Objective: Previous studies demonstrated that the risk of venous thromboembolism (VTE) is increased in patients with gout, but not whether there was a temporal association between gout flare and VTE. This study was undertaken to evaluate potential temporal associations between gout flare and VTE.
Methods: Data were obtained from electronic primary-care records from the UK's Clinical Practice Research Datalink, which links data from hospitalization and mortality registers. Using self-controlled case series analysis adjusted for season and age, we evaluated the temporal association between gout flare and VTE. The 90 days after primary-care consultation or hospitalization for gout flare was designated the exposed period. This was divided into three 30-day intervals. The baseline period was up to 2 years before the start of and up to 2 years after the end of the exposed period. The association between gout flare and VTE was measured using adjusted incidence rate ratios (IRRs) with 95% confidence intervals (95% CIs).
Results: In total, 314 patients met the inclusion criteria (age ≥18 years, incident gout, no presence of VTE or use of a primary-care anticoagulant prescription before the start of the pre-exposure period). Among the 314 patients, VTE incidence was significantly higher in the exposed period than in the baseline period (adjusted IRR 1.83, 95% CI 1.30-2.59). The adjusted IRR of VTE during the first 30 days after gout flare was 2.31 (95% CI 1.39-3.82) relative to the baseline period. No increase in the adjusted IRRs was observed in days 31-60 (adjusted IRR 1.49, 95% CI 0.79-2.81) and days 61-90 (adjusted IRR 1.67, 95% CI 0.91-3.06) relative to baseline. Results were consistent across sensitivity analyses.
Conclusion: Among patients with gout, there was a transient increase in the rate of VTE within 30 days after primary-care consultation or hospitalization for gout flare.
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http://dx.doi.org/10.1002/art.42480 | DOI Listing |
J Clin Med
December 2024
Department of Rheumatology, Päijät-Häme Central Hospital, Wellbeing Services County of Päijät-Häme, 15850 Lahti, Finland.
Gout is the most common form of inflammatory arthritis, caused by the deposition of monosodium urate crystals in the joints due to elevated serum uric acid levels. Its prevalence and associated healthcare burden have been rising in recent decades, a trend expected to continue. It is crucial to recognize that gout and hyperuricemia are not merely causes of painful joint flares, but systemic metabolic disorders linked to a broad spectrum of comorbidities such as cardiovascular diseases, chronic kidney disease, diabetes, insulin resistance, steatotic liver disease, osteoarthritis, and respiratory and eye diseases.
View Article and Find Full Text PDFGout, a common chronic disease, is characterized by the formation and deposition of monosodium urate (MSU) crystal deposition in articular and nonarticular structures. Osteoarthritis (OA), the most prevalent type of arthritis, is a progressive degenerative joint disease. Previous clinical studies have reported that gout frequently affects OA joints; however, the underlying mechanism remains unidentified.
View Article and Find Full Text PDFArthritis Care Res (Hoboken)
January 2025
University of Auckland, Auckland, New Zealand.
J Inflamm Res
December 2024
Shandong Provincial Clinical Research Center for Immune Diseases and Gout, Qingdao, People's Republic of China.
Purpose: Previous studies have linked high-density lipoprotein cholesterol (HDL-C) to gout, but little is known about the dose-effect relationship between serum HDL-C levels and gout flares. This study aimed to quantify the association between the two during urate-lowering therapy initiation and develop a regression equation to predict gout flares.
Patients And Methods: We conducted a prospective, observational, single-center cohort study of men with gout.
Cureus
November 2024
Internal Medicine, Unidade Local de Saúde de Santo António, Porto, PRT.
Although gout is a common intermittent crystalline arthropathy, tophaceous gout is a rare condition. Flares of this disease are usually treated with anti-inflammatory drugs followed by control of serum uric acid levels. We present a refractory, severe, tophaceous gout overlapping with psoriatic arthritis, presenting with a hyper-inflamed phenotype resistant to conventional anti-inflammatory and hypouricemic agents.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!