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Riccioni C., Sarcinella R., Izzo A., Stornelli G., Palermo G., Liguori M., Martocchia R., Moschetti B.
U.O. Angiologia, Ospedale “Nuovo Regina Margherita”, Roma
The annual risk of venous thrombosis in young women (<45 years) is about 1 in 10,000, which increases 4-6 fold in the course of hormonal therapy. Patients with moderate or low thrombophilia, such as factor V Leiden or Factor II mutation, have an incidence of thromboembolic diseases of 2.8% per year multiplied by 3.8% for patients using hormonal therapy. It is common opinion that the coagulation disorders due to mutation of the factor II gene appear randomly and combining one or more pathogenetic factors of thrombosis and risk factors. In June 2000, a young woman reported a sudden pain in the neck, a week after the appearance of a tumefaction with fever and asthenia. Histological examination of the swelling identified a single nodal lymphoadenopathy with dimensions 13.9±0.7 mm. At Duplex Scan we observed jugular vein thrombosis in corresponding to the place of nodal compression. The patient was using substitutive hormonal therapy per os (Fedra: gestodene+etinilestradiolo) started after a miscarriage 3 months into pregnancy. The patients immediately had antithrombotic therapy with calcic heparin at standard doses; hormonal therapy was promptly interrupted. By laboratory investigation we found: a) heterozigous gene of factor II mutation with a normal prothrombin activity of 96% (n.v.: 75-120) and a moderate increase in the aPTT 42.2 sec (n.v.: 25-40). b) seral positivity for Cytomegalovirus IgG of 86.56 UR/ml (n.v: 0.00-15.00: negative) and for Epstein Barr virus (1,34 positive). There were no clinical signs of hepatic disorder. The patient was checked weekly. After 3 months she was clinically healthy. Duplex Scan revealed the compressibility of the jugular vein wall with resolution of the thrombus. These data allow us to suppose the existence of the association of more risk factors such as minor coagulation deficiency, hormonal therapy, and local compressive events in the genesis of thrombotic phenomena in atypical sites.
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