Abstract:
Currently there is scarce data on endothelial dysfunction (ED) in patients with gout (GA), moreover there are no current studies of ED in gout comorbid with arterial hypertension (AH). The purpose of this study is to describe specific features of biochemical and instrumental markers of endothelial dysfunction in patients with GA comorbid with AH. We measured and compared the level of Von Willebrand factor (vWF), interleukin-1beta (IL-1), endothelin-1 (ET-1), plasma nitrites (NO2-) and nitrates (NO3-), the total activity of NOsynthase, endothelium-dependent (FMD) and endothelium-independent vasodilatation (NMD) in 26 patients with GA, 26 patients with AH and in 86 patients with GA+AH. The study showed that vWF concentration was highest in comorbidity group (92,9±29,0%) showing no significant difference from GA and AH (79,2% and 86,5% respectively). IL-1 was highest in GA+AH group (2,0 pg/ml) being significantly higher than in AH (p=0,01) but showing no difference from GA (p=1,0). ET-1 concentration was highest in the comorbid pathology group (3,07 fmol/ml) versus 1,58 fmol/ml in GA (p<0,0001) and 2,77 fmol/ml in AH (p=1,0). NO-synthase activity was greatest in GA and in comorbid pathology groups showing no significant intergroup difference; NO2- and NO3- concentrations, being similar in these two groups, were statistically higher that in AH. Greatest reduction of FMD and NMD was found in comorbid pathology group (5,80% and 10,35% respectively) and it was not significantly different from AH group (6,18%; p=0,83 for FMD and 13,59%; p=0,079 for NMD). FMD and NMD in gout (10,03% and 15,35% respectively) were similar to normal,
being significantly different compared to GA+AH group (p=0,045 for FMD and p=0,018 for NMD). This study shows that ED in gout is characterized by significantly higher concentration of IL-1, nitric oxide metabolites and intact FMD compared to hypertension. Hypertension is characterized by significantly higher concentrations of endothelin-1, more prominent increase in von Willebrand factor and significant FMD reduction. Endothelial dysfunction in comorbid pathology demonstrates "summation" of pathogenetic mechanisms of underlying disorders, expressed in significant increase of interleukin-1 and endothelin-1 concentrations, hyperactivation of NO synthesis together with decreased FMD and NMD.
