OBESITY AND THE CLOTTING CASCADE: MECHANISTIC INSIGHTS INTO HAEMOSTATIC ALTERATIONS

Ibrahim Kalle Kwaifa; Emmanuel Ifeanyi Obeagu

doi:10.22270/ujpr.v10i6.1463

Ibrahim Kalle Kwaifa Department of Haematology, School of Medical Laboratory Sciences, College of Health Sciences, UsmanuDanfodiyo University (UDU), Sokoto, North-Western, 2346, Nigeria.
Emmanuel Ifeanyi Obeagu Department of Biomedical and Laboratory Science, Africa University, Mutare, Zimbabwe. The Department of Molecular Medicine and Haematology, School of Pathology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.

10.22270/ujpr.v10i6.1463

Keywords:

Coagulation, fibrinolytic disorders, haemostasis, obesity

Abstract

Obesity is linked to the disruption of haemostasis. Numerous studies have indicated that obese individuals exhibit higher plasma concentrations of all pro-thrombotic factors, such as fibrinogen, von Willebrand factor, and factor VII in comparison to non-obese individuals. Additionally, elevated plasma levels of plasminogen activator inhibitor-1 have been studied in obese individuals compared to non-obese individuals. Moreover, obesity is marked by heightened plasma concentrations of anti-thrombotic agents, such as urokinase plasminogen activator, tissue-type plasminogen activator, and proteins C and S. The rise in these agents may be seen as protective measures to mitigate the impacts of the increased pro-thrombotic factors. The molecular connections between coagulation and fibrinolytic systems facilitate the targeted and efficient breakdown of fibrin accumulations, ensuring continuous blood flow and minimizing blood loss. The link between obesity, endothelial dysfunction, and haemostasis suggests that obesity features elevated levels of von Willebrand factor, fibrinogen, tissue factors, factor VII, VIII, and FX, which have been noted to promote a hypercoagulable condition. Although the coagulation and fibrinolytic systems collaborate to maintain the haemostatic equilibrium of the system, the fibrinolytic system functions to orchestrate the interactions among activators, zymogens, enzymes, cofactors, receptors, and inhibitors of fibrinolysis, facilitating the breakdown of fibrin deposits at the injury site without causing systemic negative effects. Thrombosis linked to obesity is one of the leading global health issues, and thus, continuous updates in this field are essential for improved comprehension of this treatable yet widespread condition.