Ectopic liver is defined as liver parenchyma situated outside the liver proper with no connection to native hepatic tissue. This rare developmental anomaly is most commonly described as an attachment to the gallbladder with an incidence <0.3%, but it has been reported in other locations within the abdomen and thorax.(2-4) Most cases are found incidentally in asymptomatic patients, but ectopic liver has been known to cause visceral or vascular obstruction.(4,5) Herein we present a unique case of ectopic liver attached by a thin stalk seemingly floating in the suprahepatic inferior vena cava.
Both hereditary and acquired factors increase the risk of venous thromboembolism, thus the clinical management of affected patients involves evaluation of genetic factors that predispose to hypercoagulability. Factor V Leiden (R507Q) and factor II (prothrombin) mutation (G20210A) are the two most common inherited hypercoagulability disorders among populations of European origin. Both factor V Leiden and factor II mutation (G20210A) represent gain-offunction mutations: factor V Leiden causes resistance to activated protein C, and factor II mutation (G20210A) results in higher levels of plasma prothrombin. Herein, we present an uncommon case of combined factor V Leiden mutation (R507Q) and factor II mutation (G20210A), and discuss the prevalence and features of each entity, as well as their role in the clinical management of affected patients.
ABBREVIATIONSEDTA-ethylenediaminetetraacetic acid, VTE-venous thromboembolism, APC-activated protein C,
INDEX TERMSfactor V Leiden, factor II mutation (G20210A), prothrombin, warfarin Clin Lab Sci 2012;25(4):199
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