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Revisiting the pathogenesis of podagra: why does gout target the foot?

Roddy E - J Foot Ankle Res (2011)

Bottom Line: This invited paper provides a summary of a keynote lecture delivered at the 2011 Australasian Podiatry Conference.It displays a striking predilection to affect the first metatarsophalangeal joint as well as joints within the mid-foot and ankle.The proclivity of gout for the first metatarsophalangeal joint is likely to be multi-factorial in origin, arising from the unique combination of the susceptibility of the joint to osteoarthritis and other determinants of urate solubility and crystal nucleation such as temperature and minor physical trauma which are particularly relevant to the foot.

View Article: PubMed Central - HTML - PubMed

Affiliation: Arthritis Research UK Primary Care Centre, Primary Care Sciences, Keele University, Keele, UK. e.roddy@cphc.keele.ac.uk.

ABSTRACT
This invited paper provides a summary of a keynote lecture delivered at the 2011 Australasian Podiatry Conference. Gout is the most prevalent inflammatory arthropathy. It displays a striking predilection to affect the first metatarsophalangeal joint as well as joints within the mid-foot and ankle. A number of factors are known to reduce urate solubility and enhance nucleation of monosodium urate crystals including decreased temperature, lower pH and physical shock, all of which may be particularly relevant to crystal deposition in the foot. An association has also been proposed between monosodium urate crystal deposition and osteoarthritis, which also targets the first metatarsophalangeal joint. Cadaveric, clinical and radiographic studies indicate that monosodium urate crystals more readily deposit in osteoarthritic cartilage. Transient intra-articular hyperuricaemia and precipitation of monosodium urate crystals is thought to follow overnight resolution of synovial effusion within the osteoarthritic first metatarsophalangeal joint. The proclivity of gout for the first metatarsophalangeal joint is likely to be multi-factorial in origin, arising from the unique combination of the susceptibility of the joint to osteoarthritis and other determinants of urate solubility and crystal nucleation such as temperature and minor physical trauma which are particularly relevant to the foot.

No MeSH data available.


Related in: MedlinePlus

Distribution of joints typically affected by gout (reproduced with the permission of the author and the Royal College of General Practitioners: Roddy E, Doherty M. Gout. In: RCGP Guide to MSK Disorders in Primary Care. Ed: Warburton L (in press)).
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Figure 1: Distribution of joints typically affected by gout (reproduced with the permission of the author and the Royal College of General Practitioners: Roddy E, Doherty M. Gout. In: RCGP Guide to MSK Disorders in Primary Care. Ed: Warburton L (in press)).

Mentions: After an often prolonged period of asymptomatic hyperuricaemia, the initial manifestation of gout is usually an acute attack of synovitis affecting a single peripheral joint, most commonly the first metatarsophalangeal joint (MTPJ). Other commonly affected joints include the mid-tarsal joints, ankles, knees, fingers, wrists and elbows (Figure 1). Such attacks are characterised by sudden onset of excruciating joint pain, typically taking less than 24 hours from symptom onset to reach peak intensity, with associated joint swelling, overlying erythema and exquisite tenderness to touch. Although acute gout should be treated rapidly with a non-steroidal anti-inflammatory drug (NSAID) or colchicine, it usually resolves completely over a period of two to three weeks even without treatment. A variable period of time then elapses until the patient experiences a further attack (the "intercritical period"). With time, attacks may increase in severity and frequency, involve different joint sites, and may become oligo- or polyarticular. Eventually, without treatment, the patient may develop chronic tophaceous gout, characterised by chonic pain and stiffness, joint damage and erosive arthropathy, and clinically evident subcutaneous nodular deposits of MSU crystals (tophi) which can occur at the toes, Achilles' tendons, pre-patellar tendons, fingers, olecranon processes, and less commonly, the ears (Figure 2).


Revisiting the pathogenesis of podagra: why does gout target the foot?

Roddy E - J Foot Ankle Res (2011)

Distribution of joints typically affected by gout (reproduced with the permission of the author and the Royal College of General Practitioners: Roddy E, Doherty M. Gout. In: RCGP Guide to MSK Disorders in Primary Care. Ed: Warburton L (in press)).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3117776&req=5

Figure 1: Distribution of joints typically affected by gout (reproduced with the permission of the author and the Royal College of General Practitioners: Roddy E, Doherty M. Gout. In: RCGP Guide to MSK Disorders in Primary Care. Ed: Warburton L (in press)).
Mentions: After an often prolonged period of asymptomatic hyperuricaemia, the initial manifestation of gout is usually an acute attack of synovitis affecting a single peripheral joint, most commonly the first metatarsophalangeal joint (MTPJ). Other commonly affected joints include the mid-tarsal joints, ankles, knees, fingers, wrists and elbows (Figure 1). Such attacks are characterised by sudden onset of excruciating joint pain, typically taking less than 24 hours from symptom onset to reach peak intensity, with associated joint swelling, overlying erythema and exquisite tenderness to touch. Although acute gout should be treated rapidly with a non-steroidal anti-inflammatory drug (NSAID) or colchicine, it usually resolves completely over a period of two to three weeks even without treatment. A variable period of time then elapses until the patient experiences a further attack (the "intercritical period"). With time, attacks may increase in severity and frequency, involve different joint sites, and may become oligo- or polyarticular. Eventually, without treatment, the patient may develop chronic tophaceous gout, characterised by chonic pain and stiffness, joint damage and erosive arthropathy, and clinically evident subcutaneous nodular deposits of MSU crystals (tophi) which can occur at the toes, Achilles' tendons, pre-patellar tendons, fingers, olecranon processes, and less commonly, the ears (Figure 2).

Bottom Line: This invited paper provides a summary of a keynote lecture delivered at the 2011 Australasian Podiatry Conference.It displays a striking predilection to affect the first metatarsophalangeal joint as well as joints within the mid-foot and ankle.The proclivity of gout for the first metatarsophalangeal joint is likely to be multi-factorial in origin, arising from the unique combination of the susceptibility of the joint to osteoarthritis and other determinants of urate solubility and crystal nucleation such as temperature and minor physical trauma which are particularly relevant to the foot.

View Article: PubMed Central - HTML - PubMed

Affiliation: Arthritis Research UK Primary Care Centre, Primary Care Sciences, Keele University, Keele, UK. e.roddy@cphc.keele.ac.uk.

ABSTRACT
This invited paper provides a summary of a keynote lecture delivered at the 2011 Australasian Podiatry Conference. Gout is the most prevalent inflammatory arthropathy. It displays a striking predilection to affect the first metatarsophalangeal joint as well as joints within the mid-foot and ankle. A number of factors are known to reduce urate solubility and enhance nucleation of monosodium urate crystals including decreased temperature, lower pH and physical shock, all of which may be particularly relevant to crystal deposition in the foot. An association has also been proposed between monosodium urate crystal deposition and osteoarthritis, which also targets the first metatarsophalangeal joint. Cadaveric, clinical and radiographic studies indicate that monosodium urate crystals more readily deposit in osteoarthritic cartilage. Transient intra-articular hyperuricaemia and precipitation of monosodium urate crystals is thought to follow overnight resolution of synovial effusion within the osteoarthritic first metatarsophalangeal joint. The proclivity of gout for the first metatarsophalangeal joint is likely to be multi-factorial in origin, arising from the unique combination of the susceptibility of the joint to osteoarthritis and other determinants of urate solubility and crystal nucleation such as temperature and minor physical trauma which are particularly relevant to the foot.

No MeSH data available.


Related in: MedlinePlus