PubMed · 13888181
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J DUCOS. 1961. [Normal hemostasis].. https://pubmed.ncbi.nlm.nih.gov/13888181/
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Venous thromboembolism (VTE) is a recognized complication of malignant disease and multiple risk factors contribute to the hypercoagulability that commonly accompanies malignancy. Thromboprophylaxis with antithrombotic drugs such as the low-molecular-weight heparins (LMWHs) can be used to control the hypercoagulable state and to reduce the incidence of VTE in patients with cancer. Clinical and biochemical data suggest that LMWHs may also inhibit tumor growth, leading to a survival benefit in these patients. Many cancer patients reportedly have a hypercoaguable state, with recurrent thrombosis due to the impact of cancer cells and chemotherapy or radiotherapy on the coagulation cascade. Studies have demonstrated that unfractionated heparin (UFH) or its low-molecular-weight fractions interfere with various processes involved in tumor growth and metastasis. Clinical trials in cancer patients with thromboembolic disorders have suggested a clinically relevant effect of LMWHs (as compared with UFH) on the survival of cancer patients with deep vein thrombosis. Similarly, the impact of warfarin on the survival of cancer patients with thromboembolic disorders was demonstrated in certain tumor types. Studies from our laboratory demonstrated a significant role for LMWH, warfarin, anti-VIIa, and LMWH releasable tissue factor pathway inhibitor on the regulation of angiogenesis, tumor growth, and tumor metastasis. However, a direct anticancer effect for heparin in cancer patients without thrombosis still remains to be clinically documented.
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Reperfusion fluids are administered routinely during surgical operations and following trauma. Studies performed wholly in vitro have indicated effects of some fluids on haemostasis through inhibition of platelet aggregation. Recently we performed a study to further evaluate the effects of reperfusion studies in vitro and also a study in a clinical setting to determine the extent to which the results of in vitro experiments can be extrapolated to the clinical situation. The results indicate that a combination of homeostatic and trauma response mechanisms complicate the ability to extrapolate from the findings in vitro.