Abstract
Objective. To investigate whether advanced glycation endproducts (AGEs) in the skin are increased in patients with systemic sclerosis (SSc) and are related to the presence of disease-related and traditional cardiovascular risk factors. Methods. Skin autofluorescence, as a measure for the accumulation of AGEs, was assessed by measuring UV-A light excitation-emission matrices (AF-EEMS) in 41 SSc patients and 41 age- and sex-matched controls. Traditional cardiovascular risk factors and disease-related risk factors were recorded. Results. Skin AF-EEMS did not differ between SSc patients and controls (1.68 ± 0.58 a.u. versus 1.63 ± 0.41 a.u., P = 0.684). Skin AF-EEMS in SSc patients was associated with levels of CRP (r = 0.44, P = 0.004), Medsger's severity scale (r = 0.45, P = 0.006), and use of agents intervening in the renin-angiotensin system (r = 0.33, P = 0.027). When analysing SSc patients and controls together, in multivariate analysis, only age and use of agents intervening in the renin-angiotensin system were independently associated with AF-EEMS. Conclusion. These data demonstrate that skin AGEs are not increased in SSc patients.
Highlights
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
We demonstrated that skin AF as a marker of tissue advanced glycation endproducts (AGEs) accumulation is not increased in SSc patients, while expected relations with age, prevalence of CVD, and CRP were found
AF-Excitation Emission Matrix Scanner (EEMS): autofluorescence obtained by the Excitation-Emission Matrix Scanner; ACE: angiotensin-converting enzyme; ATII: angiotensin II
Summary
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 [1, 2] 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. 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 [3, 4]. AGE generation as a result of oxidative stress has been found in inflammatory diseases, such as rheumatoid arthritis and SLE [9,10,11,12,13,14,15]
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