MVT is the least common and has the most

MVT is the least common and has the most favorable outcome amongst the three AIID categories. Resembling other venous thrombotic diseases, the most common MVT etiologies include venous stasis and heritable or acquired hypercoagulable states, which may be caused by thrombophilia, malignancies, intraabdominal infections, major operations, portal hypertension, or idiopathy. Activated protein C resistance, protein C or S deficiency, lupus anticoagulant, and factor V Leiden and prothrombin G20210A mutations have been reportedly associated with MVT. Otherwise, hypercoagulability is not associated with most AOMI cases. Hypercoagulability-related AOMI is reported only in one case report, highlighting its rare occurrence.
Thrombophilia screening is recommended for patients with unexplained, recurrent, or unusually located venous thromboembolism (VTE) and for young patients with VTE (less than 50 years). Antithrombin III, proteins C and S, factor V and prothrombin mutations, lupus anticoagulant, antiphospholipid antibodies, and occult malignancy should be screened. Routine screening for thrombophilic conditions is not recommended in most cases of arterial thromboembolism; however, recent studies have reported that venous and arterial thromboses may share some risk factors, such as age, metabolic syndromes, and inflammatory conditions. The coagulation process or platelet activation is critical in the development of both venous and arterial thrombosis. Thus, appropriate screening for hypercoagulability benefits patients with recurrent and multiple arterial thromboses and those without typical risk factors for arterial thromboembolism.
During thrombin and fibrin production, factor VIII is activated and forms a complex with activated factor IX. Factor VIII and von Willebrand factor circulate in the plasma as a complex, and a deficiency of these factors cause the inherited bleeding disorders, purchase SIRT1/2 Inhibitor IV A and von Willebrand disease, respectively. An elevated plasma level of factor VIII is positively associated with VTE. Although inconsistent, some studies have shown that factor VIII elevation is an independent risk factor for coronary artery disease and ischemic stroke. Although the reason for factor VIII hyperactivity remains unclear, hereditary factor VIII elevation is strongly believed to be a potential cause. To our knowledge, this is the first report in English reporting AOMI associated with an elevated level of factor VIII.
Except for DNA testing for factor V Leiden and prothrombin G20210A mutations, thrombophilia screening test results can be altered during an acute thrombotic phase, inflammatory state, or with anticoagulant therapy. The thrombophilia test requires a detailed explanation for patients receiving anticoagulant treatment because warfarin inhibits the vitamin K-dependent synthesis of clotting factors. A long-term warfarin usage suppresses protein C synthesis. Furthermore, warfarin reduced the plasma level of protein C in our patient to slightly below the normal range (Figure 2B). Although unaffected by anticoagulants, factor VIII is an acute-phase reactant and thus a later measurement is necessary for confirming the activity of factor VIII. The plasma factor VIII level in our patient was high at 64 months postoperatively, confirming the intrinsic hyperactivity of factor VIII. Therefore, a lifelong anticoagulant therapy is indicated to prevent the recurrence of arterial thrombosis.


Esthesioneuroblastoma (ENB), also known as olfactory neuroblastoma (ONB), is a rare type of neuroectodermal tumor, generally originating in the specialized olfactory epithelium of the upper nasal cavity. It often invades the orbital space and anterior skull base. Treatment strategy includes a wide range of surgical resection plus adjuvant postoperative radiotherapy and chemotherapy. The overall prognosis mainly depends on the histological grade and severity of the tumor invasion.