Abstract
Deep vein thrombosis (DVT) is multi-causal disease associated to high morbidity and mortality due to complications, especially from pulmonary embolism. New factors of relevance on the DVT pathophysiology enhance our understanding of disease mechanisms and can be translated into improved management of patients, prevention of recurrence and development of new therapies. In this context, the precise role of platelets in the pathogenesis of DVT is not completely understood. Our objectives were to acquire and to analyze the whole platelet protein profile of samples from 3 DVT patients and to compare them to results obtained from 1 sibling and 1 neighbor from each patient (in order to minimize genetic and environmental interferences). These patients presented unprovoked and recurrent episodes of proximal DVT as well as a family history of DVT. Platelets were washed, lysed, and the proteins were hydrolyzed by trypsin. Peptides were first separated by HPLC and peptide fractions were further detected by LC-MS/MS. Five proteins was present on patients and absent in all the controls: Apolipoprotein A1 Binding-Protein, Coatomer (zeta1 sub-unit), 17β-hydroxysteroid dehydrogenase type XI, Leukotriene A-4 Hydrolase and Sorbitol Dehydrogenase. The analysis identified proteins that currently are not related to the pathophysiology of DVT, and the persistence of these inflammatory and lipid transportation-related proteins emphasize the relevance of these phenomena on DVT.
Highlights
Thrombosis is a multi-causal pathological process resulting from the activation and propagation of the hemostatic response
Platelets are important mediators of haemostasis and thrombin generation, and there is no doubt about their relevance in the pathophysiology of Venous thromboembolism (VTE)
We employed a proteomic approach to identify platelets proteins from unprovoked and recurrent deep vein thrombosis (DVT) patients and to compare to profiles obtained from their siblings and neighbors
Summary
Thrombosis is a multi-causal pathological process resulting from the activation and propagation of the hemostatic response. Venous thromboembolism (VTE) is considered a common disease, and its incidence ranges from 1 to 3 cases per 1000 individuals [1,2]. Nearly 25% develop recurrent VTE within 10 years. Several hereditary and acquired risk factors have been identified in the last two decades, but about 25% of patients present unprovoked deep vein thrombosis (DVT), without known risk factor [3]. Patients with the same genetic alteration can present diverse clinical characteristics, suggesting a possible interaction with other factors on DVT triggering. The identification of pathways involved on the pathophisiology of DVT would have great importance in clinical practice
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