Association between venous thromboembolism and acute pancreatitis: An analysis from the nationwide inpatient sample

Abstract

Background and Aims Acute inflammation of the pancreas may trigger a systemic inflammatory response and initiate coagulation. Few studies have been conducted on the association between venous thromboembolism (VTE) and acute pancreatitis (AP). We investigated the incidence and risk of VTE in patients with AP. Methods We conducted a retrospective cohort analysis for the nationwide AP cohort. We identified 91 786 patients with AP and 183 557 controls who were frequency‐matched according to sex, age (5‐y interval), and index year from the National Health Insurance Research Database between 2000 and 2008. The patients and controls were followed until diagnosis of deep vein thrombosis (DVT) or pulmonary embolism (PE), death or the end of 2011. Results The nationwide cohort study showed that patients with AP exhibited a higher incidence of VTE (13.1 vs 5.65 per 10 000 person‐y) than did the controls. After covariates were controlled for, the patients with AP had a 1.88‐fold higher risk of VTE than did the controls (adjusted hazard ratios [aHR] = 1.88; 95% confidence intervals [CI] = 1.68‐2.10). The incidence rates of DVT and PE were higher in the patients with AP than in the controls, irrespective of sex, age or comorbidity. The patients with AP exhibited a 1.86‐fold higher aHR of DVT (95% CI = 1.63‐2.12) and a 1.92‐fold higher aHR of PE (95% CI = 1.59‐2.31) than did the controls. Conclusion Patients with AP exhibited a significantly higher risk of VTE than did the controls.

Construction and validation of risk prediction model for deep vein thrombosis in acute exacerbations of chronic obstructive pulmonary disease based on serum angiopoietin 2 levels

“…The occurrence and development of thrombotic diseases are not only related to abnormal blood coagulation and fibrinolysis processes but also to intravascular inflammation. Chung et al (32) showed that thrombosis is also an inflammatory reaction process because there is a close relationship between inflammatory reaction and thrombosis. The massive release of inflammatory mediators and the damage to the vascular endothelium during infection leads to platelet adhesion and aggregation.…”

“…Sahni et al (35) also reported that the serum level of Ang-2 is positively correlated with inflammatory mediators such as TNF-α and interleukin 6, and these two inflammatory factors have been proved to be risk factors for DVT in many studies. As a pro-inflammatory factor, Ang-2 plays an important role in the physiological activities of promoting inflammation and vascular leakage (32). D-dimer is not only the smallest fibrin degradation product but also a specific degradation product of the fibrous matrix of venous thrombosis.…”

Chemoprophylaxis to Prevent Deep Venous Thrombosis in Patients Hospitalized for Pancreatitis: Beneficial or Harmful?

“…They showed that this cohort is at a higher risk for VTE than the control patients, irrespective of age, sex, or comorbidities. The patients showed a 1.86-fold higher adjusted hazard ratio (aHR) of DVT and a 1.92-fold higher aHR of pulmonary embolism than did the controls [ 10 ].…”

Acute venous thromboembolism in acute pancreatitis based on the severity: a retrospective cohort study

“…Due to pancreatitis, the systemic acute inflammatory process increases pro-inflammatory markers such as TNF-alpha, IL-1, IL-6, IL-10, which then trigger the activation of the coagulation cascade, prevent fibrinolysis, and prevent regular anticoagulation pathways from functioning. [5] Endothelial vasculature is disrupted through the activation of inflammatory markers, leading to the weakening of vessel walls. This, in turn, leads to impediment of blood flow and stasis which allow for ensuing thrombus formation.…”