A deficiency in Factor X may be hereditary or acquired. An acquired deficiency should be suspected when certain findings are present.


General features:

(1) negative family history of a bleeding disorder

(2) personal past history indicates normal coagulation function during childhood

(3) onset of a clinical bleeding disorder associated with a prolongation in both the PT and aPTT

(4) deficiency of factor X on coagulation factor assay


Clinical bleeding can be severe and may include:

(1) GI bleeding

(2) cutaneous bleeding

(3) intracerebral hemorrhage


Parameters to consider:

(1) isolated deficiency or mixed with other factor deficiencies

(2) deficiency of the factor or the presence of an inhibitor


A mixed acquired deficiency may occur in:

(1) liver disease

(2) vitamin K deficiency or coumadin therapy


An isolated deficiency may be seen in:

(1) amyloidosis

(2) with a circulating inhibitor


In Vitro Effect of Adding Normal Plasma


PT and aPTT normal

circulating inhibitor

PT and aPTT prolonged


In amyloidosis the Factor X is absorbed onto the amyloid fibrils. Therapy is directed towards reducing the amount of amyloid protein (control of underlying disease with chemotherapy; splenectomy if splenomegaly present and the patient is refractory to all therapy)..


The causes of a circulating inhibitor are uncertain but may be due to the presence of an autoantibody.


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