Inflammation as a cause of venous thromboembolism.
Review
Overview
abstract
Inflammatory markers are highly amenable to appraise and adjust and could already serve as a diagnostic indicator and also as a predictor of prognosis over the management of many health problems. Inflammation is implicated in venous thromboembolism (VTE). However there is still an intense curiosity about whether it is a cause or only a consequence of the thromboembolic process. The more likely scenario is that some inflammatory mediators contribute to the development of VTE, which per se induces an inflammatory reaction. Here we will review evidences supporting the role of inflammation as a cause of VTE. Genetic association studies have provided possible links between inflammation-related genetic variants, especially cytokines (e.g. IL-1, IL-4, IL-6, IL-10, and IL-13), and VTE, leading to establish the fundamental role of genetic background in predisposition to VTE and variable inflammatory processes in individuals. Additionally, several inflammation-related conditions including aging, autoimmune disease, cancer, cardiovascular diseases, hormone replacement therapy, infectious diseases, metabolic diseases, overweight or obesity, pregnancy or postpartum, respiratory diseases, and trauma have been associated with an increased risk of VTE. At this moment, despite their theoretical potential, to achieve the implementation of the inflammation-related laboratory tests in practice is a long task and future studies with larger sample sizes are required to address whether the properties of the inflammatory process, particularly intensity and duration, are useful in determining the risk of VTE and following outcomes.
