Thrombin generation in severely obese children

Abstract

In recent years the prevalence of obesity has raised to an alarming level. Especially the increasing rate of obese children across all pediatric ages is a cause of concern. Several studies made likely a close connection between obesity and alterations in hemostasis by findings that obese subjects tend to have higher values of fibrinogen, prothrombin fragment 1 and 2 (F1 + 2), factor VII, factor VIII, von Willebrand factor (vWF), and plasminogen activator inhibitor (PAI) compared to non-obese subjects [1, 2]. These hemostatic alterations in obese patients may contribute to the development of cardiovascular disease. Despite its undisputed importance, data on single factors or components involved in the coagulation cascade reflect only a small part of the complex hemostaticthrombotic system and cannot replace an overall function test [3]. Therefore, we investigated the general influence of obesity in childhood on thrombin generation (TG) performing the Calibrated Automated Thrombography (CAT) representing a global test of the blood clotting system. In contrast to various conventional clotting tests, such as the partial thromboplastin time (PTT) or the prothrombin time (PT), the TG - assay is sensitive to hypercoagulable changes in the plasma [4].Measurements of the TG represent a method to estimate the individual thrombotic risk by assessing the coagulability of blood, and - determined with platelet poor plasma - reflect the function of all plasmatic pro- and anticoagulant factors [5]. The area under the curve of generated thrombin represents the so-called «endogenous thrombin potential (ETP)» and has been shown to correlate with plasma-based hypercoagulable states [4]. In this study we compared the TG of obese children with that of healthy, normal weight, and age matched controls by means of the CAT. © 2007 Springer Verlag Berlin Heidelberg.