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The Fifth Element: Is Vascular Dysfunction an Intrinsic Feature of Gout?
Michael H Pillinger1, Michael Toprover1
1Department of Medicine, Division of Rheumatology, NYU Grossman School of Medicine And Rheumatology Section, Department of Medicine, VA New York Harbor Health Care System, NY Campus, USA.
Insights
Gout significantly impacts vascular health, affecting endothelial function. Treating gout with colchicine and urate-lowering therapy can improve vascular function and reduce cardiovascular risks.
Area of Science:
- Rheumatology
- Cardiovascular Medicine
- Immunology
Background:
- Gout is a prevalent inflammatory arthritis affecting 5.1% of adults.
- Traditionally viewed in four stages, gout also involves vascular complications.
- Soluble urate and inflammatory mediators contribute to vascular damage in gout.
Purpose of the Study:
- To elucidate the mechanisms and consequences of vascular involvement in gout.
- To assess the impact of gout on endothelial function.
- To evaluate the effects of gout treatments on vascular health and cardiovascular outcomes.
Main Methods:
- Assessment of endothelial function using brachial artery flow-mediated dilation.
- Analysis of gout treatment efficacy, including guideline-concordant therapy, colchicine, and urate-lowering therapy.
- Evaluation of cardiovascular outcomes such as incident coronary artery disease (CAD) and major adverse cardiovascular events (MACE).
Main Results:
- Patients with gout exhibit diminished endothelial function.
- ACR gout guideline-concordant treatment improves endothelial function, though less effectively in patients with cardiometabolic comorbidities.
- Colchicine and urate-lowering therapy enhance endothelial function and decrease risks of CAD and MACE in gout patients.
Conclusions:
- Gout adversely affects vascular health through mechanisms involving soluble urate and inflammation.
- Standard gout treatments can improve endothelial function and mitigate cardiovascular risks.
- Comprehensive management of gout, including vascular health, is crucial, especially in patients with comorbidities.
Abstract:
Gout, the most common inflammatory arthritis, affects as many as 5.1% of the adult population. Classically, gout is conceived as four sequential phenotypic states: 1) asymptomatic hyperuricemia 2) acute gout flare 3) inter-critical gout (gout between flares); and 4) tophaceous gout. However, these four states are paralleled by a fifth state, consisting of vascular involvement. The mechanisms and consequences of vascular gout are incompletely elucidated. In vitro and animal models indicate that soluble urate adversely affects vascular endothelium and smooth muscle. The recent discovery that soluble urate can be transported intracellularly to alter cell metabolism and epigenetics (trained innate immunity) suggests additional impacts of urate on leukocytes and endothelium. Once gout has progressed to flares, the vasculature is exposed to inflammatory mediators, both during flares and to a lesser but persistent extent inter-critically, suggesting additional mechanisms of gout's effect. We have reported that patients with gout have diminished endothelial function measured by brachial artery flow-mediated dilation. ACR gout guideline-concordant treatment improves endothelial function but is less effective in patients with cardiometabolic comorbidities. Moreover, treatment of gout patients with the anti-inflammatory colchicine and urate lowering therapy improves endothelial function and reduces the risk of both incident coronary artery disease (CAD), and MACE in patients with established CAD.
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