PLATELET SURVIVAL STUDIES AND BODY SCANNING IN IDIOPATHIC THROMBOCYTOPENIC PURPURA

1967 ◽  
Vol 254 (6) ◽  
pp. 777-784 ◽  
Author(s):  
Richard B. Solomon ◽  
Dallas V. Clatanoff
PEDIATRICS ◽  
1966 ◽  
Vol 37 (2) ◽  
pp. 339-341
Author(s):  
WILLIAM KRVIT ◽  
EDMUND YUNIS ◽  
JAMES G. WHITE

1. Normal platelets were transfused into 4 patients with Aldrich syndrome. The response in platelet count indicated that little destruction of platelets was occurring. The survival of platelets was considered to be normal. Plasma transfusion alone did not correct the platelet counts. Platelet antibodies were not detected in two of these patients. 2. For control studies, normal platelets were transfused into two patients with amegakaryocytotic congenital thrombocytopenia and sex-linked recessive (non-Aldrich) familial thrombocytopenia. Their survival was normal. Similarly, normal platelets were transfused into three patients with idiopathic thrombocytopenic purpura. Minimal increase in platelets and no significant length of survival of platelets was seen. The thrombocytopenia of Aldrich syndrome was considered to be due to a defect in procduction and/or release of platelets.


1971 ◽  
Vol 24 (7) ◽  
pp. 621-625 ◽  
Author(s):  
G. W. K. Donaldson ◽  
A. C. Parker ◽  
M. McArthur ◽  
J. Richmond

1976 ◽  
Vol 89 (3) ◽  
pp. 388-390 ◽  
Author(s):  
Sinasi Özsoylu ◽  
Hüseyin Allahverdi ◽  
Yahya Lâleli ◽  
Aysel Pirnar

1996 ◽  
Vol 76 (06) ◽  
pp. 1020-1029 ◽  
Author(s):  
Laurent Macchi ◽  
Gisèle Clofent-Sanchez ◽  
Gérald Marit ◽  
Claude Bihour ◽  
Catherine Durrieu-Jais ◽  
...  

SummaryIn idiopathic thrombocytopenic purpura (ITP), autoantibodies reacting with antigens on the platelet membrane bring about accelerated platelet destruction. We now report PAICA (“Platelet-Associated IgG Characterization Assay”), a method for detecting autoantibodies bound to specific membrane glycoproteins in total platelet lysates. This monoclonal antibody (MAb) capture assay takes into account the fact that antibodies on circulating platelets may be translocated to internal pools as well as being on the surface. A total of twenty ITP patients were examined by PAICA, and the results compared with those obtained by measuring (i) serum antibodies bound to paraformaldehyde-fixed control platelets by ELISA, (ii) IgG bound to the surface of the patient’s own platelets by flow cytometry (PSIgG), (iii) total platelet-associated IgG (PAIgG) by ELISA and (iv) serum antibodies reacting with control platelets by MAIPA (“Monoclonal Antibody-specific Immobilization of Platelet Antigens”). Of twelve patients with elevated PAIgG, nine had increased PSIgG yet eleven reacted positively in PAICA. Of these, eight possessed antibodies directed against GP Ilb-IIIa, two against GP Ib-IX and one patient possessed antibodies directed against GP Ilb-IIIa and GP Ia-IIa respectively. Only seven of the patients possessed serum antibodies detectable by MAIPA. PAICA was also able to detect platelet-associated c7E3 (the chimeric form of Fab fragments of the MAb 7E3) following its infusion during antithrombotic therapy, when it proved more sensitive over a seven-day period than a MAIPA assay adapted for assessing surface-bound antibody. We propose that PAICA provides added sensitivity to the detection of platelet-associated antibodies in immune thrombocytopenias or following therapy with humanized MAbs.


1975 ◽  
Vol 34 (01) ◽  
pp. 050-062
Author(s):  
Dale H Cowan ◽  
Richard C Graham ◽  
Patricia Shook ◽  
Ronda Griffin

SummaryTo determine the effect on platelet behavior of transient exposure of platelets to ascorbic acid, studies of platelet function and ultrastructure were done before exposure to ascorbic acid at pH 6.5, during exposure to pH 6.5, and after restoration of pH to pre-acidifìcation levels. The effect of ascorbic acid (A. A.) was compared to that of HCl and citric acid (C. A.). ADP- and collagen-induced aggregation of normal platelets were significantly impaired by both A. A. and C. A. but were less affected by HCl. The release of 14C-serotonin was significantly reduced by each agent. The ultra-structure of normal platelets brought to pH 6.5 by A.A. was normal. After neutralization, there was marked dilatation of the open channel system and loss of the disc shape. When platelets were brought to pH 6.5 by A. A., then neutralized, the aggregates which formed after stimulation by ADP or collagen were smaller than normal, the platelets were less closely approximated, and degranulation was less complete. The data show that exposure of platelets to ascorbic acid for short intervals impairs their function when measured after restoration of pH to levels compatible with maximal responses. Platelet survival studies using autologous platelets labelled with 51Cr in the presence or absence of ascorbic acid showed that the recovery of normal platelets was unaffected by ascorbic acid, whereas recovery of platelets from patients with idiopathic thrombocytopenic purpura, idiopathic thrombocythemia, and alcohol-related thrombocytopenia was markedly reduced. The injury resulting from the use of ascorbic acid in preparing platelets for studies of platelet survival in patients with disorders affecting platelets may impair the recovery of the cells, resulting in artifactual changes in the survival studies.


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