scholarly journals Peribiliary Intravascular Fibrin Occlusions and Bile Duct Necrosis in DCD Livers During Ex Situ Perfusion: Prevention With Tissue Plasminogen Activator and Fresh Frozen Plasma

2021 ◽  
Vol 105 (12) ◽  
pp. e401-e402
Author(s):  
Christopher J.E. Watson ◽  
Rebecca Brais ◽  
Rohit Gaurav ◽  
Lisa Swift ◽  
Corrina Fear ◽  
...  
Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Jason M Meunier ◽  
Brent Bluett ◽  
Evan P Wenker ◽  
Wan-Tsu W Chang ◽  
George J Shaw

Introduction: Recombinant tissue plasminogen activator (rt-PA) is the only FDA approved thrombolytic therapy for acute ischemic stroke. Recent studies have shown hypothermia to be beneficial in patient outcome in stroke. However, rt-PA is less effective at temperatures less than 37°C. Interest in improving the lytic efficacy of rt-PA thrombolysis has led to the study of adjunctive therapies such as GP IIb-IIIa inhibitors like eptifibatide (Epf) and ultrasound (US) enhanced thrombolysis. However, the thrombolytic efficacy of combination therapy with rt-PA over a clinically applicable temperature range is unknown. Objective: The effects of temperature on the thrombolytic efficacy of combination rt-PA-driven thrombolysis were determined in an in-vitro human clot model. Methods: Human whole blood clots were made from blood obtained from volunteers, after local Institutional Review Board approval. Clots were made in 20-µL pipettes and placed in a water tank for microscopic visualization during treatment. Sample clots were exposed to human fresh-frozen plasma (hFFP) alone (Control); hFFP and rt-PA ([0.5 µg/ml]; “+rt-PA”); hFFP, rt-PA ([0.5 µg/ml]), and Epf ([0.63 µg/ml]; “+Epf”); and hFFP, rt-PA, Epf, and ultrasound supplied by a 2-MHz transcranial Doppler (TCD) unit (“+TCD”). Exposures were for 30 minutes at 30-37°C. Clot width was measured using a microscopic imaging technique and mean percent fractional clot loss (FCL) at 30 minutes was used to determine thrombolytic efficacy. Results: Each of 15 treatment groups had a minimum of 6 clots (range: 6-148) from 2 different donors (range: 2-21), for a total of 409 clots. At 37°C, FCLs for +rt-PA and +TCD groups were 44% (95% Confidence Interval: 37-52%) and 59% (54-64%) respectively (p<0.01). At 30°C, FCLs for +rt-PA and +TCD groups were 32% (27-36%) and 30% (26-33%) respectively (p not significant). Conclusion: Combination therapy using rt-PA, Epf, and 2-MHz US exhibits temperature dependence over a clinically applicable temperature range.


2020 ◽  
Vol 8 (1) ◽  
pp. 33-36
Author(s):  
Giovanna Bertini ◽  
◽  
Serena Elia ◽  
Venturella Vangi

Aortic thrombosis during neonatal period is a rare event especially when it is not related to umbilical arterial catheters. A case of a premature infant with a gestational age of 25 weeks who suddenly developed, at the age of 44 days, poor arterial saturation (SaO2 60%) and legs pale and painful, is reported. In this patient, arterial and venous eco-color Doppler showed a complete aortic thrombosis distal to the renal arteries of unknown etiology. Thrombolytic therapy with tissue-type plasminogen activator (t-PA) was immediately started with a bolus dose of 0.5 mg/kg/h followed by a continuous infusion of 0.2 mg/kg/h. Fresh frozen plasma was also infused in order to increase the concentration of plasminogen. We tried with success to avoid bleeding complications maintaining fibrinogen concentration over 500 mg/L and platelets over 100,000x109/L. Heparinisation with enoxaparin was started after 5 days of t-PA treatment and continued for 85 days. The premature infant recovered but physiotherapy and splints were needed for talipes equinovarus resulted as a consequence of distal thrombosis. Conclusion: The strategy for treating an acute arterial thrombosis in a neonate may include thrombolytic therapy with t-PA, taking into account that the rate of plasmin generation in newborns and overall activity is decreased compared to adults. The impaired response of newborns may be enhanced not by increasing the dose of t-PA but increasing plasminogen through fresh frozen plasma infusion.


