著者

Ismail Sari Levent Kebapcilar Ahmet Alacacioglu Oktay Bilgir Yasar Yildiz Ali Taylan Arif Yuksel Didem L. Kozaci

出版者

The Japanese Society of Internal Medicine

雑誌

Internal Medicine (ISSN:09182918)

巻号頁・発行日

vol.48, no.16, pp.1363-1368, 2009 (Released:2009-08-17)

参考文献数

28

被引用文献数

29 35 28

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Objective Endothelial dysfunction is present in ankylosing spondylitis (AS). However, the etiology of events is still unclear. The aim of the present study was to investigate whether there are abnormalities in nitric oxide (NO) metabolism and endothelin-1 (ET-1) in AS patients. Methods Subjects without any classical cardiovascular (CV) risk factors were studied. Fasting glucose, serum lipids, high sensitive CRP (hsCRP), ESR, asymmetric dimethylarginine (ADMA) and ET-1 were studied. Patients were also evaluated with the Bath Ankylosing Spondylitis Metrology Index, Bath Ankylosing Spondylitis Functional Index, and the Bath Ankylosing Spondylitis Disease Activity Index. Results A total of 48 AS patients (38.6±10.6 years; 36M/12F) and 38 controls (36.4±11.1 years; 27M/11F) were studied. Acute phase reactants including hsCRP, and ESR were significantly increased in the patients group (p<0.05). Serum ADMA concentrations were also significantly higher in AS than in controls. Plasma levels of ET-1 did not differ between the groups (p>0.05). Comparison of three groups (conventional and anti-TNF treatment groups and controls) revealed that ADMA was significantly higher in the conventional treated AS than in controls. The levels of ADMA were not different between anti-TNF group and healthy subjects. Plasma ET-1 concentrations were similar between groups (p>0.05). Correlation analysis yielded significant correlations between ADMA, hsCRP, LDL cholesterol, HDL cholesterol and triglycerides (p<0.05). Conclusion The increased ADMA levels obtained in a group of relatively young AS patients who did not have classical CV risk factors suggest that NO metabolism is impaired in AS. On the other hand, anti-TNF treatments may have a beneficial effect on vascular function in AS.