Specificities of anti‐platelet antibodies in multitransfused patients with haemato‐oncological disorders

Kurz, Markus; Greinix, Hildegard; Höcker, P; Kalhs, Peter; Knöbl, Paul; Wr, Mayr; Pober, Michael; Panzer, Sarah E.

doi:10.1046/j.1365-2141.1996.d01-1936.x

Cited by 58 publications

(42 citation statements)

References 26 publications

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“…M-SPRCA indicated that patients with thrombocytopenia had antiplatelet antibodies (61.2%; range, 48%-74%; mean, 64.3%). The number of patients with both antiplatelet and anti-HLA antibodies was 37.5% (range, 16%-52%; mean, 34.1%), consistent with previous reports 7,20,40-44. More interesting, there were 3 cases of idiopathic thrombocytopenia (1.3%) that could be investigated and confirmed to have only anti-HLA by this modified technique.…”

Section: Discussionsupporting

confidence: 89%

“…There were reports that platelet antibody specificity in transfusion recipients differed significantly from that observed in patients with neonatal alloimmune thrombocytopenia or posttransfusion purpura 6,7. Immunologic platelet destruction, mediated by alloantibodies directed against antigens on platelets, is frequently the principal or an important contributing factor in the platelet refractory state 7,8. There is a general correlation between alloimmunization to HLA and platelet antigens and clinical platelet refractoriness 4,9-13.…”

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confidence: 99%

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Modification of Solid Phase Red Cell Adherence Assay for the Detection of Platelet Antibodies in Patients With Thrombocytopenia

2008

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Platelet refractoriness is caused by HLA antibodies and platelet-specific antibodies. Current methods used to detect antiplatelet antibodies have limitations. Solid phase red cell adherence (SPRCA) lacks sensitivity and requires a second assay using chloroquine-treated intact platelets to specify the response due to anti-HLA. We modified SPRCA by using 2 types of antihuman platelet antibodies with different specificities toward platelet lysate and tested samples from 361 patients (69 with unexplained thrombocytopenia and 292 with poor response to platelet transfusions not explicable by alloimmunization or the clinical situation) and 50 from healthy volunteers. Our method compared favorably with platelet suspension direct immunofluorescence. All samples from healthy volunteers were negative; of the samples from the patient population, 240 were positive (147 samples had only antiplatelet and 3 samples had only anti-HLA antibodies). This modified technique had a sensitivity of 98% and a specificity of 91%.

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Section: Discussionsupporting

confidence: 89%

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confidence: 99%

Modification of Solid Phase Red Cell Adherence Assay for the Detection of Platelet Antibodies in Patients With Thrombocytopenia

2008

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“…Schnaidt et al [40]found that in 9/36 (25%) of the patients with multiple HLA antibodies HPA antibodies were formed. Kurz et al [41]studied a group of 81 haemato–oncological patients and found HPA antibodies in 7/81 patients and HLA antibodies in 32/81 patients of whom 7 had a combination of HLA and HPA antibodies. HPA antibodies seem to be less rare and their role in platelet transfusion refractoriness, especially if present in combination with HLA antibodies, needs further investigation.…”

Section: Alloimmune Factors and Refractorinessmentioning

confidence: 99%

Prevention and Management of Platelet Transfusion Refractoriness

Novotný¹

1999

Vox Sanguinis

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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.

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“…By the MAIPA assay platelet reactive antibodies were uncovered even before their detection by the LCT. As previously demonstrated [3,11,12], panreactive platelet and HLA antibodies may wax and wane at the time of chemotherapy-induced severe aplasia. The induction of antibody production coincided with feverish episodes.…”

Section: Discussionmentioning

confidence: 86%

Platelet Antibodies and Fever: Their Association in Multitransfused Patients with Hemato-Oncological Diseases

Kurz¹,

Eichelberger²,

Greinix³

et al. 1999

Transfus Med Hemother

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The posttransfusion platelet increment depends significantly on the clinical condition of the patient and the presence of platelet-reactive antibodies. We prospectively determined the development of platelet-reactive antibodies in weekly intervals at the time of chemotherapy in 17 multitransfused patients with hemato-oncological diseases. Sera were tested by both the MAIPA technique and the lymphocytotoxicity test (LCT) for antiplatelets against HLA class I antigens. In addition, we applied the MAIPA technique to determine the presence of platelet-reactive antibodies against human platelet-specific alloantigens (HPA-1, -2, -3, -5) and the platelet membrane glycoproteins (GP) Ia/IIa, Ib/IX, IIb/IIIa (panreactive). Platelet-reactive HLA antibodies were the most common antibodies, found in the sera of 8 patients. They were transient in 5 patients and were constantly detectable throughout the observation period in the other 3. Ten sera from 7 patients were positive for HLA antibodies by MAIPA, but negative by LCT. Of note, in 5 patients the presence of antibodies was indicated by MAIPA, but the LCT became positive only in the consecutive sample.

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Specificities of anti‐platelet antibodies in multitransfused patients with haemato‐oncological disorders

Cited by 58 publications

References 26 publications

Modification of Solid Phase Red Cell Adherence Assay for the Detection of Platelet Antibodies in Patients With Thrombocytopenia

Modification of Solid Phase Red Cell Adherence Assay for the Detection of Platelet Antibodies in Patients With Thrombocytopenia

Prevention and Management of Platelet Transfusion Refractoriness

Platelet Antibodies and Fever: Their Association in Multitransfused Patients with Hemato-Oncological Diseases

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