Determination of antiplatelet antibodies on the surface of platelets from patients with various forms of immune thrombocytopenia by direct radioimmunoassay

1991 ◽  
Vol 111 (6) ◽  
pp. 846-849 ◽  
Author(s):  
A. I. Kuznetsov ◽  
L. I. Idel'son ◽  
A. V. Mazurov
2020 ◽  
Vol 9 (6) ◽  
pp. 1998 ◽  
Author(s):  
Thomas Rogier ◽  
Maxime Samson ◽  
Guillaume Mourey ◽  
Nicolas Falvo ◽  
Nadine Magy-Bertrand ◽  
...  

Immune thrombocytopenia (ITP) is a rare autoimmune disease due to autoantibodies targeting platelet glycoproteins (GP). The mechanism of platelet destruction could differ depending on the specificity of antiplatelet antibodies: anti-GPIIb/IIIa antibodies lead to phagocytosis by splenic macrophages, in a Fcγ receptor (FcγR)-dependent manner while anti-GPIb/IX antibodies induce platelet desialylation leading to their destruction by hepatocytes after binding to the Ashwell–Morell receptor, in a FcγR-independent manner. Considering the FcγR-dependent mechanism of action of intravenous immunoglobulins (IVIg), we assumed that the response to IVIg could be less efficient in the presence of anti-GPIb/IX antibodies. We conducted a multicentric, retrospective study including all adult ITP patients treated with IVIg who had antiplatelet antibodies detected between January 2013 and October 2017. Among the 609 identified, 69 patients were included: 17 had anti-GPIb/IX antibodies and 33 had anti-GPIIb/IIIa antibodies. The response to IVIg was not different between the patients with or without anti-GPIb/IX (88.2% vs. 73.1%). The response to IVIg was better in the case of newly diagnosed ITP (odds ratio (OR) = 5.4 (1.2–24.7)) and in presence of anti-GPIIb/IIIa (OR = 4.82 (1.08–21.5)), while secondary ITP had a poor response (OR = 0.1 (0.02–0.64)). In clinical practice, the determination of antiplatelet antibodies is therefore of little value to predict the response to IVIg.


Author(s):  
V.M. Dudnyk ◽  
O.I. Izyumets ◽  
V. H. Furman ◽  
O. V. Kutsak ◽  
O.O. Stetsun

Annotation. The aim of the study was to analyze with the help of literature data the features of the clinical course of immune thrombocytopenia, to monitor the mechanisms of reactions, as well as to reproduce them on their own observation. Features of clinical course and differential diagnosis of immune thrombocytopenia are described. It is established that the main manifestation of this pathology is hemorrhagic syndrome, accompanied by skin hemorrhages, bleeding, possible hepatosplenomegaly, jaundice. Detection of antiplatelet antibodies is used to confirm the diagnosis.


1975 ◽  
Author(s):  
E. Pogliani ◽  
E. Cofrancesco ◽  
A. Della Volpe ◽  
M. Cortellaro ◽  
G. Masera ◽  
...  

15 sera from never transfused thrombocytopenic children (idiopathic thrombocytopenic purpura, drug induced and post-viral thrombocytopenia) were performed in a microtechnique according to the modified sedimentation pattern test of Myllyla (1). Eighter percent of these sera, tested against a pannel of at least five healthy donors, gave a positive result at different dilutions (from ¼ to ⅙). This quantitative platelet agglutination assay, compared with platelet aggregometry and 14 C-serotonin release, seems to be a sensitive, simple and reliable method to detect antiplatelet antibodies. Therefore it could have clinical applicability to the study of patients affected by immune thrombocytopenia.(1) Myllyla, G.: Aggregation of human blood platelet by immune complexes in the sedimentation pattern test.Scand, J. Haemat. suppl. 19, 1973.


Blood ◽  
2016 ◽  
Vol 128 (17) ◽  
pp. 2183-2185 ◽  
Author(s):  
Silvia Cantoni ◽  
Monica Carpenedo ◽  
Michele Nichelatti ◽  
Lanfranco Sica ◽  
Silvano Rossini ◽  
...  

