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

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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