Hyperfibrinogenemia is associated with inflammatory mediators and poor prognosis in patients with gastric cancer
A proportion of human monocytes form long needles of fibrin on their surfaces when they are briefly exposed to human plasma. A number of coagulation factor deficient plasmas (II, V, VII, VIII, von Willebrand, IX, X, XI and XII) were tested for their ability to promote formation of this fibrin. Monocytes failed to make fibrin only in Factor II or prothrombin deficient plasma. Thrombin is involved in the manufacture of monocyte fibrin as shown by the ability of the thrombin specific inhibitor, hirudin, to block the process and by the demonstration that monocytes are able to cleave prothrombin to thrombin, an activity which increases with time of monocyte incubation at 37 degrees C. These results indicate that human monocytes possess a prothrombin cleaving activity although it remains unclear how this activity is generated. It is speculated that thrombin serves a necessary role in both wound healing and tissue repair.