Tumor Necrosis Factor blockade in patients with Rheumatoid Arthritis inhibits Atherothrombosis.

Rationale:

Rheumatoid arthritis is associated with an increased incidence of atherosclerotic vascular disease. It is suggested that systemic inflammation is a risk factor for enhanced atherogenesis which is for instance also observed in SLE. In line with this, TNF-alpha is a central mediator of inflammation in RA and inhibition thereof may exert anti-atherothrombotic effects.


Objective:

In the current study we aim to establish whether TNF-alpha plays a central role in inflammation-mediated acceleration of atherogenesis and the propencity towards development of atherothrombotic disease in RA.


Study design:

This is an observational study in RA patients undergoing therapy with TNF-alpha blockade. Prior to receiving treatment surrogate markers for atherosclerosis, thrombosis, inflammation and angiogenesis will be assessed. These measurements will be repeated to evaluate short-term and long-term effects.


Study population:

We will include RA patients who are experiencing an inflammatory exacerbation of RA and who will be treated with TNF-alpha blockade.


Main study parameters:

Surrogate markers for atherosclerosis (endothelial function, glycocalyx), thrombosis (PMC, plasma markers), inflammation and angiogenesis (plasma markers).


Nature and extent of the burden and risks associated with participation, benefit and group telatedness: This is an observational study evaluating additional benefits (anti-atherothrombotic effects) of standard clinical practice (TNF-alpha blockade). Measurement of endothelial function and glycocalyx volume are routinely performed at the department of vascular medicine.

In the current study we aim to establish whether TNF-alpha plays a central role in inflammation-mediated acceleration of atherogenesis and the propencity towards development of atherothrombotic disease in RA.

N/A

TNF-alpha blockade.
(patients are their own control)