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.