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Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
Published on: April 27, 2016
Initiating guideline-concordant gout treatment improves arterial endothelial function and reduces intercritical
Michael Toprover1,2, Binita Shah3,4, Cheongeun Oh5
1Section of Rheumatology, VA New York Harbor Health Care System, New York, NY, USA.
Insights
Initiating guideline-concordant gout therapy with colchicine and a urate-lowering xanthine oxidase inhibitor (XOI) significantly reduces inflammation and improves arterial function in gout patients. These improvements were most notable in patients without pre-existing cardiovascular risk factors.
Area of Science:
- Rheumatology
- Cardiovascular Medicine
- Pharmacology
Background:
- Gout patients exhibit arterial dysfunction and systemic inflammation, posing risks for adverse cardiovascular events.
- These vascular and inflammatory markers persist even between gout attacks (intercritical periods).
Purpose of the Study:
- To investigate if guideline-concordant gout treatment with colchicine and a xanthine oxidase inhibitor (XOI) improves arterial function and reduces systemic inflammation.
- To assess the impact of initiating urate-lowering therapy (ULT) during intercritical periods.
Main Methods:
- A prospective observational study involving 38 untreated gout patients meeting ACR/EULAR criteria.
- Patients received staggered treatment with colchicine and an XOI (allopurinol or febuxostat) to achieve target serum urate (sU) levels.
- Arterial responsiveness was measured using flow-mediated dilation (FMD) and nitrate-mediated dilation (NMD). Systemic inflammation markers included hsCRP, IL-1β, IL-6, MPO, and ESR.
Main Results:
- Four weeks after achieving target sU, FMD significantly increased by 58% (p=0.03), indicating improved endothelial-dependent arterial function.
- Systemic inflammation markers (hsCRP, ESR, IL-1β, IL-6) significantly decreased (18.8%–30%; all p≤0.03).
- Improvements in FMD and inflammation were more pronounced in patients without established cardiovascular risk factors.
Conclusions:
- Guideline-concordant gout treatment effectively reduces intercritical systemic inflammation.
- Initiating therapy with colchicine and an XOI improves endothelial-dependent arterial function in gout patients.
- The benefits on arterial function are particularly significant in patients without comorbidities like hypertension or hyperlipidemia.
Background:
Patients with gout have arterial dysfunction and systemic inflammation, even during intercritical episodes, which may be markers of future adverse cardiovascular outcomes. We conducted a prospective observational study to assess whether initiating guideline-concordant gout therapy with colchicine and a urate-lowering xanthine oxidase inhibitor (XOI) improves arterial function and reduces inflammation.
Methods:
Thirty-eight untreated gout patients meeting American College of Rheumatology (ACR)/European League Against Rheumatism classification criteria for gout and ACR guidelines for initiating urate-lowering therapy (ULT) received colchicine (0.6 mg twice daily, or once daily for tolerance) and an XOI (allopurinol or febuxostat) titrated to ACR guideline-defined serum urate (sU) target. Treatment was begun during intercritical periods. The initiation of colchicine and XOI was staggered to permit assessment of a potential independent effect of colchicine. Brachial artery flow-mediated dilation (FMD) and nitrate-mediated dilation (NMD) assessed endothelium-dependent and endothelium-independent (smooth muscle) arterial responsiveness, respectively. High-sensitivity C-reactive protein (hsCRP), IL-1β, IL-6, myeloperoxidase (MPO) concentrations, and erythrocyte sedimentation rate (ESR) assessed systemic inflammation.
Results:
Four weeks after achieving target sU concentration on colchicine plus an XOI, FMD was significantly improved (58% increase, p = 0.03). hsCRP, ESR, IL-1β, and IL-6 also all significantly improved (30%, 27%, 19.5%, and 18.8% decrease respectively; all p ≤ 0.03). Prior to addition of XOI, treatment with colchicine alone resulted in smaller numerical improvements in FMD, hsCRP, and ESR (20.7%, 8.9%, 13% reductions, respectively; all non-significant), but not IL-1β or IL-6. MPO and NMD did not change with therapy. We observed a moderate inverse correlation between hsCRP concentration and FMD responsiveness (R = - 0.41, p = 0.01). Subgroup analyses demonstrated improvement in FMD after achieving target sU concentration in patients without but not with established cardiovascular risk factors and comorbidities, particularly hypertension and hyperlipidemia.
Conclusions:
Initiating guideline-concordant gout treatment reduces intercritical systemic inflammation and improves endothelial-dependent arterial function, particularly in patients without established cardiovascular comorbidities.
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