Abstract
Hypercoagulable state and neoangiogenesis are common phenomena associated with malignancy. Cancer patients have increased levels of circulating endothelium-derived microparticles (EMPs), which have been hypothesized to be involved in numerous pathophysiological processes. Hemostasis and angiogenesis are also activated in colorectal cancer (CRC) patients. The study aimed to investigate potential influence of chemotherapy on EMPs, thrombin anti-thrombin complex (TAT) and vascular endothelial growth factor (VEGF) levels in CRC patients undergoing chemotherapy. The study group consisted of 18 CRC patients: 8 stage III colon cancer (CC) and 10 stage IV rectal cancer (RC) patients. EMPs, TAT and VEGF levels were assessed before chemotherapy and after the third course. Results were compared with 10 healthy subjects. EMP concentration was measured by flow cytometry, while TAT and VEGF concentrations were assayed employing ELISA. Compared to the control group, CC and RC patients had significantly higher levels of tissue factor (TF)-bearing and non-TF-bearing EMPs before and after three courses of chemotherapy. VEGF concentrations in CRC patients were higher than in the control groups and increased following chemotherapy. TAT levels were elevated in CRC patients before chemotherapy compared to healthy subjects and significantly increased after the third course of chemotherapy. No significant correlation was found either between EMP and TAT levels, or between EMP concentrations and VEGF levels in the study group. CRC patients have increased EMPs, and TAT as well as VEGF levels tend to increase during chemotherapy.
Highlights
Close association between malignancy and blood coagulation disorders has been recognized for over 130 years [1]
Rectal cancer patients were given first line palliative chemotherapy (PC) according to the CLF1 regimen, which was a standard therapy in Poland at the time
tissue factor (TF)−endothelium-derived microparticles (EMPs) concentrations in rectal cancer (RC) patients were significantly higher in comparison with the control group before PC (1646 ± 884/μl vs. 834 ± 667/μl, p < 0.05), as well as after the 3rd course of chemotherapy (2087 ± 324/μl, p < 0.05) (Table 2)
Summary
Close association between malignancy and blood coagulation disorders has been recognized for over 130 years [1]. Cancer is one of the major independent risk factors for development of venous thromboembolic disease (VTE) [2, 3], which is the second most frequent reason for mortality in cancer patients [4, 5]. Cancer patients bear significantly higher (4–7-fold) risk of VTE than their healthy counterparts [6]. The risk of VTE is increased in colorectal cancer (CRC) patients [7]. Chemotherapy, for example, has been linked to 4.5 to 6-fold incremented risk of VTE [8]. Coagulopathy and angiogenesis are among the most consistent host reactions associated with malignancy
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