Inflammation and Coagulation: A “Continuum” Between Coagulation Activation and Prothrombotic State

Review Article

J Blood Disord. 2015;2(1): 1023.

Inflammation and Coagulation: A “Continuum” Between Coagulation Activation and Prothrombotic State

Guido D’Angelo*

Laboratorio di Chimica-Clinica, Ematologia e Microbiologia Azienda Ospedaliera “S. Antonio Abate” Gallarate Varese, Italy

*Corresponding author: Guido D’Angelo,(Ematologia/Coagulazione) Laboratorio di Chimica-Clinica, Ematologia e Microbiologia, Azienda Ospedaliera“S. Antonio Abate” – Gallarate Via Pastori 4, Varese,Italy.

Received: February 20, 2015; Accepted: March 11, 2015; Published: March 19, 2015


The close relationship between inflammation and coagulation is expressed mainly in three stages: blood coagulation activation, a decrease in natural anticoagulants activity and fibrinolytic process decrease. The connection between inflammation and coagulation is now well established. The inflammation also acts on the antithrombotic endothelial normal functions. The loss of homeostasis in normal coagulation processes, promotes not only a stressed thrombotic condition, but it leaves the inflammatory process constantly turned on.

The inflammation/coagulation interaction could be represented like “a dog that bites its tail”.

The review also considers the main coagulation testing and some therapeutic indications. The latter, although experimental and more expensive, in severe sepsis can replace the deficiency of natural anticoagulants, as well as reduce the inflammatory state.

Keywords: Inflammation; Coagulation; Prothrombotic state; Endogen anticoagulant; Fibrinolysis; Coagulation tests


The severe and systemic inflammatory response may cause significant pathological damage. There is a thin line between inflammation and coagulation system, and often coagulation disorders are associated with inflammatory diseases.

In severe inflammation, the onset of coagulation disorder is due to the imbalance between coagulation and fibrinolysis activity, with a consequent hypercoagulable state. The outcome is a thrombotic condition with microvascular failure and the development of Multiple Organ Dysfunction Syndrome (MODS) [1-3].

Inflammation and coagulation

The activated coagulation, the endogenous anticoagulants down-regulation and the fibrinolysis inhibition, are the three main mechanisms by which inflammation occurs in the clotting process. During inflammation, the cytokines, which are immune system mediators, are released. The release of cytokine Interleukin-6 (IL- 6) stimulates the production of platelets [4]. In addition, several inflammatory mediators, such as bacterial endotoxins, thromboxane A2, Platelet Activating Factor (PAF) and the neutrophil cathepsin G enzyme, activate the platelets [5]. The production and activation of processes mediated by inflammation give thrombogenic characteristics to the platelets, resulting in increased sensitivity to platelet agonists. Platelet activation induced by inflammation can trigger a loop that perpetuates the inflammatory state through two conditions. In the first case, the activated platelet aggregate make the phospholipid surfaces able to trigger the secondary hemostasis by acquiring negative charge (Figure 1). The resulting production of Thrombin binds to specific cell surface receptors known as “Protease- Activated Receptor” (PAR) and is itself a strong inflammation mediator [6]. In the second case, the interaction between activated platelets and sub endothelial cells stimulates the adhesion and the recruitment of inflammatory leukocytes that release the cytokine Interleukin-1β (IL-1β), which is able to enhance the adhesion properties of endothelial cells [7,8] (Figure 1).