Plasma From Patients Undergoing Liver Transplantation Is Resistant to Anticoagulant Activity of Soluble Thrombomodulin

Burlage, Laura C.; Bos, Sophie; Adelmeijer, Jelle; Sakai, Takumi; Porte, Robert J.; Lisman, Ton

doi:10.1002/lt.25318

Cited by 2 publications

(1 citation statement)

References 39 publications

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“…Given the importance of acute liver dysfunction in explaining risk for microvascular thrombosis (by predisposing to reduced levels of PC and AT), it is possible that rhsTM might not decrease SPG risk in patients with shock liver. Indeed, Burlage and coworkers 70 found that plasma from patients undergoing liver transplantation was resistant to anticoagulant action of ART-123, an effect they attributed to decreased levels of PC and protein S (cofactor for APC) in patients with severe liver disease.…”

Section: Thrombomodulin Concentrates As a Treatment For Dicmentioning

confidence: 99%

Microvascular Thrombosis and Ischaemic Limb Losses in Critically Ill Patients

Warkentin

2019

Hamostaseologie

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Relatively little scientific attention has been given to the small subset of critically ill patients with circulatory shock who develop ischaemic limb losses (symmetrical peripheral gangrene [SPG]). The clinical picture consists of acral (distal extremity) tissue necrosis involving lower limbs in a largely symmetrical fashion and with detectable arterial pulses; in one-third of patients the upper extremities are also affected (potential for four-limb amputations). The laboratory picture includes thrombocytopenia, coagulopathy, and normoblastemia (circulating nucleated red blood cells). The explanation for limb losses is microvascular thrombosis caused by disseminated intravascular coagulation usually secondary to cardiogenic or septic shock. A common myth is that vasopressors cause the ischaemic limb injury. However, the more likely explanation is failure of the natural anticoagulant systems (protein C and antithrombin) to downregulate thrombin generation in the microvasculature. This is because more than 90% of patients with SPG have preceding ‘shock liver’, which occurs 2 to 5 days (median, 3 days) prior to ischaemic limb injury, with impaired hepatic production of protein C and antithrombin.

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Section: Thrombomodulin Concentrates As a Treatment For Dicmentioning

confidence: 99%