Fixation of C3 to Platelets in Vitro by Antiplatelet Antibody from Patients with Immune Thrombocytopenic Purpura

1981 ◽  
Vol 47 (2) ◽  
pp. 251-256 ◽  
Author(s):  
R. McMillan ◽  
M. Martin
Keyword(s):  
Immune Thrombocytopenic Purpura ◽  
Antiplatelet Antibody ◽  
Thrombocytopenic Purpura

scholarly journals Platelet-associated and plasma anti-glycoprotein autoantibodies in chronic ITP

Blood ◽  
1987 ◽  
Vol 70 (4) ◽  
pp. 1040-1045 ◽  
Author(s):  
R McMillan ◽  
P Tani ◽  
F Millard ◽  
P Berchtold ◽  
L Renshaw ◽  
...  
Keyword(s):  
Immune Thrombocytopenic Purpura ◽  
Platelet Glycoprotein ◽  
Antiplatelet Antibody ◽  
Platelet Destruction ◽  
Thrombocytopenic Purpura ◽  
Chronic Immune Thrombocytopenic Purpura ◽  
Chronic Itp ◽  
Negative Results ◽  
Well Assay ◽  
Positive Results

Chronic immune thrombocytopenic purpura (ITP) is due to platelet destruction by circulating antiplatelet antibody. Although autoantibodies against the platelet glycoprotein IIb/IIIa (GPIIb/IIIa) complex and GPIb have been demonstrated using various methods, practical assays for detection of platelet-associated or plasma autoantibodies have not been available. We studied 59 patients with chronic immune thrombocytopenic purpura in whom platelet-associated and plasma autoantibodies against the GPIIb/IIIa complex and GPIb were measured using a newly developed immunobead assay and a previously reported microtiter-well assay. Platelet-associated autoantibody was detected using the immunobead assay in 21 of 28 patients (75.0%; 13 with anti-GPIIb/IIIa, 8 with anti-GPIb). Plasma autoantibodies were noted in 34 of 59 patients (57.6%; 21 with anti-GPIIb/IIIa, 11 with anti-GPIb, and 2 with both). Positive results were noted in 30 of 59 patients using the immunobead assay and in only 14 of 59 using the microtiter-well assay, suggesting that solubilization of the platelets prior to antibody addition, as in the microtiter-well assay, alters epitope stability. Of the 31 thrombocytopenic control patients studied, all gave negative results using both assays. We conclude that these clinically adaptable assays allow detection of autoantibodies in most patients with chronic ITP, confirming the presence of an autoimmune process.

scholarly journals Platelet-associated and plasma anti-glycoprotein autoantibodies in chronic ITP

Blood ◽  
1987 ◽  
Vol 70 (4) ◽  
pp. 1040-1045 ◽  
Author(s):  
R McMillan ◽  
P Tani ◽  
F Millard ◽  
P Berchtold ◽  
L Renshaw ◽  
...  
Keyword(s):  
Immune Thrombocytopenic Purpura ◽  
Platelet Glycoprotein ◽  
Antiplatelet Antibody ◽  
Platelet Destruction ◽  
Thrombocytopenic Purpura ◽  
Chronic Immune Thrombocytopenic Purpura ◽  
Chronic Itp ◽  
Negative Results ◽  
Well Assay ◽  
Positive Results

Abstract Chronic immune thrombocytopenic purpura (ITP) is due to platelet destruction by circulating antiplatelet antibody. Although autoantibodies against the platelet glycoprotein IIb/IIIa (GPIIb/IIIa) complex and GPIb have been demonstrated using various methods, practical assays for detection of platelet-associated or plasma autoantibodies have not been available. We studied 59 patients with chronic immune thrombocytopenic purpura in whom platelet-associated and plasma autoantibodies against the GPIIb/IIIa complex and GPIb were measured using a newly developed immunobead assay and a previously reported microtiter-well assay. Platelet-associated autoantibody was detected using the immunobead assay in 21 of 28 patients (75.0%; 13 with anti-GPIIb/IIIa, 8 with anti-GPIb). Plasma autoantibodies were noted in 34 of 59 patients (57.6%; 21 with anti-GPIIb/IIIa, 11 with anti-GPIb, and 2 with both). Positive results were noted in 30 of 59 patients using the immunobead assay and in only 14 of 59 using the microtiter-well assay, suggesting that solubilization of the platelets prior to antibody addition, as in the microtiter-well assay, alters epitope stability. Of the 31 thrombocytopenic control patients studied, all gave negative results using both assays. We conclude that these clinically adaptable assays allow detection of autoantibodies in most patients with chronic ITP, confirming the presence of an autoimmune process.

