Skin Autofluorescence Is Not Increased in Patients with Systemic Sclerosis PDF Print E-mail
Thursday, 01 March 2012 15:52
M. E. Hettema, H. Bootsma, R. Graaff, R. de Vries, C. G. M. Kallenberg, and A. J. Smit
Received 24 May 2011; Accepted 8 August 2011

Vascular involvement is a key factor in major manifestations of systemic sclerosis (SSc), such as Raynaud’s phenomenon (RP), myocardial dysfunction, pulmonary hypertension, and renal involvement. Microvascular involvement, in which endothelial injury is present, is the main characteristic of SSc. Oxidative stress has been suggested as a major player in the process of endothelial dysfunction found in SSc. Endothelial damage may be induced by oxygen free radicals and reactive nitrogen species, generated locally by the inflammatory process and by periods of tissue ischemia followed by postischaemic reperfusion. This socalled ischaemic-reperfusion injury can be seen in RP. Increased levels of antibodies against oxidised low-density lipoproteins (LDL) and increased serum levels of 8-isoprostane, being markers of oxidative stress, have, indeed, been observed in SSc.

Oxidative or carbonyl stress, leading to formation of so-called reactive carbonyl compounds, is an important source for the generation of so-called advanced glycation endproducts (AGEs). AGE generation as a result of oxidative stress has also been found in inflammatory diseases, such as rheumatoid arthritis and SLE.

Tissue autofluorescence (AF) is a marker of the accumulation of AGEs, validated in different patient groups and healthy controls. Therefore, we assessed AGE accumulation in patients with SSc and hypothesized that AGE accumulation is increased in patients with SSc compared to healthy controls based on the presence of oxidative stress and endothelial dysfunction in SSc. We related AGE accumulation to the presence of disease-related and traditional cardiovascular risk factors.

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