37 publications

Genotyping for Human Platelet Alloantigen Polymorphisms: Applications in the Diagnosis of Alloimmune Platelet Disorders

Genotyping for Human Platelet Alloantigen Polymorphisms: Applications in the Diagnosis of Alloimmune Platelet Disorders

Management of Patients Refractory to Platelet Transfusion

Thrombocytopenia and Critical Care Medicine

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