PhD ceremony: mw. K. de Leeuw, 16.15 uur, Academiegebouw, Broerstraat 5, Groningen
Thesis: Premature atherosclerosis in systemic autoimmune diseases
Promotor prof. C.G.M. Kallenberg
Faculty: Medical Sciences
Systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and Wegener’s granulomatosis (WG) are associated with a significantly increased prevalence of cardiovascular disease (CVD). Many risk factors are involved in the pathogenesis of atherosclerosis, the major underlying cause of CVD.
Intima-media thickness (IMT), as a marker for subclinical atherosclerosis, was increased in SLE and WG patients. Traditional risk factors cannot fully explain this increased IMT, and disease-related risk factors are contributing as well.
After follow-up, SLE patients had an increased IMT progression. However, IMT progression was not different between WG patients and controls, probably because disease activity was low and reduction of traditional risk factors was achieved during follow-up.
Measurement of endothelial dysfunction, as one of the earliest steps in the development of atherosclerosis, was performed using laser Doppler fluxmetry combined with iontophoresis. Endothelial function was impaired in SLE patients with Raynaud’s phenomenon. However, SLE patients without Raynaud’s phenomenon had no altered microvascular responses. In WG patients, this technique showed increased microvascular vasodilatation.
Recently, the accumulation of advanced glycation endproducts (AGEs) has been recognized as a contributing factor in the progression of atherosclerosis. AGEs were increased in SLE and were correlated to disease duration and IMT.
Furthermore, the development of atherosclerosis might be accelerated by the decreased quantity and quality of circulating progenitor cells (CPCs) found in SLE patients, as CPCs play an important role in the repair of vascular damage.
In conclusion, accelerated atherosclerosis in systemic autoimmune diseases is caused by a combination of traditional and disease-related risk factors. Therefore, reduction of traditional risk factors and control of disease activity may result in prevention of CVD in these patients.
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