Coagulopathies and inflammatory diseases, ostensibly, have distinct underlying molecular bases. Notwithstanding, both are host defense mechanisms to physical injury. In invertebrates, clotting can function directly in anti-pathogen defense. Molecules of the vertebrate clotting cascade have also been directly linked to the regulation of inflammation. We posit that thrombophilia may provide resistance against pathogens in vertebrates. The selective pressure of improved anti-pathogen defense may have retained mutations associated with a thrombophilic state in the human population and directly contributed to enhanced inflammation. Indeed, in some inflammatory diseases, at least a subset of patients can be identified as hypercoagulable. Therefore, anticoagulants such as warfarin or apixaban may have a therapeutic role in some inflammatory diseases.
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