Rheumatology Advance Access originally published online on August 25, 2006
Rheumatology 2006 45(10):1319-1320; doi:10.1093/rheumatology/kel261
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Impaired endothelial function in patients with ankylosing spondylitis: reply
Division of Rheumatology, Department of Internal Medicine, Dokuz Eylul University School of Medicine, Turkey
Correspondence to: N. Akkoc, Dokuz Eylul Universitesi Tip Fakultesi, Ic Hastaliklari AD, Romatoloji BD 35340 Inciralti, Izmir, Turkey. E-mail: nurullah.akkoc{at}deu.edu.tr
SIR, We thank Pieringer for his interest and valuable comments on our recent publication [1].
The association between endothelial dysfunction [2] and smoking has clearly been demonstrated in various studies as pointed out quite rightly by Pieringer [3–6]. Acute [6], chronic [4] and even passive smoking [3] have been shown to be associated with impaired endothelial function. Nonetheless, smokers were not excluded from our study, because of high prevalence of smoking among Turkish adults, which has been reported to be about 44% [7]. However, as explained in the manuscript, the percentages of smokers were similar both in ankylosing spondylitis (AS) patients and healthy controls, 37 and 35%, respectively. The only differences between the baseline clinical and laboratory characteristics of the patients and controls were inflammatory markers [erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and fibrinogen] and Bath Ankylosing Spondylitis Metrology Index (BASMI), suggesting that the disease itself may be responsible for the impaired endothelial function [1]. This is further supported by the subgroup analysis including only non-smokers, which still shows a lower flow-mediated dilation (FMD) in patients with AS compared with the controls (Table 1).
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The effect of smoking on endothelial function was not the focus of this study. However, to satisfy Pieringer's curiosity, we have made a subgroup analysis comparing smokers with non-smoking individuals regardless of their disease status which has revealed only a slightly reduced FMD in smokers compared with the non-smoking individuals (Table 1). The lack of correlation between smoking and endothelial function may probably be due to the definition of smokers and non-smokers in our study. Subjects classified as smokers and non-smokers based on their self-report at the time of interview in our study may be quite different than the subjects described in those studies that Pieringer has cited in which non-smokers had never smoked. But, our non-smoker group may actually have included former smokers. Moreover, the dose of smoking in the smokers may be less in our study, which was not aimed at studying the effect of smoking on FMD. In one of the studies [4], smokers had smoked at least 20 cigarettes per day for 1 yr and average cigarette consumption in these subjects was 16 pack-years. In the second study, one group of smokers had smoked an average of 17 cigarettes per day for 5–15 yrs, and another group of smokers had smoked an average of 21 cigarettes per day for more than 15 yrs [8]. Average cumulative cigarette consumption was 12 pack-years in the third study [9]. The first two studies also suggested that impaired endothelial function due to smoking is dose related [4, 8]. Thus, we believe that the inconsistency between our study and those studies may be due to the difference in dose of smoking of the subjects studied.
In conclusion, because the proportion of smokers and non-smokers were quite similar in patient and control groups, and presence of decreased FMD in AS patients compared with controls even when only non-smokers are analysed, we believe AS may be associated with impaired endothelial function.
The authors have declared no conflicts of interest.
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