Mesothelioma and venous thrombosis
==================================

* Ami Schattner

We agree with Henry Schneiderman that in the patient we described1 the proximity of the tumour to the thrombosed vessels was far from coincidental and that the tumour was likely material to the pathogenesis of thrombosis. One of 2 mechanisms could be involved: either, as Schneiderman suggests, mechanical compression of proximal veins causing venous stasis or elaboration by the tumour cells of specific procoagulants, whose concentration and effects are more prominent close to their site of origin. Both mechanisms have been demonstrated in patients with adenocarcinoma of the pancreas.2 However, reports of thrombosis in patients with mesothelioma are much rarer than in patients with adenocarcinoma of the pancreas or lung, for example, which suggests that the first mechanism is the more likely in the case we described;1 the chest CT shown in our report is consistent with this hypothesis. The surgery report did not allude to the state of the veins, and, unfortunately,3 an autopsy was not authorized. As for our description of Virchow's triad, use of the word “epithelial” was a typographic error, and the text should have referred to “endothelial damage” (on page 465, third column).

The case reported by Mehlika Isildak and associates is an additional vivid reminder that cancer-associated thrombosis can affect veins at almost any site; it also emphasizes the greater risk with more advanced disease.1 However, thrombotic complications in mesothelioma remain an unusual occurrence in both early4 and advanced disease. Interleukin 6 (IL-6) may indeed be produced by mesothelioma and other tumours.5 It affects not only the number of platelets but, more important, their function. Platelets responding to IL-6 have increased sensitivity to activation by thrombin and increased procoagulant activity, which may be further enhanced by the elevated levels of fibrinogen and plasminogen activator inhibitor (which suppresses fibrinolysis) caused by IL-6 and other inflammatory mediators.6 The exact relevance of these observations to thromboembolism in vivo remains unproven.

**Ami Schattner** Hebrew University Hadassah Medical School Jerusalem, Israel

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