Compared with healthy controls, subjects with gout have reduced arterial function, according to a recent study. Individual comorbidities are insufficient to account for differences between gout and control groups, but multiple comorbidities may collectively contribute to impairment in endothelium-dependent arterial responsiveness. Endothelial impairment is also related to serum rate (sUA) and high-sensitivity C-reactive protein (hsCRP), markers of gout severity and inflammation, respectively. Researchers conducted a cross-sectional study of untreated gout subjects (n=34) and non-gout healthy controls (n=64). High-resolution dynamic ultrasound-measured flow-mediated dilation (FMD) and nitroglycerin-mediated dilation (NMD) assessed endothelium-dependent and endothelium-independent arterial responsiveness, respectively. sUA and hsCRP were measured in the gout group, and correlated with FMD and NMD responses. They found:
- Both FMD and NMD were impaired in the gout vs control group.
- Stratification for individual comorbidities suggested that no single risk factor accounted for impaired FMD/NMD in the gout subjects.
- However, the degree of association between gout and FMD, but not NMD impairment, was dampened after multivariable adjustment.
- Within the gout group, there was an inverse correlation between FMD and sUA, and between FMD and hsCRP, but not between NMD and sUA or hsCRP.
Krasnokutsky S, Romero AG, Bang D, et al. Impaired arterial responsiveness in untreated gout patients compared with healthy non-gout controls: association with serum urate and C-reactive protein. [Published online ahead of print February 15, 2018]. Clin Rheumatol. doi:10.1007/s10067-018-4029-y.
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