Gout pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Gout occurs when mono-sodium urate crystals form on the articular cartilage of joints, on tendons, and in the surrounding tissues. Purine metabolism gives rise to uric acid, which is normally excreted in the urine. Uric acid is more likely to form into crystals when there is a hyperuricaemia, although it is 10 times more common without clinical gout than with it[1]
Purines can be generated by the body via breakdown of cells in normal cellular turnover, or can be ingested in purine-rich foods such as seafood. the kidneys are responsible for approximately one-third of uric acid excretion, with the gut responsible for the rest. It may be possible that defects in the kidney that may be genetically determined are responsible for the predisposition of individuals for developing gout.
There are also different racial propensities to develop gout. Gout is high among the peoples of the Pacific Islands, and the Māori of New Zealand, but rare in the Australian aborigine despite the latter's higher mean concentration of serum uric acid.[2] In the United States, gout is twice as prevalent in African American males as it is in Caucasians.[3]
A seasonal link also may exist, with significantly higher incidence of acute gout attacks occurring in the spring.[4] [5]
Hyperuricemia is considered an aspect of metabolic syndrome, although its prominence has been reduced in recent classifications. This explains the increased prevalence of gout among obese individuals.
Gout is a form of arthritis that affects mostly men between the ages of 40 and 50. The high levels of uric acid in the blood are caused by protein rich foods. Alcohol intake often causes acute attacks of gout and hereditary factors may contribute to the elevation of uric acid. Typically, persons with gout are obese, predisposed to diabetes and hypertension, and at higher risk of heart disease. Gout is more common in affluent societies due to a diet rich in proteins, fat, and alcohol.[6] It is known that lead sugar was used to sweeten wine, and that chronic lead poisoning is a cause of gout,[7][8] which condition is then known as saturnine gout, because of its association with alcohol and excess.[9]
Gout also can develop as co-morbidity of other diseases, including polycythaemia, leukaemia, intake of cytotoxics, obesity, diabetes, hypertension, renal disorders, and hemolytic anemia. This form of gout is often called secondary gout. Diuretics (particularly thiazide diuretics) have traditionally been blamed for precipitating attacks of gout, but a Dutch case-control study from 2006 appears to cast doubt on this conclusion.[10]
References
- ↑ Virsaladze D, Tetradze L, Djavashvili L, Esakia N, Tananashvili D. (2007). "Levels of uric Acid in serum in patients with metabolic syndrome". Georgian Med News. 146: 34&ndash, 7. PMID 17595458.
- ↑ Roberts-Thomson R, Roberts-Thomson P (1999). "Rheumatic disease and the Australian aborigine". Ann Rheum Dis. 58 (5): 266&ndasgh, 70. PMID 10225809.
- ↑ Rheumatology Therapeutics Medical Center. "What Are the Risk Factors for Gout?". Retrieved 2007-01-26.
- ↑ Schlesinger N, Gowin KM, Baker DG, Beutler AM, Hoffman BI, Schumacher HR Jr. "Acute gouty arthritis is seasonal". Retrieved 2007-09-27.
- ↑ Gallerani M, Govoni M, Mucinelli M, Bigoni M, Trotta F, Manfredini R. "Seasonal variation in the onset of acute microcrystalline arthritis". Retrieved 2007-09-27.
- ↑ Robert S. Ivker, D.O. ; et al. (1999). The Complete Self-Care guide to Holistic Medicine. pp. 186&ndash, 8. ISBN0-87477-986-J.
- ↑ Lin JL, Huang PT. (1994). "Body lead stores and urate excretion in men with chronic renal disease". J Rheumatol. 21 (4): 705&ndash, 9. PMID 8035397.
- ↑ Shadick NA, Kim R, Weiss S, Liang MH, Sparrow D, Hu H. (2000). "Effect of low level lead exposure on hyperuricemia and gout among middle aged and elderly men: the Normative Aging Study". J Rheumatol. 27 (7): 1708&ndash, 12. PMID 10914856.
- ↑ Ball GV. (1971). "Two epidemics of gout". Bull Hist Med. 45 (5): 401&ndash, 8. PMID 4947583.
- ↑ Janssens H, van de Lisdonk E, Janssen M, van den Hoogen H, Verbeek A (2006). "Gout, not induced by diuretics? A case-control study from primary care". Ann Rheum Dis. 65 (8): 1080&ndash, 3. doi:10.1136/ard.2005.040360. PMID 16291814.