2020 ◽  
Vol 26 (2) ◽  
pp. 215-226 ◽  
Author(s):  
Qiang Liu ◽  
Ahmed Hassan ◽  
Daniele Pezzati ◽  
Basem Soliman ◽  
Laura Lomaglio ◽  
...  

VASA ◽  
2014 ◽  
Vol 43 (6) ◽  
pp. 450-458 ◽  
Author(s):  
Julio Flores ◽  
Ángel García-Avello ◽  
Esther Alonso ◽  
Antonio Ruíz ◽  
Olga Navarrete ◽  
...  

Background: We evaluated the diagnostic efficacy of tissue plasminogen activator (tPA), using an enzyme-linked immunosorbent assay (ELISA) and compared it with an ELISA D-dimer (VIDAS D-dimer) in acute pulmonary embolism (PE). Patients and methods: We studied 127 consecutive outpatients with clinically suspected PE. The diagnosis of PE was based on a clinical probability pretest for PE and a strict protocol of imaging studies. A plasma sample to measure the levels of tPA and D-dimer was obtained at enrollment. Diagnostic accuracy for tPA and D-dimer was determined by the area under the receiver operating characteristic (ROC) curve. Sensitivity, specificity, predictive values, and the diagnostic utility of tPA with a cutoff of 8.5 ng/mL and D-dimer with a cutoff of 500 ng/mL, were calculated for PE diagnosis. Results: PE was confirmed in 41 patients (32 %). Areas under ROC curves were 0.86 for D-dimer and 0.71 for tPA. The sensitivity/negative predictive value for D-dimer using a cutoff of 500 ng/mL, and tPA using a cutoff of 8.5 ng/mL, were 95 % (95 % CI, 88–100 %)/95 % (95 % CI, 88–100 %) and 95 % (95 % CI, 88–100 %)/94 %), respectively. The diagnostic utility to exclude PE was 28.3 % (95 % CI, 21–37 %) for D-dimer and 24.4 % (95 % CI, 17–33 %) for tPA. Conclusions: The tPA with a cutoff of 8.5 ng/mL has a high sensitivity and negative predictive value for exclusion of PE, similar to those observed for the VIDAS D-dimer with a cutoff of 500 ng/mL, although the diagnostic utility was slightly higher for the D-dimer.


2005 ◽  
Vol 5 (04) ◽  
pp. 178-182
Author(s):  
Wieland Kiess ◽  
Manuela Schulz ◽  
Sabine Liebermann ◽  
Roland Pfäffle ◽  
Peter Bührdel ◽  
...  

ZusammenfassungDas Smith-Lemli-Opitz-Syndrom wird durch einen Defekt des letzten Schrittes der Cholesterolbiosynthese, den Mangel an 7-Dehydrocholesterolreduktase, verursacht. Die Akkumulation der Metaboliten 7-Dehydrocholesterol und 8-Dehydrocholesterol, die die wichtigsten biochemischen Marker für die Diagnose der Erkrankung darstellen, sowie der Mangel an Cholesterol können zu multiplen kongenitalen Anomalien führen. Die Ursache des Enzymmangels sind Mutationen innerhalb des DHCR7-Gens, welches auf Chromosom 11q13 lokalisiert ist. Therapeutische Möglichkeiten bestehen in der Gabe von Cholesterol und im Notfall Fresh Frozen Plasma (FFP); der therapeutische Nutzen von Statinen befindet sich zurzeit in der klinischen Erprobung.


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