Gout is a multifactorial ailment with predisposing factors of high purine diet, usage of diuretics, kidney dysfunction and alcohol consumption. It is a chronic disease characterized by the deposition of monosodium urate (MSU) crystal in the joints and hyperuricemia,
In most cases, gout occurs due to under excretion or overproduction of uric acid. In an acute exacerbation of gout, the accumulation of crystalized MSU in the joints activates the release of inflammatory cytokines and neutrophil, mast cells, macrophages, and lymphocytes which manifests symptomatically as warmth, redness, pain, swelling, and loss of joint movement.
The end product of purine metabolism in the liver is urate. Overproduction of urate is caused by a deficiency of the enzyme responsible for purine metabolism in the body. This accounts for 10% of the causes of gout. Whereas, under excretion due to renal insufficiency accounts for the remaining 90% of hyperuricemia, as two thirds of the uric acid is excreted through the renal system. Decreased function of the transporter enzyme “ATP-binding cassette super-family G member 2” (ABCG2) in the kidneys causes a reduction of uric acid elimination causing an increase in uremia.
Hypertension and diabetes mellitus are known risk factor gout. Elevated blood pressure leads to a reduction in the glomerular filtration rate culminating to lessen blood flow to the glomeruli and consequently causing a reduced elimination of uric acid. While insulin increases the uptake of uric acid from the renal tubules.
Diagnosing gout is done through the examination of extracted joint fluids under polarized light microscopy. Uric acid levels should not be used as a diagnostic tool as uric acid levels decrease or remain within normal limits during flare-ups due to interleukin-6 and endogenous cortisol secretion.
In management of gout, the goal is to ensure the reduction and maintenance of the serum urate level below normal values. In patients with chronic gout, tophi which are granulomatous inflammation of MSU crystal deposits, are located in different parts of the joint and skin.
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References
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5512152/
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5512152/
- https://oxfordmedicine.com/view/10.1093/med/9780199668847.001.0001/med-9780199668847-chapter-39
- Oxford Textbook of Osteoarthritis and Crystal Arthropathy (3 ed.) Edited by Michael Doherty, David J. Hunter, Hans Bijlsma, Nigel Arden, and Nicola Dalbeth. Publisher: Oxford University PressPrint Publication Date: Oct 2016Print ISBN-13: 9780199668847Published online: Nov 2016DOI: 10.1093/med/9780199668847.001.0001
- Pathophysiology of Gout. Chapter: Pathophysiology of Gout. Author(s):Nicola Dalbeth. DOI:10.1093/med/9780199668847.003.0039