Objective: To establish the association between serum levels of reactive oxygen species (ROS) products, nitric oxide (NO) radicals and ascorbate radicals with renal resistive index (RRI), common carotid artery resistive index (CCARI) and intima-media thickness (IMT) in gout patients, and to find out whether the connection is more pronounced when tophi are present.
Methods: A cross-sectional study including 71 consecutive gout patients, divided into two groups according to the presence of subcutaneous tophi. Serum concentrations of ROS products, NO radicals and ascorbate radicals were determined by ex vivo electron paramagnetic resonance (EPR) study. RRI was measured in both kidneys at the level of interlobar arteries with 3.5 MHz transducer. By applying ultrasound of the common carotid arteries, conducted with 10 MHz linear transducer CCARI and IMT were measured.
Results: Gouty arthritis without tophi and gouty tophi subjects were age-matched. Serum uric acid and distribution of conventional cardiovascular risk factors was equal in the groups. However, in tophi patients CRP and the number of individuals who had suffered a cardiovascular event were higher. In the two stages of the disease serum levels of ROS products, NO radicals, ascorbate radicals, as well as RRI and CCARI were comparable but intima-media was thicker in gouty tophi. Serum concentrations of ROS products, NO radicals and ascorbate radicals did not correlate with RRI, CCARI and IMT. Among untreated and treated with Allopurinol or Febuxostat patients the means of ROS products, NO radicals, ascorbate radicals, RRI, CCARI and IMT were similar.
Conclusions: In the earlier and advanced stage of the disease we found no difference in oxidative stress level but the degree of inflammation was higher in tophi subjects. No connection was established between serum ROS products, NO radicals and ascorbate radicals with renal and carotid arteries arteriosclerotic vascular changes. We suggest that in gout individuals intrinsic inflammation has a leading role in the process of atherogenesis.
