Gout pathophysiology
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Gout pathophysiology On the Web |
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American Roentgen Ray Society Images of Gout pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
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]
(Images courtesy of Charlie Goldberg, M.D., UCSD School of Medicine and VA Medical Center, San Diego, CA)
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Gout of Left MCP Joints: Diffuse redness and swelling over MCP joints caused by inflammation induced by gout. Right hand is normal, for comparison.
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Gout of the Right Wrist: Note swelling and redness over right wrist area. Left wrist is normal.
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Gout of the Left Wrist: Note swelling and redness over left wrist area.
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A normal wrist for comparison.
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Tophaceous Gout
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Tophaceous Gout
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Tophaceous Gout
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Gout of the Left Great Toe: Diffuse swelling and redness centered at the left MTP joint.
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Gout of the Right Great Toe: Diffuse swelling and redness centered at the right MTP joint, but extending over much of the foot.
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Tophaceous Gout
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Gout of the Knee: Image demonstrates redness and swelling caused by acute gouty arthritis.
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Picture demonstrates normal knee for comparison. skin changes seen in both legs are related to burns that patient suffered previously.
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Gout with tophi on elbow and knee.
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![Gout (Needles, no birefringence, monosodium urate) [11]](/images/0/02/Gout_%28no_birefringence%29.jpg)
Gout (Needles, no birefringence, monosodium urate) [11]
![Gout (Needles, no birefringence, monosodium urate) [11]](/index.php/File:Gout_(no_birefringence).jpg)
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.
- ↑ http://picasaweb.google.com/mcmumbi/USMLEIIImages