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3537-3537
Author(s):  
John W. Semple ◽  
Kristin Hunt ◽  
Yu Hou ◽  
Rukhsana Aslam ◽  
Edwin R. Speck ◽  
...  

Abstract Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder characterized by increased peripheral immune platelet destruction and megakaryocyte defects in the bone marrow. Although ITP was originally thought to be primarily due to humoral mediated autoimmunity it is now evident that T cells can also play a contributing role to the thrombocytopenia. In fact, the exact interplay between platelet destruction, megakaryocyte dysfunction, and the elements of both the humoral and cell mediated immune systems still remain incompletely defined. In murine passive models of ITP, the direct administration of anti-platelet antibodies can result in severe thrombocytopenia which is evident within 24 hours of injection. While most studies have focused on immune platelet destruction in the spleen, an additional possibility is that the anti-platelet antibody also has an effect on megakaryocytes. To unequivocally determine if antiplatelet antibodies have an effect on megakaryocytes in an in vivo model, BALB/c mice were intravenously administered 2 ug of an anti-GPIIbIIIa antibody (MReg30) or 50 uL of a high tittered anti-GPIIIa (anti-β3) serum from BALB/c GPIIIa (CD61) knockout mice immunized with wild type platelets. Platelet counts were assessed over time and the bone marrow and spleens were harvested for histological examination of megakaryocytes. Both preparations of antiplatelet antibodies significantly reduced platelet numbers within 1 day of antibody or serum administration. This thrombocytopenia could be rescued by administration of 2 g/kg of IVIg ip. Compared with naïve control mice, histological (H&E staining) examination of the bone marrow and spleens revealed that megakaryocytes were significantly increased in number and all exhibited abnormalities consistent with apoptosis e.g. pyknotic nuclei. IVIg administration completely prevented these megakaryocyte abnormalities. These results show that passively administered anti-platelet antibodies not only affect platelet counts but also significantly affect megakaryocyte physiology in the absence of cell mediated immunity. Disclosures: No relevant conflicts of interest to declare.


2013 ◽  
Vol 93 (2) ◽  
pp. 309-315 ◽  
Author(s):  
David Grimaldi ◽  
Florence Canouï-Poitrine ◽  
Laure Croisille ◽  
Ketty Lee ◽  
Françoise Roudot-Thoraval ◽  
...  

Blood ◽  
1996 ◽  
Vol 88 (1) ◽  
pp. 194-201 ◽  
Author(s):  
TA Brighton ◽  
S Evans ◽  
PA Castaldi ◽  
CN Chesterman ◽  
BH Chong

Abstract The diagnosis of idiopathic immune thrombocytopenia remains a clinical diagnosis based on the exclusion of other causes of immune and nonimmune thrombocytopenia. Measurement of platelet-associated Ig (PAIg), while sensitive, is nonspecific for the diagnosis of immune thrombocytopenia. Published experience of antigen capture assays (including monoclonal antibody immobilization of platelet antigens or MAIPA) suggest a high sensitivity and specificity (70% to 80%) in selected groups of patients. In a prospective evaluation of 158 patients with thrombocytopenia from all causes, we report a sensitivity of 51% and specificity of 80% for direct MAIPA assays. MAIPA was considerably better in discriminating immune from nonimmune thrombocytopenia than two assays of PAIgG. Antiplatelet antibodies detected by MAIPA were more frequently directed against the glycoprotein (GP) IIb/IIIa than the GP Ib/IX complex. Our experience suggests that MAIPA assays are useful in the laboratory assessment of thrombocytopenia, should be performed before therapy, and that some patients with ‘nonimmune’ thrombocytopenia may have genuine antiplatelet antibodies.


JRSM Open ◽  
2014 ◽  
Vol 5 (6) ◽  
pp. 205427041453112 ◽  
Author(s):  
Kriti Mittal ◽  
Michael J McNamara ◽  
Brian R Curtis ◽  
Keith R McCrae

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