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13-02-2011 | Cardiology | Article

Contact phase coagulation defects offer no thrombosis protection

Abstract

Free abstract

MedWire News: Defects of the contact phase of blood coagulation do not protect people with such defects from thrombosis, according to Italian researchers.

Antonio Girolami and colleagues from the University of Padua Medical School note that patients with clotting factor deficiencies associated with excessive bleeding, such as hemophilias and von Willebrand Disease (vWD), have occasionally been shown to present thrombotic phenomena.

However, "it is not clear yet whether defects of the contact phase of blood coagulation, which are not associated with a bleeding tendency, represent a mild prothrombotic state or not," they add.

The researchers therefore reviewed published data to evaluate the incidence of thrombosis in all reported patients with factor (F)XII, prekallikrein, and kininogen deficiencies.

Of 341 patients identified with these conditions, 43 (12.6%) had a thrombotic event, including 17 cases of deep vein thrombosis with or without pulmonary embolism, 11 myocardial infarctions, and nine ischemic stroke cases.

More specifically, thrombotic events occurred in 32 (13.9%) of 231 patients with FXII deficiency (16 arterial and 16 venous), nine (12.0%) of 75 patients with prekallikrein deficiency (five arterial and four venous), and two (5.7%) of 35 patients with total or high molecular weight kininogen deficiencies (one arterial and one venous).

Three patients with thrombosis had associated congenital risk factors: one heterozygous and one homozygous FV leiden deficiency, and one heterozygous antithrombin deficiency. A further 30 thrombosis patients had acquired risk factors including diabetes, hypertension, trauma, and obesity.

The researchers note that their findings probably do not represent the actual incidence of thrombosis in these patients because of the potential for reporting bias, with patients who develop thrombosis secondary to the clotting defect more likely to be identified than those who have the clotting defect but remain symptom-free.

Even so, "this study clearly indicates that the severe in vitro coagulation defect seen in these conditions does not protect from thrombosis," conclude Girolami and co-authors.

They add that the only two conditions that may provide protection from thrombosis are congenital FII and FX deficiency, as no patient with either of these defects has been reported to have thrombosis.

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2011

By Laura Dean

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