Produced in the liver FX when activated cleaves prothrombin to generate thrombin in the intrinsic pathway of coagulation.

This process is vitamin K dependent and enhanced by activated factor V. The condition may be inherited or, more commonly, acquired.

Symptoms may differ greatly, as apparently modifiers control to some degree the amount of FX that is produced.

Other bleeding can be encountered in muscles or joints, brain, gut, or urine[1][2] While in congenital disease symptoms may be present at birth or show up later, in patients with acquired FX deficiency symptoms typically show up in later life.

[citation needed] In the acquired form of FX deficiency an insufficient amount of factor X is produced by the liver due to liver disease, vitamin K deficiency, buildup of abnormal proteins in organs (amyloidosis) or certain medications (i.e.

[4] Treatment of FX deficiency in amyloidosis may be more complex and involve surgery (splenectomy) and chemotherapy.