Experimental study demonstrates factor XI supports thrombin generation without factor XII, suggesting alternative coagulation pathways promote clot formation.
Factor XIa (FXIa), the activated form of the plasma zymogen FXI, is a trypsin‐like protease that contributes to thrombin generation and hemostasis primarily by activating factor IX (FIX).1 In humans, severe FXI deficiency may cause excessive bleeding with trauma or surgery, particularly when injury involves the mouth, nasopharynx, or urinary tract.2,3 Bleeding severity varies, and many individuals who are FXI deficient do not experience abnormal hemostasis. A variable trauma‐induced bleeding disorder has also been reported in FXI‐deficient dogs,4 cats,5 and cattle.
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Mohammed et al. (2022) studied this question.
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