1 Contrast-enhanced computed tomography findings. to chronic period pulmonary thromboembolism for most patients. However, the effects of DOAC on acute pulmonary thromboembolism (APTE) in patients with antiphospholipid syndrome (APS) remain obscure. The standard treatment for thrombotic APS is initial anticoagulation with unfractionated heparin or a low-molecular-weight heparin followed by warfarin. DOAC may be useful for some APTE patients with APS. strong class=”kwd-title” Keywords: Anti-cardiolipin antibody, Lupus anticoagulant, Thrombus, Venous thromboembolism Introduction Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by arterial, venous, or microvascular thrombosis and/or obstetric morbidity in association with persistent antiphospholipid antibodies (APLA), such as lupus anticoagulant (LA) and anti-2-glycoprotein I (anti-2GPI) antibody, and/or anti-cardiolipin MG-132 (ACL) antibodies. The most prevalent type of venous thrombosis associated with APS is deep vein thrombosis (DVT) in the lower extremities with or without pulmonary thromboembolism. Direct oral anticoagulants (DOAC) have become agents of first choice in the treatment of acute to chronic period pulmonary thromboembolism for most patients [1]. However, the effects of DOAC on acute pulmonary thromboembolism (APTE) in patients with APS remains obscure. We describe a patient with primary APS and venous thromboembolism (VTE) that disappeared while under the oral DOAC rivaroxaban. The patient has remained on rivaroxaban for two years and has been free of recurrent VTE. Case report A 73-year-old man with no medical or family history, or a history of cigarette smoking or alcohol consumption, suddenly developed dyspnea while gardening two days before admission. He attended a local general practitioner because the dyspnea persisted. Electrocardiographic findings and swollen lower extremities indicated venous thromboembolism (VTE) and he was referred to our hospital. On admission, his vital signs were as follows: blood pressure 170/93?mmHg, heart rate 94?bpm, body temperature 36.9?C, respiratory rate 12 breaths/min, and oxygen saturation of 96% on 2?L/min oxygen via nasal cannula. He was 160?cm tall, weighed 75?kg, and had a body mass index of 29.3?kg/m2. Respiratory sounds were normal, and no heart murmur was evident. Both lower legs were swollen and warm to the touch, the left more than the right. Electrocardiography (ECG) showed sinus rhythm, a heart rate of 92 bpm and negative T waves in leads III and V1-2. A chest X-ray revealed mild TMPRSS2 enlargement of the bilateral hilar pulmonary arteries and cardiomegaly, with a cardiothoracic ratio of 52%. Echocardiography showed mild, right ventricular dilation and mild pulmonary hypertension (tricuspid valve regurgitation MG-132 pressure gradient, 38?mmHg) with normal right ventricular function (tricuspid annular plane systolic excursion, 1.9?cm; fractional area change, 38%). Laboratory data upon admission revealed mildly reduced platelets 151,000/L, and elevated high-sensitivity troponin T 0.042?ng/mL, C-reactive protein 1.27?mg/dL, N-terminal pro-brain natriuretic peptide 867?pg/mL, fibrinogen MG-132 degradation product 30.0?g/mL, and D-dimer 11.6?g/mL. Normal renal function was indicated by blood urea nitrogen 24?mg/dL and creatinine 0.73?mg/dL. Arterial blood gas analysis on 2?L/min oxygen by nasal cannula revealed normoxia (PO2, 83.6?mmHg), hypocapnia (PCO2 29.7?mmHg), and mild lactic acidemia (lactate 1.9?mmol/L) with a pH of 7.463. Ultrasound imaging revealed venous thrombi in the left popliteal and soleal veins in the lower extremities. Contrast-enhanced computed tomography (CT) revealed several thrombi in the bilateral pulmonary arteries (Fig. 1A, B) in addition to the thrombi in the left popliteal vein (Fig. 1C). There was no finding on CT and laboratory data that suggested cancer, and the present patients pulmonary embolism severity score (PESI) was 93 points [Class III (intermediate risk)]. Open in a separate window Fig. 1 Contrast-enhanced computed tomography findings. Findings on admission show multiple thrombi in bilateral pulmonary arteries (arrows; A, B) and thrombus in the enlarged left popliteal vein (arrow; C). Findings at 15 days after admission show that bilateral pulmonary arteries are almost completely free of all thrombi (D, E) and that thrombus in the left popliteal vein has decreased in size (arrow; F). Hemodynamically stable APTE with DVT was diagnosed and therapy with the DOAC rivaroxaban was immediately started at a dose of 15?mg twice.
1 Contrast-enhanced computed tomography findings