CMAJ • July 6, 2004; 171 (1). doi:10.1503/cmaj.1040715.
© 2004 Canadian Medical Association or its licensors
All editorial matter in CMAJ represents the opinions of the authors and not necessarily those of the Canadian Medical Association.
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Letters
Correspondance

Mesothelioma and venous thrombosis

Ami Schattner

Hebrew University, Hadassah Medical School, Jerusalem, Israel

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

References

  1. Schattner A, Lugassy G, Klepfish A. Thromboembolism in pancreatic cancer. Pathogenesis, manifestations and management. In: Columbus F, editor. Progress in pancreatic cancer research. New York: Nova Science Publishers. In press.
  2. Schattner A, Kozack N. A 47-year-old man with mesothelioma and neck swelling. CMAJ 2004; 170(4):465. [Free Full Text]
  3. Lundberg GD. Low-tech autopsies in the era of high-tech medicine. Continued value for quality assurance and patient safety. JAMA 1998; 280: 1273-4.[Free Full Text]
  4. Sorensen HT, Mellemkjaer L, Steffensen FH, Olsen JH, Nielsen GL. The risk of a diagnosis of cancer after primary deep venous thrombosis or pulmonary embolism. N Engl J Med 1998; 338: 1169-73.[Abstract/Free Full Text]
  5. Suzuki S, Tanaka K, Nogawa S, Umezawa A, Hata J, Fukuuchi Y. Expression of interleukin-6 in cerebral neurons and ovarian cancer tissue in Trousseau syndrome. Clin Neuropathol 2002; 21: 232-5.[Medline]
  6. Esmon CT. Possible involvement of cytokines in diffuse intravascular coagulation and thrombosis. Baillieres Best Pract Res Clin Haematol 1999; 12: 343-59.[Medline]




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