scholarly journals Platelet turnover and kinetics in immune thrombocytopenic purpura: results with autologous 111In-labeled platelets and homologous 51Cr- labeled platelets differ

Blood ◽  
1986 ◽  
Vol 67 (1) ◽  
pp. 86-92 ◽  
Author(s):  
P Heyns A du ◽  
PN Badenhorst ◽  
MG Lotter ◽  
H Pieters ◽  
P Wessels ◽  
...  
Keyword(s):  
Immune Thrombocytopenic Purpura ◽  
Severe Disease ◽  
Reticuloendothelial System ◽  
Computer Assisted ◽  
Scintillation Camera ◽  
Antiplatelet Antibody ◽  
Thrombocytopenic Purpura ◽  
Computer Assisted Image ◽  
The Difference

Abstract Mean platelet survival and turnover were simultaneously determined with autologous 111In-labeled platelets (111In-AP) and homologous 51Cr- labeled platelets (51Cr-HP) in ten patients with chronic immune thrombocytopenic purpura (ITP). In vivo redistribution of the 111In-AP was quantitated with a scintillation camera and computer-assisted image analysis. The patients were divided into two groups: those with splenic platelet sequestration (spleen-liver 111In activity ratio greater than 1.4), and those with diffuse sequestration in the reticuloendothelial system. The latter patients had more severe ITP reflected by pronounced thrombocytopenia, decreased platelet turnover, and prominent early hepatic platelet sequestration. Mean platelet life span estimated with 51Cr-HP was consistently shorter than that of 111In-AP. Platelet turnover determined with 51Cr-HP was thus over-estimated. The difference in results with the two isotope labels was apparently due to greater in vivo elution of 51Cr. Although the limitations of the techniques should be taken into account, these findings indicate that platelet turnover is not always normal or increased in ITP, but is low in severe disease. We suggest that this may be ascribed to damage to megakaryocytes by antiplatelet antibody. The physical characteristics in 111In clearly make this radionuclide superior to 51Cr for the study of platelet kinetics in ITP.

Mannose Labeled Liposome-Encapsulated Doxorubicin Is Effective in the Management of Experimental Immune Thrombocytopenic Purpura Model Mice.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3995-3995
Author(s):  
Yoji Ishida ◽  
Kazunori Murai ◽  
Syugo Kowata ◽  
Tatsuo Oyake ◽  
Ryo Suzuki ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Intravenous Injection ◽  
Immune Thrombocytopenic Purpura ◽  
Mannose Receptor ◽  
Reticuloendothelial System ◽  
Peritoneal Macrophages ◽  
Thrombocytopenic Purpura ◽  
Murine Macrophages

