
THE PROTHROMBIN FACTOR II G20210A MUTATION
WITH PULMONARY THROMBOEMBOLISM AND A
NORMAL LEVEL OF FIBRIN DEGRADATION PRODUCTS Nagorni-Obradovic Lj1,2, Miljic P1,3, Djordjevic V4, Pešut DP1,2*,
Jovanovic D1,2, Stojsic J2, Stevic R2, Radojkovic D4 *Corresponding Author: Dragica P. Pešut, School of Medicine University of Belgrade, Clinical
Centre of Serbia, Institute of Lung Disease and Tuberculosis, Research and Epidemiology
Department, Visegradska 26/20, 11000 Belgrade, Serbia; Tel.: +381-11-3615561; Fax: +381-11-
2681591; E-mail: dragica. pesut@ gmail.com page: 69
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INTRODUCTION
Pulmonary infarction usually results from pulmonary thromboembolism (PTE), and typically appears on radiological examination as a peripheral wedge-shaped density above the diaphragm [1,2]. Nodular opacities are rare and may not be distinguished from nodular infiltrates produced by malignant disorders, granulomatous disorders or infections [3]. It is generally accepted that normal plasma level of D-dimer (specific degradation products of cross-linked fibrin) excludes PTE, and argues in favor of an alternative diagnosis [4]. Surgical lung biopsy and histological examination may be required in order to establish the nature of nodular opacities [3]. In theory, surgical intervention in a patient with recent pulmonary infarction may increase the risk of additional thrombotic events, however, the occurrence of thromboembolic complications following surgical lung biopsy has not been reported. Appropriate perioperative antithrombotic prophylaxis in patients undergoing surgical biopsy, especially when blood hypercoagulability is also present, is essential to prevent thrombotic events.We here report on a patient with atypical pre-sentation of pulmonary infarction, who developed pulmonary embolism soon after open lung biopsy. Hematological investigation revealed the presence of thrombophilia which was then shown to be due to heterozygous FII G20210A mutation [5].
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