Molecular regulatory mechanisms of depression-related thrombosis risk
Abstract
Background: This is largely because depression is a common psychiatric condition affecting more than 280 million people worldwide and is increasingly linked to an increased risk of thrombotic events, including deep vein thrombosis (DVT) and pulmonary embolism (PE). For example, underlying pathophysiological mechanisms remain inadequatly understood and thus further research on the association between depression, systemic inflammation, platelet activation and coagulation abnormalities is warranted. The objective of this study is to identify biological pathways linking thombosis and depression by examination of inflammatory and coagulation biomarkers, platelet activation, and risk of thrombosis independent predictors. In addition, the study investigates the possibility of nursing interventions in reducing thrombotic complications among depressed individuals.
Methods: A case control study was performed with 500 subjects (250 who had major depressive disorder and 250 healthy control subjects) were included. Enzyme-linked immunosorbent assays (ELISA) and quantitative polymerase chain reaction (qPCR) were employed to quantify key inflammatory (IL-6, TNF-, CRP) and coagulation (D-dimer, fibrinogen) biomarkers. An assessment of platelet activation (CD62P, PAC1 binding, GPIIbIIIa activation) was performed by flow cytometry. The study was carried out by a longitudinal follow-up over 12 months and by multivariate regression models to identify independent risk predictors.
Results: Thrombophilic and inflammatory parameters were significantly higher in depressed patients as compared to controls (p 0.001). The system was markedly hypercoagulable, as platelet activation markers were greatly upregulated. Through multivariate regression analysis, we determined that thrombosis risk was independent of severity level of depression (OR = 2.10, p 0.001), IL-6 levels (OR = 1.92, p 0.001), and platelet activation (OR = 2.50, p 0.001).
Conclusion: The results indicate that depression is an independent risk factor for thrombosis, through systemic inflammation and platelet hyperactivity. These results reinforce the value of licking psychiatric screening into thrombosis risk assessment and suggest the possible benefits of targeted anti-inflammatory or antiplatelet interventions in the psychiatric population at high risk of thrombosis.
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