R. Gancheva 1, T. Velikova 2, T. Kundurzhiev 3, Z. Kolarov 1, A. Koundurdjiev 4
1. Clinic of Rheumatology, University Hospital St. Iv. Rilski, 2. Clinical Immunology, University Hospital Lozenetz, 3. Faculty of Public Health, 4. Clinic of Nephrology, University Hospital St. Iv. Rilski, Medical University, Sofia
Background: In the literature there are reports that the key interleukins, IL-1β and IL-18, for the initiation and maintenance of gouty inflammation are associated with renal and cardiovascular disorders. They have a major regulatory function in the innate immune response and in vascular pathology.
Objectives: We aimed to determine serum levels of IL-1β and IL-18 in controls with inactivated osteoarthritis, patients with asymptomatic hyperuricemia, gouty arthritis without tophi subjects and gouty tophi individuals out of flare, and to establish whether their serum concentrations are connected to ultrasound alterations of the kidneys and heart.
Methods: The study is cross-sectional in design. A total of 83 consecutive patients were included: 18 with inactivated osteoarthritis, 29 with asymptomatic hyperuricemia, 22 gouty arthritis without tophi and 18 gouty tophi individuals out of flare. Serum interleukin concentrations were determined by enzyme-linked immunosorbent assay (ELISA) with Human IL-1β and IL-18 ELISA kits (Platinum, eBioscience, Vienna, Austria). By applying ultrasound were measured: renal resistive index (RRI) with 3.5 MHz transducer working with pulse Doppler frequency of 2.5 MHz and left ventricular mass index (LVMi), determined with 2.5 MHz transducer Phased Array. Data were analyzed by One-Sample Kolmogorov-Smirnov, ANOVA, Tukey HSD, Kruskal Wallis, Mann-Whitney and Fisher’s exact test. Correlational analyzes were performed by using the Spearman correlation coefficient.
Results: In gouty tophi subjects serum IL-1β level was undetectable compared to the other three groups, (p<0.001). The serum concentration of IL-18 was comparable across the groups, (p=0.154). Given that the level of IL-1β was undetectable in gouty tophi patients, a correlation analysis in this group with serum uric acid concentration, RRI and LVMi was not performed. In patients with osteoarthritis, asymptomatic hyperuricemia and gouty arthritis without tophi subjects, we did not detect an association between IL-1β and serum uric acid (r=0.074, p=0.777; r= -0.324, p=0.086; r=0.327, p=0.138), RRI (r=-0.013, p=0.960; r= -0.308, p=0.105; r= -0.224, p=0.316) and LVMi (r= -0.217, p=0.402; r=0.131, p=0.506, r=0.259, p=0.271). Similarly, in patients with osteoarthritis, asymptomatic hyperuricemia, gouty arthritis without tophi and gouty tophi no correlation was found between IL-18 concentration and serum uric acid (r=0.279, p=0.277, r= -0.037, p=0.847; r=0.068, p=0.771; r=0.134, p=0.648), RRI (r= -0.090, p=0.732; r=0.035, p=0.856; r=0.253, p=0.255; r=-0.099, p=0.736) and LVMi (r= -0.164, p=0.529; r=0.325, p=0.091; r=0.128, p=0.591; r=0.368, p=0.216).
Conclusions: We suggest that serum IL-1β and IL-18 levels do not reflect the severity of the disease and cardiovascular risk in the examined gout patients.