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Gout can lead to intense pain, swelling, and stiffness. Acute gouty arthritis is characterized by sudden onset and severe pain in the affected joint, usually the big toe. Gout affects millions of people worldwide, and its prevalence is increasing due to the rising incidence of obesity and other risk factors. The management of gout involves controlling inflammation, reducing pain, and preventing recurrent attacks.

“This study aimed to evaluate the change in uric acid level during the acute phase and explore the relationship between uric acid level, glucocorticoids, and inflammatory factors, providing additional evidence for clinical practice,” researchers of a study published in Frontiers in Endocrinology wrote.

Serum uric acid (SUA) is a critical biomarker in gout management, as its levels are directly associated with the development and progression of gout. In recent years, several studies have investigated the role of SUA in acute gouty arthritis, aiming to elucidate the underlying mechanisms and potential therapeutic targets. One of these studies is a prospective, longitudinal study conducted on 50 acute gout patients at the dedicated gout clinic of the Affiliated Hospital of Qingdao University.

The primary objective of the study was to explore the relationship between the changes in SUA levels and free glucocorticoids and inflammatory factors in patients with acute gouty arthritis. The study enrolled patients who presented with acute gouty arthritis and treated them primarily with colchicine and nonsteroidal anti-inflammatory drugs. Blood and 24-hour urine samples were collected during the acute phase and 2 weeks after the initial visit.

The results of the study showed that SUA levels were significantly downregulated during the acute flare than after the flare, indicating that SUA levels may be a useful biomarker for diagnosing acute gouty arthritis. Additionally, the 24-hour fractional excretion of uric acid (24 h FEur) and 24-hour urinary uric acid excretion (24 h Uur) increased significantly in patients during the acute phase, suggesting that these factors may contribute to the development of acute gouty arthritis.

Moreover, the study found that the percent change in SUA was associated with those in 24 h FEur and C-reactive protein, while the percent change in 24 h Uur was associated with those in 24-hour urinary free cortisol and percent change in interleukin 1β and interleukin 6. These findings suggest that inflammatory factors and bioactive free glucocorticoids may play significant roles in the process of decreased SUA levels during the acute gout flare.

“Decreased SUA level during acute gout flare is associated with increased excretion of urinary uric acid. Inflammatory factors and bioactive free glucocorticoids may play significant roles in this process; however, further studies need to be conducted to understand the mechanism,” the authors of the study concluded.

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