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22-08-2011 | Cardiology | Article

Superficial vein thrombosis may increase VTE risk

Abstract

Free abstract

MedWire News: Clinically diagnosed superficial vein thrombosis (SVT) is associated with an increased risk for venous thromboembolism (VTE), show results of a population-based study conducted in the Netherlands.

Previously called thrombophlebitis, SVT is regarded a self-limiting disorder, although recent studies showed that ultrasonographically diagnosed SVT is a precursor for VTE, explain Suzanne Cannegieter and colleagues from Leiden University Medical Center.

"While current literature defines 'real' SVT as a disorder diagnosed both clinically and through an ultrasound, in reality, clinical practice does not necessarily follow this model. In fact, most physicians are able to identify SVT by the presence of a red, painful, palpable cord in the course of a patient's superficial vein, for which additional testing with ultrasound is not necessary," said Cannegieter.

"However, it is uncertain whether patients with clinically diagnosed, but not necessarily ultrasonographically confirmed SVT are at risk of VTE and whether this risk can be explained by underlying thrombogenic causes," the researchers add.

To investigate, Cannegieter and team reviewed data for 4290 patients with VTE (deep vein thrombosis [DVT] or pulmonary embolism [PE]) and 5754 controls without the condition who participated in the MEGA study, a large, population-based, case-control study that assessed VTE risk in the Netherlands between 1999 and 2004.

At study entry, the prevalence of SVT was 10% in patients and 2% in controls.

The researchers report, in the journal Blood, that participants with prior SVT were a significant 6.3 times more likely to develop DVT and 3.9 times more likely to develop PE than controls, during the study.

When the team assessed whether the presence of a thrombophilia could explain the association between SVT and VTE, they found that having a non-O blood group and carrying the factor V Leiden mutation were associated with a marginal increase in SVT risk in controls.

Adjusting for these factors only slightly attenuated the association between SVT and DVT, suggesting that, while a small part of the association could be explained by prothrombotic mutations, it is likely that other factors (varicosis, obesity, stasis) also play a role in SVT etiology, the researchers remark.

"Our results, which are in line with recent studies that regard SVT diagnosed by ultrasonography as a precursor of VTE, show that a history of clinically diagnosed SVT is a risk factor for future VTE," said Cannegieter.

"We recommend that clinicians should actively ask patients for a history of clinically diagnosed SVT and use this information in their risk stratification analysis.

"Furthermore, people who experience symptoms of SVT are advised to see a doctor, particularly when these symptoms do not pass or grow worse, as SVT appears not to be a separate and benign form of venous thrombosis, as previously thought," she concluded.

By Laura Dean

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