Coagulation defects ‘do not protect against thrombosis’
MedWire News: Researchers in Italy believe they have cleared up the uncertainty over links between risk for adverse thrombotic events and coagulation defects.
Antonio Girolami (Padua City Hospital) and co-workers explain that it remains unclear whether defects of the contact phase of blood coagulation that are not associated with increased bleeding place patients at an increased risk of thrombosis. They therefore evaluated the incidence of thrombosis in 341 patients with deficiencies in factor (F)XII, prekallikrein, or kininogens.
Analysis of data from the 341 patients showed that 43 had experienced thrombosis. Specifically, 32 patients with FXII deficiency suffered a total of 16 arterial and 16 venous thrombotic events. Prekallikrein deficiency was associated with five arterial and four venous events, and kininogen deficiencies were linked to one arterial and one venous event.
Overall, the most common thrombotic event was myocardial infarction, accounting for 11 cases.
It has recently been suggested that FXII deficiency does not necessarily result in a pro-thrombotic state "since most, if not all patients with the deficiency who presented with thrombosis were also carriers of other congenital or acquired known risk factors," say the authors.
Similarly, the investigators write "the question is not settled for prekallikrein deficiency, since recent studies have demonstrated the occurrence of thrombosis in occasional patients."
The link between kininogen deficiency and thrombotic events also remains uncertain since very few cases have been reported, the researchers add.
Commenting on their results, the authors say that "the only sure conclusion that can be drawn from this study, is that the defects of the contact phase do not protect from thrombosis."
"This should not be surprising," add Girolami et al, "since thrombotic events, particularly arterial, have been noticed even in patients with severe bleeding conditions."
The results are reported in the Journal of Thrombosis and Thrombolysis.
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By Philip Ford