Gout (crystal deposition disorders)

• What is Gout (Crystal Deposition Disorders)
• Statistics on Gout (Crystal Deposition Disorders)
• Risk Factors for Gout (Crystal Deposition Disorders)
• Progression of Gout (Crystal Deposition Disorders)
• Symptoms of Gout (Crystal Deposition Disorders)
• Clinical Examination of Gout (Crystal Deposition Disorders)
• How is Gout (Crystal Deposition Disorders) Diagnosed?
• Prognosis of Gout (Crystal Deposition Disorders)
• How is Gout (Crystal Deposition Disorders) Treated?
• Gout (Crystal Deposition Disorders) References

What is Gout (Crystal Deposition Disorders)

Gout is the most common form of crystal-induced arthritis, characterised by the deposition of crystals in and around joints and tendons. In some patients this may be asymptomatic, in others it will cause an acute inflammatory reaction (acute gout), or it may result in the slow destruction of the involved tissue after repeated attacks (chronic gout).

Statistics on Gout (Crystal Deposition Disorders)

It is estimated that gout affects 0.2% of the population in Europe and the USA. However it is thought that raised uric acid levels in the blood (often a feature of gout) is far more common. Gout is seen more often in developed countries (perhaps due to the influence of diet, high cholesterol and diabetes), and is more common in men than women. It commonly occurs in middle age for men and after menopause in women.

Risk Factors for Gout (Crystal Deposition Disorders)

A family history of gout is commonly seen. Raised uric acid levels (hyperuricaemia) in the blood predispose to the development of gout, however most people with increased levels of uric acid do not develop symptoms. Hyperuricaemia is more common in certain ethnic groups such as Maoris. Uric acid levels increase with age, obesity, diabetes, heart disease and raise blood pressure, foods such as liver and oily fish, high cholesterol and excess consumption of alcohol.

Progression of Gout (Crystal Deposition Disorders)

Gout is caused by a metabolic disorder characterised by raised uric acid levels and the deposition of urate crystals in joints and tissues, resulting in acute inflammation of the joint.
Two forms of gout have been described:

1. Primary gout (95%): An inherited condition with either overproduction or underexcretion of uric acid;
2. Secondary gout (5%): Due to an acquired condition causing either overproduction or underexcretion of uric acid (e.g. renal failure).

How is Gout (Crystal Deposition Disorders) Diagnosed?

The signs and symptoms of gout are usually enough to make a diagnosis. Fluid can be taken from the affect joint and examined under microscopy but this is often inconvient and unecessary, unless infection is suspected. Uric acid levels are often raised in gout. Joint damage in chronic gout can be seen on x-ray.

Prognosis of Gout (Crystal Deposition Disorders)

With early treatment and control, prognosis is excellent. Recurrent attacks of gout may require life long treatment with medications to control uric acid levels, but this is usually effective.

How is Gout (Crystal Deposition Disorders) Treated?

Acute attacks of gout are treated with anti-inflammatory medications to reduce pain and swelling. The patient is advised to rest the joint. Between attacks attention may be given to reducing risk of further attacks by losing weight, reducing alcohol consumption and modifying diet if necessary.
If attacks of gout are frequent, or tophi (crystal deposits) develop in the joints, long term therapy is considered. A medication called allopurinol is usually prescribed, in combination with anti-inflammatory drugs (to minimise the risk of allopurinol precipitating acute gout in the first few months).

Gout (Crystal Deposition Disorders) References

1. Solomon L, Warwick D, Apley AG, Nayagam S. Apley’s Concise System of Orthopaedics and Fractures (2nd edition). London: Arnold; 2001. [Book]
2. Collier JAB, Longmore JM, Scally P. Oxford Handbook of Clinical Specialties (6th edition). Oxford: Oxford University Press; 2003. [Book]
3. Harris MD, Siegel LB, Alloway JA. Gout and hyperuricemia. Am Fam Physician. 1999;59(4):925-37. [Full text]
4. Kaplan J. Gout and pseudogout in emergency medicine [online]. Omaha, NE: eMedicine; 2004 [cited 19 September 2004]. Available from: URL link
5. Kumar P, Clark M (eds). Clinical Medicine (5th edition). Edinburgh: WB Saunders Company; 2002. [Book]