How would you interpret a patient with prolonged PT and normal aPTT, normal fibrinogen, and normal platelets?

How would you interpret a patient with prolonged PT and normal aPTT, normal fibrinogen, and normal platelets?

• A. Isolated Factor VII deficiency or warfarin or vitamin K deficiency
• B. Hemophilia A
• C. DIC with hyperfibrinolysis
• D. Von Willebrand disease

Answer: (A)

Prolonged PT with a normal aPTT points to an issue in the extrinsic pathway, since PT measures tissue factor–activated clotting (factor VII) while aPTT probes the intrinsic pathway. When only the extrinsic pathway is affected, the most likely cause is deficiency or inhibition of vitamin K–dependent factors that feed into that pathway—most notably factor VII. This pattern can arise from true factor VII deficiency, or from vitamin K deficiency, or from anticoagulant therapy with warfarin, which lowers the vitamin K–dependent factors (II, VII, IX, X). Normal fibrinogen and normal platelets argue against a consumptive process or platelet disorder, which would typically disturb those components and usually affect both PT and aPTT. Hemophilia A would extend the aPTT (intrinsic pathway) rather than PT. Von Willebrand disease can affect bleeding and sometimes aPTT (via reduced factor VIII) but PT is typically normal. So the best interpretation is an extrinsic pathway issue due to factor VII deficiency or vitamin K–dependent factor deficiency (or warfarin effect).

Prolonged PT with a normal aPTT points to an issue in the extrinsic pathway, since PT measures tissue factor–activated clotting (factor VII) while aPTT probes the intrinsic pathway. When only the extrinsic pathway is affected, the most likely cause is deficiency or inhibition of vitamin K–dependent factors that feed into that pathway—most notably factor VII. This pattern can arise from true factor VII deficiency, or from vitamin K deficiency, or from anticoagulant therapy with warfarin, which lowers the vitamin K–dependent factors (II, VII, IX, X). Normal fibrinogen and normal platelets argue against a consumptive process or platelet disorder, which would typically disturb those components and usually affect both PT and aPTT. Hemophilia A would extend the aPTT (intrinsic pathway) rather than PT. Von Willebrand disease can affect bleeding and sometimes aPTT (via reduced factor VIII) but PT is typically normal. So the best interpretation is an extrinsic pathway issue due to factor VII deficiency or vitamin K–dependent factor deficiency (or warfarin effect).