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Transfusion ◽  
2021 ◽  
Author(s):  
Justin E. Juskewitch ◽  
Micah D. Zuccarelli ◽  
Kristie K. Clymer ◽  
Laurie L. Wakefield ◽  
Justin D. Kreuter ◽  
...  

Transfusion ◽  
2020 ◽  
Vol 60 (12) ◽  
pp. 3055-3059
Author(s):  
Rachel K. Horton ◽  
Micah D. Zuccarelli ◽  
Laurie L. Wakefield ◽  
Margaret A. DiGuardo ◽  
Manish J. Gandhi ◽  
...  

Author(s):  
Wanxin Chen ◽  
Ziping Li ◽  
Bohan Yang ◽  
Ping Wang ◽  
Qiong Zhou ◽  
...  

ABSTRACTThe pandemic COVID-19 pneumonia has engulfed the entire world. Hematopoietic system can also be affected by COVID-19. Thrombocytopenia at admission was prevalent, while late-phase or delayed-phase thrombocytopenia is obscure. This retrospective single-center case series analyzed patients with COVID-19 at the Union Hospital, Wuhan, China, from January 25th to March 9th, 2020. Analysis began on March 11th, 2020. COVID-19 associated delayed-phase thrombocytopenia was occurred in 11.8% percent of enrolled patients. The delayed-phase thrombocytopenia in COVID-19 is prone to develop in elderly patients or patients with low lymphocyte count on admission. The delayed-phase thrombocytopenia is significantly associated with increased length of hospital stay and higher ICU admission rate. Delayed-phase nadir platelet counts demonstrated a high and significantly negative linear correlation with B cell percentages and serum IL-6 levels. We also presented bone marrow aspiration pathology of three patients with delayed-phase thrombocytopenia, showing impaired maturation of megakaryocytes. We speculated that the delayed-phase platelet destruction might be mediated by antibodies, and suggest immunoregulatory treatment in severe patients to improve outcomes. Besides, clinicians need to pay attention to the delayed-phase thrombocytopenia especially at 3-4 weeks after symptom onset.


1999 ◽  
Vol 69 (1) ◽  
pp. 83-86
Author(s):  
Chi-Woon Kong ◽  
Chun-Jo Shih ◽  
Hsiang-Chiang Hsiao ◽  
Hsin-Ya Chang ◽  
Ho-Chang Tai ◽  
...  

1979 ◽  
Vol 87 (2) ◽  
pp. 268-273 ◽  
Author(s):  
Joan T. Zajtchuk ◽  
William H. Falor ◽  
Miller F. Rhodes

Fourteen patients with a documented sudden neurosensory hearing loss and four patients with other diseases causing neurosensory hearing loss were studied. The standardized coagulation workup included hematocrit, activated partial thromboplastin generation time, thrombin generation, prothrombin time, phase platelet count, platelet adhesivity, protamine sulfate, serum antithrombin III activity, fibrinogen, and Factor VIII values. Only those patients having documented evidence of a neurosensory hearing loss occurring within hours or days were included in this study. Eight of the 14 patients with a documented sudden neurosensory hearing loss satisfied our laboratory criteria for a diagnosis of in vitro hypercoagulability. Three of these patients had abnormal thrombin generation values, 4 had abnormal serum antithrombin III values, and 1 had an elevated platelet count Four other patients with other diseases causing neurosensory hearing loss did not show evidence of in vitro hypercoagulability. It would appear from this data that coagulation abnormalities play a role in the pathogenesis of sudden neurosensory hearing loss.


1979 ◽  
Vol 87 (2) ◽  
pp. 268-273 ◽  
Author(s):  
Joan T. Zajtchuk ◽  
Maj William H. Falor ◽  
Mai Miller F. Rhodes

Fourteen patients with a documented sudden neurosensory hearing loss and four patients with other diseases causing neurosensory hearing loss were studied. The standardized coagulation workup included hematocrit, activated partial thromboplastin generation time, thrombin generation, prothrombin time, phase platelet count, platelet adhesivity, protamine sulfate, serum antithrombin III activity, fibrinogen, and Factor VIII values. Only those patients having documented evidence of a neurosensory hearing loss occurring within hours or days were included in this study. Eight of the 14 patients with a documented sudden neurosensory hearing loss satisfied our laboratory criteria for a diagnosis of in vitro hypercoagulability. Three of these patients had abnormal thrombin generation values, 4 had abnormal serum antithrombin III values, and 1 had an elevated platelet count. Four other patients with other diseases causing neurosensory hearing loss did not show evidence of in vitro hypercoagulability. It would appear from this data that coagulation abnormalities play a role in the pathogenesis of sudden neurosensory hearing loss.


1979 ◽  
Author(s):  
N.K. Furkalo ◽  
R.M. Bolshakova ◽  
M.A. Dukhina

Hemostatic parameters (including the contact activated phase, platelet functional state, anticoagulational activity, detection of soluble fibrin and fibrinogen (fibrin degradation products) as well as blood viscosity and the character of microcirculation disturbances evaluated by biomicroscopy, microphotographing and filming of bulbar conjunctival vessels, were studied in 394 patients with chronic IHD. Microthrombosis parallel with generalized sludge were discovered within the microcirculatory bed. Analysis of hemostatic rheologic and microcirculatory data has revealed features of chronic, moderately pronounced DIMC, which did not result in marked consumption of coagulational factors. At equal severity grades of IHD, myocardial infarction occured more often in those patients, who bore microthrombosis, microhemorrhage and perivascular edema in the microcirculation system. Hence the detection of DIMC features may become an early diagnostic criterion of IHD severity and its possible complications.


1977 ◽  
Vol 38 (02) ◽  
pp. 0552-0561 ◽  
Author(s):  
Yale S. Arkel ◽  
Jacob I. Haft ◽  
William Kreutner ◽  
Joseph Sherwood ◽  
Rae Williams

Summary23 healthy house staff officers were studied for platelet aggregation changes immediately prior to, immediately after and at a 7 to 11 day interval after their presenting a case before the Medical Mortality Conference. In 12 of the 23 with epinephrine (2.5 × 10−6M) and 11 of the 23 with ADP (2.0 × 10−6M) an absence of second phase aggregation was noted. A total of 19 of the 23 with epinephrine (2.5 × 10−6M) either had absent second phase or had a decreased slope of second phase aggregation. In all subjects except two a return to normal pattern was noted in the recovery samples 7 to 11 days later.In 5 subjects who had absent second phase aggregation with epinephrine (2.5 × 10-6M) immediately after presentation, one had a return toward normal at 24 hours while the others were resistant to higher concentrations of epinephrine (2.5 × 10−5M and 2.5 × 10−4M). One subject in the immediate post presentation period had a slight improvement in second phase aggregation with 2.5 × 10−4M epinephrine.Platelet counts increased in 5 of 6 subjects in the immediate post presentation period and did not necessarily correlate with the absence of second phase aggregation.ADP/ATP platelet content increased in the post presentation samples.We can conclude that during and immediately after an activity associated with stress, platelet changes can occur characterized by a decreased second phase aggregation with epinephrine or ADP. These changes last for at least 24 hours and are resistant to higher concentrations of epinephrine.


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