Normal Purine Metabolism and Pathogenesis of Gout in Metabolic Disorders
- VernacularTitle:Пурины хэвийн солилцоо, түүний алдагдлын үед үүсэх тулай өвчний эмгэг жам
- Author:
Gombosuren B
1
Author Information
1. School of Medicine, Ikh Zasag International University
- Publication Type:Review
- Keywords:
Monosodium urate, Nucleotide, Uric acid, NLRP3 inflammasome, Neutrophil extracellular traps
- From:
Mongolian Journal of Health Sciences
2025;90(6):210-221
- CountryMongolia
- Language:Mongolian
-
Abstract:
Background:Gout is the most common inflammatory arthropathy among adults and develops due to hyperuricemia and
the long-term deposition of monosodium urate (MSU) crystals in the joints and tissues. Hyperuricemia results either from
increased production of uric acid or decreased renal and intestinal excretion, with impaired urate excretion being the predominant
underlying cause in most individuals. Although genetic variations in urate transporters significantly influence
serum urate levels, not all individuals with hyperuricemia develop MSU crystal deposition or gout.
Aim:To review and analyze the pathophysiology of gout arising from normal and disrupted purine metabolism.
Materials and Methods:Using a narrative literature review approach, we examined published research on purine metabolism
and the pathophysiological mechanisms of gout. Sources included Thomson Reuters, PubMed Central, Cochrane
Library, Medline, Web of Science, and Google Scholar. A total of more than 670 publications were screened, of which 31
key studies relevant to the pathophysiology of gout were included in the final analysis.
Results:The inflammatory response triggered by MSU crystals is primarily driven by activation of the NLRP3 inflammasome,
which converts IL-1β (pro-IL-1β) and IL-18 (pro-IL-18) into their active forms, IL-1β and IL-18, thereby initiating
inflammation. IL-1β and IL-18 further enhance cytokine and chemokine expression, recruiting neutrophils and other
immune cells to the site of inflammation. Neutrophils not only amplify the inflammatory response but also contribute to
its resolution through the formation of neutrophil extracellular traps (NETosis), which capture and degrade inflammatory
mediators.
Severe gout is characterized by tophus formation, chronic inflammation, and structural joint damage. Tophaceous deposits
consist of aggregated MSU crystals surrounded by inflammatory cells and connective tissue and are closely associated
with persistent inflammation and tissue injury.
Conclusion:A clear, logically structured understanding of disease pathophysiology—including cause-and-effect mechanisms—
is essential for making evidence-based decisions in diagnosis and treatment.
- Full text:2025121016381838311Пурины хэвийн солилцоо, түүний алдагдлын үед үүсэх тулай өвчний эмгэг жам.pdf
