Rheumatology Advance Access originally published online on May 16, 2006
Rheumatology 2006 45(7):923-924; doi:10.1093/rheumatology/kel138
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LETTER TO THE EDITOR |
Response to Dr Cracowski
Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
Correspondence to: Shinichi Sato, MD, PhD, Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki 852-8501, Japan. E-mail: s-sato{at}net.nagasaki-u.ac.jp
SIR, We thank Cracowski for his interest in our study that showed elevated serum 8-isoprostane levels in patients with systemic sclerosis (SSc) and their correlation with lung fibrosis, vascular damage renal vascular damage and autoantibody production [1]. Previously, he investigated urinary 8-isoprostane levels in SSc patients [2,3] and suggested the limitations for determination of 8-isoprostane levels in serum samples from SSc patients.
Cracowski mentioned stability of 8-isoprostane in –80°C during different storage times and suggested that such a condition might cause the difference in serum 8-isoprostane levels between SSc patients and controls. As we described in our study, serum samples from SSc patients were collected over the last 7 years. However, all the control serum samples from healthy individuals used in our study were also collected during the same period. In fact, we studied the direct correlation between serum 8-isoprostane levels and the serum storage period; however, there was no significant correlation between them. Similarly, there was no significant difference in serum storage period between SSc patients and normal persons examined in this study. Although the possibility of auto-oxidation of ‘any’ samples could not be completely excluded, we believe that the difference of 8-isoprostane levels we detected was not due to the different storage periods.
He also suggested that renal failure associated with SSc might contribute to increased 8-isoprostane levels via decreased excretion. We presented in our study the correlation between serum 8-isoprostane levels and pulsatility index that reflects renal vascular damage. However, almost all patients examined in this study exhibited normal renal function despite the increased pulsatility index. Only one patient suffered from renal failure in our study. This reflected the fact that the frequency of scleroderma renal crisis in Japanese SSc patients (
2%) is much lower than that in Caucasian SSc patients (20%) [4]. The correlation between serum creatinine levels, which reflects renal function, and serum 8-isoprostane levels in SSc patients was also investigated in our study; however, no significant correlation was detected between them. Thus, serum 8-isoprostane levels in SSc patients did not correlate with the ‘renal failure’ in our study, indicating that elevated serum 8-isoprostane levels in SSc were not caused by decreased renal function. Finally, our finding that serum 8-isoprostane levels significantly correlated with clinical and laboratory parameters, such as lung fibrosis, lung function and autoantibody production, could not be explained by ‘auto-oxidization’. Collectively, these results indicate that our observation of elevated serum 8-isoprostane levels in SSc reflect the oxidative stress and that serum determination of 8-isoprostane levels is a useful clinical parameter for assessing it.
The authors have declared no conflicts of interest.
References
- Ogawa F, Shimizu K, Muroi E et al. Serum levels of 8-isoprostane, a marker of oxidative stress, are elevated in patients with systemic sclerosis. Rheumatology 2006.
- Cracowski JL, Marpeau C, Carpentier PH et al. Enhanced in vivo lipid peroxidation in scleroderma spectrum disorders. Arthritis Rheum 2001;44:1143–8.[CrossRef][Web of Science][Medline]
- Cracowski JL, Carpentier PH, Imbert B et al. Increased urinary F2-isoprostanes in systemic sclerosis, but not in primary Raynaud's phenomenon: effect of cold exposure. Arthritis Rheum 2002;46:1319–23.[CrossRef][Web of Science][Medline]
- Nishijima C, Sato S, Hasegawa M et al. Renal vascular damage in Japanese patients with systemic sclerosis. Rheumatology 2001;40:406–9.
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