The protein C pathway.
Review published in Critical care medicine (2000)
Abstract
OBJECTIVE: To examine the role of the protein C anticoagulant pathway in the regulation of microvascular thrombosis. The mechanisms by which inflammation impairs the function of this pathway are also reviewed; conversely, we will survey emerging knowledge of the multiple mechanisms by which the protein C anticoagulant pathway can control the inflammatory response. DATA SOURCES: The information reviewed here was taken from the primary literature, including recent abstracts. STUDY SELECTION: All studies that bear directly on the interrelationship between the protein C anticoagulant pathway and inflammation were included, as was a summary of the initial clinical experience with protein C/activated protein C therapy in sepsis. DATA EXTRACTION AND SYNTHESIS: The results from each of the experimental approaches are summarized. Clinical experience with protein C supplementation in sepsis, although promising, is still in the early stages of study. CONCLUSIONS: The protein C anticoagulant pathway is a major mechanism in controlling microvascular thrombosis. Protein C deficiency that can occur in sepsis facilitates thrombin generation in the microvasculature, probably augmenting inflammatory responses and contributing to endothelial cell dysfunction. Animal studies and preliminary clinical results suggest that protein C/activated protein C supplementation may be useful in reversing microvascular dysfunction.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Summary
To examine the role of the protein C anticoagulant pathway in the regulation of microvascular thrombosis. The mechanisms by which inflammation impairs the function of this pathway are also reviewed; conversely, we will survey emerging knowledge of the multiple mechanisms by which the protein C...
Why This Matters for Hirudotherapy
This review examines the protein C anticoagulant pathway's role in regulating microvascular thrombosis, surveying both how inflammation impairs this pathway and how protein C may modulate inflammatory responses. The authors summarize experimental and preliminary clinical data suggesting that protein C deficiency during sepsis facilitates microvascular thrombin generation, contributing to endothelial dysfunction, and that protein C supplementation may help reverse this dysfunction. The abstract contains no mention of leeches, hirudin, or hirudotherapy at any point. Consequently, this article has no direct connection to the American Society of Hirudotherapy's domain, and any relevance would be limited to general background on anticoagulation physiology that is not specific to leech-based therapies.
Citation
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