Introduction
As the third most frequent cardiovascular disease, venous thromboembolism (VTE) can be divided into two types, i.e., deep vein thrombosis (DVT) and pulmonary embolism (PE). There are 100 to 200 cases of VTE per 100,000 people per year [1-3]. Although VTE can cause death in the acute phase or result in chronic illness and disability, it can usually be prevented. PE to the phenomenon of a substance in the bloodstream blocking the lung aorta or its branches, and the most common cause is DVT. Acute PE is the most serious clinical manifestation of VTE because it can be asymptomatic or discovered by chance, and in some situation, the initial manifestation of PE may even be sudden death. Thus PE is responsible for death, disability, and hospitalization of a large portion of patients [4, 5].
Anticoagulation is a recommended treatment for the patients with acute PE to prevent early death and recurrent symptoms of lethal VTE. For these patients, the standard treatment is a superposition of unfractionated heparin (UFH) with low molecular weight heparin (LMWH) or fondaparinux followed by a vitamin K antagonist (VKA) or a direct and reversible inhibitor of factor Xa (rivaroxaban, apixaban, dabigatran or edoxaban) is the standard treatment [1]. The common adverse reactions of these anticoagulant drugs are drug-induced liver injury and bleeding.
Due to that liver is the primary site to synthesize most of the coagulation factors and fibrin which are related to the coagulation process, it is logical that liver dysfunction may be related to the disorders of coagulation process and that the coagulation abnormalities become more pronounced as the liver disease progresses. Since liver can synthesize coagulation factors, including factors V, VII, IX, X, and Xi), and anticoagulation factors such as proteins, protein C, antithrombin (AT), fibrinolytic factors, etc., hemorrhage or thrombosis may occur in liver disease [6]. Furthermore, the level of vitamin K in patients with alcoholic fatty liver is often low, which reduces the produced amount of coagulation factorsⅡ,Ⅶ,Ⅸ, and Ⅹ, as well as anticoagulation factors, protein C, and protein S [7]. In this case, the shift to a balance between hemorrhage and thrombosis is a difficult point in clinical treatment. For patients with pulmonary embolism and fatty liver, how to rationally select anticoagulants is indeed a challenge for clinical pharmacists and doctors. This study reported a case of a patient with pulmonary embolism and fatty liver requiring anticoagulant therapy.