Coexistence of endothelial dysfunction, fibrinolysis activation and diminished interleukin 6 level in morbid obesity

Iza Iwan-Ziętek, Katarzyna Szot, Małgorzata Michalska, Przemysław Adamczyk, Jacek Chojnowski, Krzysztof Góralczyk, Barbara Ruszkowska-Ciastek, Grażyna Bednarek, Tadeusz Sulikowski, Zbigniew Ziętek, Danuta Rość



Introduction: The aim of the study was to assess selected parameters of endothelial dysfunction and haemostasis in morbidly obese patients. So far, reports related to the disorders within the cells of the endothelium in morbid obesity are surprisingly sparse.

Materials and methods: The study was conducted in 74 morbidly obese patients with body mass index (BMI) >40 kg/m2 and in 30 healthy volunteers with normal BMI. The following tests were performed on the citrated plasma of venous blood: soluble Thrombomodulin concentrations (sTM), von Willebrand factor (vWF:Ag), tissue plasminogen activator antigen (t-PA:Ag), plasminogen activator inhibitor type 1 antigen (PAI-1:Ag) concentrations, and soluble fraction of selectin E and P (sE-selectin and sP-selectin) and interleukin 6 (Il-6) concentrations.

Results: The findings of the study indicate that there were markedly higher concentrations of sTM, tPA:Ag, PAI-1:Ag, sE-selectin and reduced concentrations of vWF:Ag and sP-selectin in the plasma of the patients with morbid obesity. The mean concentration of Il-6 was also significantly lower in morbid obesity.

Conclusions: Morbid obesity coexists with endothelial injury, which increases the risk of possible thromboembolic complications. Increased fibrinolytic system components and inhibition of platelet activation can be treated as compensatory mechanisms that reduce the risk of these complications. A decrease in Il-6 may be an indicator of inhibited inflammation, but it may also lead to increased susceptibility to infectious diseases.


morbid obesity; haemostasis; platelet; thromboembolic complications; inflammation


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