How we approach an acquired thrombotic thrombocytopenic purpura patient

Transfusion ◽  
2014 ◽  
Vol 54 (10) ◽  
pp. 2375-2382 ◽  
Author(s):  
Jay S. Raval ◽  
Marshall A. Mazepa ◽  
Mark E. Brecher ◽  
Yara A. Park
2017 ◽  
Vol 27 (4) ◽  
pp. 300-302 ◽  
Author(s):  
C. Sam ◽  
P. Desai ◽  
D. Laber ◽  
A. Patel ◽  
N. Visweshwar ◽  
...  

2020 ◽  
Vol 9 (3) ◽  
pp. 84-88
Author(s):  
Nicolas Cilla ◽  
Julie Dallemagne ◽  
Marie Vanhove ◽  
Patrick Stordeur ◽  
Serge Motte ◽  
...  

2020 ◽  
Author(s):  
Mohammad- Reza Rostami ◽  
Amirmasoud Kazemzadeh Houjaghan ◽  
Sahar Tavakoli shiraji ◽  
Hosein Kamranzadeh Fumani

Abstract Background and purpose: thrombotic thrombocytopenic purpura (TTP) is associated with microangiopathic hemolytic anemia, thrombocytopenia, and micro vascular thrombus plus fever, fluctuating neurologic abnormalities and renal damage. The purpose of this study was to investigate clinical symptom, laboratory finding and prognosis in TTP patient from 2010 to 2017 in Shariati hospital. In the present study we assessed clinical presentation and laboratory finding to predict mortality in patients with TTP. Methods: the study was a retrospective cohort study in patient with TTP in Shariati hospital from 2010 to 2017. 114 subjects with TTP after rule out of other microangiopathic hemolytic anemia were included in this study.Results: 114 case of TTP (80 female and 34 male) were identified. Mean ages of participated in the study were 39 years. Hematologic and neurologic symptoms were most common manifestations. Laboratory result at the time of diagnosis revealed mean thrombocytopenia (Plt: 29100), anemia (Hb:8/1), elevated LDH (15100).all patient were treated with PEX, using a cut-off value for the platelet count of 150000/ml. 75% of patient responded . In this study mean of ages, Neurologic manifestation, category of immunologic and reticulocyte count predicted mortality.Conclusion: finally, it can be concluded that mortality rate similar to other study but: in difference clinical symptom and laboratory finding may be predict mortality and occurrence of relapse.


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

1979 ◽  
Author(s):  
H. C. Kwaan

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.


1979 ◽  
Author(s):  
J. G. Kelton ◽  
P. B. Neame ◽  
I. Walker ◽  
A. G. Turpie ◽  
J. McBride ◽  
...  

Thrombotic thrombocytopenic purpura (TTP) is a rare but serious illness of unknown etiology. Treatment by plasmapheresis has been reported to be effective but the mechanism for benefit is unknown. We have investigated the effect of plasmapheresis in 2 patients with TTP by quantitating platelet associated IgG (PAIgG) levels prior to and following plasmapheresis. Both patients had very high levels of PAIgG at presentation (90 and A8 fg IgG/platelet respectively, normal 0-5). in both, the PAIgG levels progressively fell to within the normal range and the platelet count rose following plasmapheresis. One patient remained in remission with normal platelet counts and PAIgG levels. The other relapsed after plasmapheresis and the PAIgG level rose prior to the fall in platelet count. Plasmapheresis was repeated and resulted in normalization of both the platelet count and PAIgG level. It is suggested that plasmapheresis removes antiplatelet antibody or immune complexes which may be of etiological importance in this illness.


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