GOUT: UNVEILING THE COMPLEX INTERPLAY BETWEEN PATHOPHYSIOLOGY, EPIDEMIOLOGY, GENETICS, AND THERAPEUTIC OPTIONS - A COMPREHENSIVE REVIEW
Sethuramani A.*, Ajith P., Chandrasamy M., Raxshiya Smily J., Safia farvin S. and Sedhulakshmi K.
ABSTRACT
Gouty arthritis, one of the earliest known diseases, was first identified by the Egyptians around 2640 BC. Known as 'the unwalkable disease' by Hippocrates, gout is linked historically to the consumption of rich foods and alcohol, grossing it the name 'the disease of kings'. Gout results from monosodium urate (MSU) crystals accrued due to elevated serum uric acid (SUA) levels. Although hyperuricemia is the primary cause, only a marginal with high uric acid levels ripens gout. Hyperuricemia ascends from amplified fabrication or declined seepage of uric acid, allied with circumstances like metabolic syndrome and cardiovascular disease. Pathophysiology of gout encompasses genetic insights with SLC2A9 and ABCG2 and, metabolic causes like an interruption of the xanthine oxidase enzyme activation and synthesis, and inclined levels of triglycerides are in concert with momentous roles. Common treatments include NSAIDs, corticosteroids, and medications to reduce uric acid levels, though these have side effects. There is growing interest in herbal medicines for gout, as some plants can act as xanthine oxidase inhibitors with fewer side effects.
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