Elevated prothrombin time activity may be caused by vitamin K deficiency, liver disease, use of anticoagulant drugs, genetic coagulation factor deficiency, disseminated intravascular coagulation, and other factors.
1. Vitamin K deficiency:
Vitamin K is a key cofactor in the synthesis of coagulation factors II, VII, IX, and X. Insufficient intake, such as long-term fasting, biliary obstruction affecting absorption, or broad-spectrum antibiotic use disrupting gut microbiota, may lead to reduced synthesis of vitamin K-dependent coagulation factors, manifested as prolonged prothrombin time and elevated activity. Mild deficiency can be improved by supplementing vitamin K or adjusting diet.
2. Liver diseases:
Liver diseases such as cirrhosis and hepatitis can reduce the synthesis ability of coagulation factors. The liver is the main site for the synthesis of coagulation factors II, V, VII, IX, and X. When liver function is impaired, the levels of these factors decrease, leading to an abnormal increase in prothrombin time activity. Patients often experience symptoms such as jaundice and ascites, and require targeted treatment for the underlying disease and monitoring of coagulation function.
3. Effects of anticoagulant drugs:
Vitamin K antagonists such as warfarin can interfere with the carboxylation process of coagulation factors and inhibit the activation of coagulation factors II, VII, IX, and X. High activity of prothrombin time during medication is an expected pharmacological effect and requires regular monitoring of INR values to adjust dosage and avoid bleeding risks.
4. Hereditary coagulation factor deficiency:
Rare hereditary coagulation factor II, V, VII deficiency can lead to prolonged prothrombin time. These patients may have abnormal bleeding tendencies from a young age and need to be diagnosed through coagulation factor activity testing. If necessary, plasma or specific coagulation factor concentrates may be administered for treatment.
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