Credit: Original article published here.
Gout is a common type of arthritis caused by the accumulation of urate crystals in the joints, leading to inflammation and pain. Serum uric acid (SUA) is a crucial factor in the development of gout, and elevated SUA levels are associated with an increased risk of gout.
“Spontaneous serum uric acid decrease has been found in many patients during acute gout attacks, but its mechanism remains unclear,” researchers of a study published in Rheumatology wrote. They aimed to investigate the mechanism behind the spontaneous decrease in SUA during acute gout attacks.
The study involved both human patients with gout and a mouse model of gout induced by monosodium urate (MSU) crystals. The researchers evaluated the spontaneous regulation of SUA during gout attacks and its possible causes. They also studied the mechanism of the spontaneous SUA decrease in Caco2 cells and the MSU-induced gout model of wild-type mice and ABCG2-/- mice.
The results of the study suggested that SUA levels decreased during acute gout attacks in both human patients and mice models. This decrease was found to be associated with increased levels of inflammation markers, including C-reactive protein and IL-1β. Additionally, the authors noted that intestinal uric acid excretion and expression of ABCG2, a protein involved in urate transport, were upregulated during gout attacks.
“Increased intestinal urate excretion resulted in spontaneous SUA downregulation during acute gout attacks. Inflammation-induced PI3K/Akt activation and ABCG2 expression in epithelial cells might contribute to the upregulation of intestinal uric acid excretion,” the authors concluded.
Source: Rheumatology