Abstract Immune thrombocytopenic purpura (ITP) is an autoimuune disease in which platelet antibodies cause increased platelet consumption. The destruction of platelets is mediated by the reticuloendothelial system (RES), especially hepatic and splenic macrophages. The depletion of these cells was carried out by the intravenous injection of mannose labeled liposome-encapsulated doxorubicin (mannose-DXR-liposome). The reason why mannose labeled liposome was used was that the macrophage expressed mannose receptor on the surface. Therefore, mannose-DXR-liposome is considered to be phagocyted specifically by macrophages. In this study, we evaluated the effects of mannose-DXR-liposome in a mouse model of ITP. In vitro experiments: Murine peritoneal macrophages were obtained by the intraperitoneal injection of thioglycolate (TGC) to ddY mice. The uptake of fluorescence by peritoneal macrophages was measured using rhodamine-liposome by flow cytometry. The macrophages were incubated with mannose labeled rhodamine-liposome (mannose(+)-rhodamine-liposome) or mannose unlabeled rhodamine-liposome (mannose(−)-rhodamine-liposome) for 30 min at 37 °C. After washing with PBS, they were applied for flow cytometry. Rhodamine fluorescence intensity in macrophages was higher in mannose(+)-rhodamine-liposome treatment than that in mannose(−)-rhodamine-liposome treatment (Figure 1). The viability of peritoneal macrophages was measured by MTT assay after 30 min incubation with DXR-liposome. The viability in the treatment with mannose(+)-DXR-liposome was much less than that in the treatment with mannose(−)-DXR-liposome (Figure 2). In vivo experiment: Anti-mouse platelet serum (APS) was injected intraperitoneally to ddY mice at 24 hr after intravenous injection of mannose(+)-DXR-liposome or mannose(−)-DXR-liposome. Platelet count was measured at 12 hr after APS injection. It was 89.3 ± 22.1 x104 / μl (n=6) in mannose(+)-DXR-liposome treatment, while 4.5 ± 2.0 x104 / μl (n=8) in mannose(−)-DXR-liposome treatment. The platelet counts were 3.2 ± 0.5 x104 / μl (n=4), 96.1 ± 15.0 x104 / μl (n=4) or 99.3 ± 26.2 x104 / μl (n=4) in mice with only APS administration, mannose(+)-DXR-liposome+saline or mannose(−)-DXR-liposome+saline administrations instead of APS, respectively. These in vivo data indicated that APS induced thrombocytopenia was not observed in mice treated with mannose(+)-DXR-liposome, because of the destruction of macrophages by mannose(+)-DXR-liposome administration. These in vitro and in vivo results strongly suggest that mannose(+)-DXR-liposome treatment specifically delete the macrophages and can be effective in the management of experimental ITP model mice. Figure 1 The Uptake of Rhodamine –liposome by Murine Macrophages. Figure 1. The Uptake of Rhodamine –liposome by Murine Macrophages. Figure 2. The Viability of Murine Macrophages after incubation with Doxorubicin-liposome. Figure 2. The Viability of Murine Macrophages after incubation with Doxorubicin-liposome.

Different Antiplatelet Antibody Specificities in Immune Thrombocytopenic Purpura

1976 ◽  
Vol 34 (1) ◽  
pp. 147-151 ◽  
Author(s):  
R. L. DONNELL ◽  
R. Mcmillan ◽  
R. J. Yelenosky ◽  
R. L. Longmire ◽  
A. L. Lightsey
Keyword(s):  
Immune Thrombocytopenic Purpura ◽  
Antiplatelet Antibody ◽  
Thrombocytopenic Purpura ◽  
Antibody Specificities

scholarly journals Infection of megakaryocytes by human immunodeficiency virus in seropositive patients with immune thrombocytopenic purpura

Blood ◽  
1991 ◽  
Vol 78 (7) ◽  
pp. 1697-1705 ◽  
Author(s):  
F Louache ◽  
A Bettaieb ◽  
A Henri ◽  
E Oksenhendler ◽  
JP Farcet ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Immune Thrombocytopenic Purpura ◽  
Hiv Positive ◽  
Thrombocytopenic Purpura ◽  
Colony Forming Units ◽  
Immunodeficiency Virus ◽  
Hiv Antibodies ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

Abstract Twenty-one human immunodeficiency virus (HIV)-positive patients, including 11 acquired immunodeficiency syndrome (AIDS)-free patients with immune thrombocytopenic purpura (ITP), were studied to determine whether the megakaryocytic/platelet lineage was infected by HIV. Because purification of platelets did not reach a level sufficient for unequivocal results by the polymerase chain reaction, in situ hybridization was thus performed. Purified marrow megakaryocytes (MK) from 10 HIV-infected ITP patients were studied using a 35S HIV riboprobe, antisense of an HIV ENV sequence. HIV transcripts were clearly detected in MK from five of these 10 patients, although heterogeneity among MK was observed. In three of these five cases, small amounts of HIV glycoproteins were detected in MK by means of immunofluorescence. In addition anti-HIV antibodies could be eluted from platelets of all patients. In contrast, HIV transcripts were not detected in MK derived from colony-forming units-MK (CFU-MK) cultured in suspension, suggesting either that MK are infected by HIV during terminal differentiation or that HIV-infected CFU-MK are unable to differentiate in vitro. In conclusion, this study suggests that HIV infection of MK may be implicated in the pathogenesis of thrombocytopenia of HIV-positive patients.

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