2006
DOI: 10.1093/annonc/mdl140
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Chemotherapy with bevacizumab, irinotecan, 5-fluorouracil and leucovorin (IFL) associated with a large, embolizing thrombus in the thoracic aorta

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Cited by 17 publications
(8 citation statements)
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“…Combined modality treatment consisting of chemotherapy, radiotherapy, and the antiangiogenic agent thalidomide led in NSCLC patients to excessive toxicity as well as a higher incidence of thromboembolic events [48], as already seen in previous studies in other malignancies. Yoon and coworkers [49] reported that chemotherapy with bevacizumab, irinotecan, 5-fluorouracil, and leucovorin was associated with a high incidence of thromboembolism.…”
Section: Discussionmentioning
confidence: 99%
“…Combined modality treatment consisting of chemotherapy, radiotherapy, and the antiangiogenic agent thalidomide led in NSCLC patients to excessive toxicity as well as a higher incidence of thromboembolic events [48], as already seen in previous studies in other malignancies. Yoon and coworkers [49] reported that chemotherapy with bevacizumab, irinotecan, 5-fluorouracil, and leucovorin was associated with a high incidence of thromboembolism.…”
Section: Discussionmentioning
confidence: 99%
“…7,10,11 Thus, we can only speculate that the rapid growth of the AAA might have been induced by the toxic effects of chemotherapy, even though there is only an anecdotal report to support this assumption. 9 Acute cardiac toxicity of 5-fluorouracil is a well-known adverse event, 12 but thrombus formation in a normal aorta 13,14 and aortic dissection 15 represent other and very rare cardiovascular adverse events of chemotherapy. The disturbed synthesis of DNA, collagen, and elastin, release of cytokines, inhibition of smooth muscle cell proliferation, and induction of metalloproteinases are so far predominately hypothetically formulated effects of chemotherapeutics that might induce AAA development.…”
Section: Discussionmentioning
confidence: 99%
“…77,78 Endothelial damage, reduction of endothelial renewal capacity, exposure of subendothelial collagen, subsequent tissue factor activation and overexpression of proinflammatory cyclooxygenase2 and Eselectin genes all lead to activation of the coagulation pathway, thereby causing intravascular thrombosis. [79][80][81] Scappaticci et al reported the absolute rate of arterial thromboembolic events as 5.5 events per 100 personyears in their popula tion of patients concurrently receiving bevacizumab and chemotherapy. 82 Pereg and Lisher reported that lowdose aspirin effectively prevented cardiovascular complications in patients receiving bevacizumab who were 65 years or older with a prior history of cardiovascular ischemic events.…”
Section: Malignancy Treatment-related Thrombotic Events Chemotherapymentioning
confidence: 99%