Abstract
Erythrocyte glutathione transferase (e-GST) is a detoxifying enzyme hyper-expressed in nephropathic patients and used recently as a biomarker for blood toxicity. Systemic sclerosis (SSc) is characterized by endothelial dysfunction and fibrosis of the skin and internal organs. Renal involvement is frequent in SSc patients. Here we show that e-GST is hyper-expressed in SSc patients (n=102) and correlates (R2=0.49, P<0.0001) with the Medsger DSS and DAI Valentini indices that quantify the severity and activity of this disease. Interestingly, e-GST does not correlate with the impairment of kidney or other specific organs taken separately. e-GST hyper-expression seems to be linked to the presence of a factor (i.e., toxin) that triggers the autoimmune disease, and not to the damage of specific organs or to oxidative stress. e-GST may be proposed as an innovative non-antibody biomarker for SSc useful to check the progress of this disease and the efficiency of new therapeutic strategies.
Highlights
The pathogenesis of Systemic sclerosis (SSc) is complex and, progress in the understanding of the multiple processes underlying SSc has been made in recent years, no single unifying hypothesis explaining all aspects of this disease exists.[4]
A very similar positive correlation was found, analyzing separately patients affected by the diffuse cutaneous SSc (dcSSc) as well as those affected by the limited cutaneous SSc (lcSSc) (Figures 1b and c and Table 1)
In the case of the Disease Activity Index (DAI), which gives a quantitative estimation of the degree of activity of this disease, we found a positive correlation with the expression of erythrocyte glutathione transferase Data are expressed (e-GST) both considering all sclerodermic patients (Figure 1d and Table 1; R2 1⁄4 0.49, Po0.0001) and when analyzing separately patients affected by the limited cutaneous or diffuse cutaneous scleroderma (Figures 1e and f and Table 1)
Summary
The pathogenesis of SSc is complex and, progress in the understanding of the multiple processes underlying SSc has been made in recent years, no single unifying hypothesis explaining all aspects of this disease exists.[4]. Received 09.4.13; revised 07.5.13; accepted 08.5.13; Edited by A Stephanou e-GST and scleroderma: a surprising correlation R Fabrini et al elevated e-GST levels that correlate with the gravity of the kidney disease,[7] and this property is likely caused by abnormal levels of circulating toxins not filtered efficiently by the kidney All these findings suggest that e-GST behaves like an endogenous biosensor, which reveals the levels of circulating toxic compounds and the efficiency of dialytic procedures.[8] The rationale of the present study was that SSc often causes kidney damage and a possible correlation might exist between the severity of this disease and e-GST expression. The aim of the present study was to verify if e-GST activity is correlated to the severity or activity of this disease as evaluated using the Medsger Disease Severity Scale (DSS) and the Valentini Scleroderma Disease Activity Index (DAI)
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