Cancers: Earlier, we reviewed evidence that many cancers lead through the Egr-1/ cytokine mechanism to increased circulating levels of TF. Egr-1 can also lead to angiogenesis and neointimal hyperplasia during tissue repair. C-reactive protein activates macrophages, enhancing the destruction of injured endothelium. VEGF enhances the regeneration of the parietalis endothelium, thus protecting against DVT. It may therefore be predicted that VEGF inhibitors used in cancer therapy increase the risk of venous thrombosis (Gupta and Zhang 2005).
Septicaemia: Bacterial endotoxin causes slow loss of thrombomodulin and protein C receptor from the EC surfaces; it also promotes neutrophil binding to vein EC and enhances the production of E-selectin. For these reasons, bacterial infections - in particular those associated with septicaemia - may increase the likelihood of DVT. Septicaemia can be a sequel of inflammatory bowel disease, and this condition is sometimes noted as a distinct 'risk factor'.
Hormones: There is a very substantial literature on the relationships between hormone levels and thrombosis. The vast majority of this literature pertains to sex hormones used e.g. for oral contraception or hormone replacement therapy, and this matter was discussed briefly in Chapter 3. However, perturbed thyroid hormone levels also appear to increase the likelihood of DVT (as well as atherosclerosis); the mechanisms remain elusive (Squizzato et al. 2005), but protein C levels may be abnormally low (Nagumo et al. 2007). According to an intriguing recent paper, leptin increases TF production by peripheral monocytes, suggesting a possible reason why obesity is a 'risk factor' for DVT (Napoleone et al. 2007).
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