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Rivista di Angiologia
Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
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International Angiology 2009 August;28(4):298-302
Superficial venous thrombosis: role of inherited deficiency of natural anticoagulants in extension to deep veins
Milio G., Siragusa S., Malato A., Grimaudo S. 2, Pinto A. 2
1 Department of Internal Medicine, Cardiovascular and Nephrourological diseases, University of Palermo, Palermo, Italy
2 Biomedical Department of Internal and Special Medicine, University of Palermo, Palermo, Italy
Aim. Superficial venous thrombosis (SVT) has been considered for a long time a limited clinical condition of low importance, but this approach has changed in recent years, when several studies demonstrated that extension to deep veins occurs in 7.3 to 44% of patients, with high prevalence of pulmonary embolism. The aim of this study was to evaluate the prevalence of inherited deficiency of natural coagulation inhibitors in patients suffering from SVT in both normal and varicose veins, and to understand their role in extension to deep veins.
Methods. The study included 83 patients with SVT, without clinically obvious risk factors. Ultrasound examination was performed, and deficiencies of Protein C, Protein S and Antithrombin (AT) were investigated.
Results. In the patients where SVT occurred in normal veins, coagulation inhibitor deficiencies were 6.45% in the absence of extension and 62.5% in patients with extension to deep veins. In the patients with varicose vein SVT, the presence of these factors was less evident, but their prevalence was considerably higher in those with extension to deep veins (36.3%) than in non-extension (6.06%).
Conclusion. Present data confirm the role of inherited thrombophilic states related to inhibitor deficiency, considering them as risk factors for SVT in normal veins. Furthermore, an association has been found between their presence and the progression of SVT to deep veins.