scholarly journals Dramatic presentation of acquired thombotic thrombocytopenic purpura associated with COVID-19

Haematologica ◽  
2020 ◽  
Vol 105 (10) ◽  
pp. e540 ◽  
Author(s):  
Marco Capecchi ◽  
Cristina Mocellin ◽  
Chiara Abbruzzese ◽  
Ilaria Mancini ◽  
Daniele Prati ◽  
...  
Keyword(s):  
Thrombocytopenic Purpura ◽  
Dramatic Presentation

Naturally Occurring IgG Autoantibodies to Platelet Cytoskeleton Tropomyosin

1996 ◽  
Vol 75 (04) ◽  
pp. 642-647 ◽  
Author(s):  
Ming Hou ◽  
Dick Stockelberg ◽  
Jack Kutti ◽  
Hans Wadenvik
Keyword(s):  
Molecular Weight ◽  
Human Platelet ◽  
Chronic Idiopathic Thrombocytopenic Purpura ◽  
Thrombocytopenic Purpura ◽  
Immunoblot Assay ◽  
Specific Antibodies ◽  
Platelet Protein ◽  
Naturally Occurring ◽  
Normal Individuals ◽  
Cytoskeleton Protein

SummaryWe have observed that naturally occurring serum antibodies generated a 30 Kd band in a platelet immunoblot assay. The target protein had the same molecular weight (30 Kd) under nonreduced and reduced electrophoretic conditions, and could be immunoblotted from either autologous or homologous platelet lysates. Also, the 30 Kd reactive autoantibodies could be totally adsorbed by platelet cytoskeletons. From these data one likely candidate for the autoantibody target was the intracellular platelet protein tropomyosin. Indeed, a commercially available monoclonal antitropomyosin antibody reacted with proteins comigrating with this 30 Kd band; affinity purified human platelet tropomyosin was bound by the antibodies that recognized the 30 Kd protein. This body of evidence conclusively demonstrated that naturally occurring serum autoantibodies reacted with the platelet cytoskeleton protein - tropomyosin. These tropomyosin specific antibodies were found in roughly the same percentage of sera from patients with chronic idiopathic thrombocytopenic purpura (ITP) as from normal individuals.

Acquired Disorder of Platelet Function Associated with Autoantibodies against Membrane Glycoprotein IIb-IIIa Complex - 1. Glycoprotein Analysis

1991 ◽  
Vol 65 (05) ◽  
pp. 491-496 ◽  
Author(s):  
M Meyer ◽  
C M Kirchmaier ◽  
A Schirmer ◽  
P Spangenberg ◽  
Ch Ströhl ◽  
...  
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Adhesion ◽  
Bleeding Time ◽  
Membrane Glycoprotein ◽  
Membrane Glycoproteins ◽  
Abnormal Behaviour ◽  
Thrombocytopenic Purpura ◽  
Immunoelectrophoretic Analysis ◽  
Prolonged Bleeding Time

SummaryA patient with idiopathic thrombocytopenic purpura developed after splenectomy a thrombasthenia-like severe haemor-rhagic diathesis characterized by a normal or subnormal platelet count, prolonged bleeding time, strongly reduced platelet adhesion to glass and defective platelet aggregation in response to ADP and collagen. In contrast to hereditary thrombasthenia membrane glycoproteins (GP) lib and Ilia were normally present in the patient’s platelets. Immunoelectrophoretic analysis revealed an abnormal behaviour of the patient’s GP IIb-IIIa complex. Autoantibodies against GP IIb-IIIa were detected in Triton-extracted washed platelets. Incubation of normal platelets with plasma from the patient resulted in a similar immunoelectrophoretic abnormality of the GP IIb-IIIa complex indicating that bound autoantibodies (IgG) are responsible for the abnormal immunoelectrophoretic behaviour of the patient’s GP IIb-IIIa complex. Platelet fibrinogen was severely reduced similar to classical thrombasthenia suggesting that the GP IIb-IIIa complex is involved in platelet fibrinogen storage.

PAICA: A Method for Characterizing Platelet-Associated Antibodies - Its Application to the Study of Idiopathic Thrombocytopenic Purpura and to the Detection of Platelet-bound c7E3

1996 ◽  
Vol 76 (06) ◽  
pp. 1020-1029 ◽  
Author(s):  
Laurent Macchi ◽  
Gisèle Clofent-Sanchez ◽  
Gérald Marit ◽  
Claude Bihour ◽  
Catherine Durrieu-Jais ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Flow Cytometry ◽  
Idiopathic Thrombocytopenic Purpura ◽  
Antithrombotic Therapy ◽  
Membrane Glycoproteins ◽  
Serum Antibodies ◽  
Platelet Destruction ◽  
Thrombocytopenic Purpura ◽  
Capture Assay ◽  
Specific Membrane

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.

Normal Prostacyclin-Like Activity in Thrombotic Thrombocytopenic Purpura

1981 ◽  
Vol 46 (02) ◽  
pp. 571-571 ◽  
Author(s):  
M Pini ◽  
C Manotti ◽  
R Quintavalla ◽  
A G Dettori
Keyword(s):  
Thrombotic Thrombocytopenic Purpura ◽  
Thrombocytopenic Purpura

The Pathogenesis of Thrombotic Thrombocytopenic Purpura

1979 ◽  
Author(s):  
H. C. Kwaan
Keyword(s):  
Plasminogen Activator ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Degradation Products ◽  
Vascular Lesions ◽  
Local Defect ◽  
Laboratory Findings ◽  
Thrombocytopenic Purpura ◽  
Fibrin Degradation Products ◽  
Severity Of The Disease ◽  
Circulating Levels

The vascular lesions with microthrombi were studied in 12 patients with thrombotic thrombocytopenic purpura (TTP), diagnosed by the characteristic clinical and laboratory findings and confirmed histologically in each case. While defibrination was not observed, and with only minimal changes in the circulating levels of fibrinogen, fibrin degradation products and plasminogen activator, the microthrombotic lesion was invariably present. Immunofluorescent and histochemical studies indicated that both platelet and fibrin were present in the microthrombi with the platelet components dominant in many cases. Using the fibrin slide method, plasminogen activator was demonstrated in the uninvolved blood vessels but totally absent in the vessels occluded by microthrombi. in contrast, fibrinolysis is always present in the vessels afflicted with other types of thrombosis, such as the microthrombi in disseminated intravascular coagulation. Since circulating fibrinolytic activity was normal in TTP, the absence of vascular fibrinolysis is a local defect due to either inhibition by the platelet deposits or by local vascular damage. The inability of thrombolysis may explain the absence of systemic defibrination and the severity of the disease.

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