See also our records on Management of Acute Gout and Gout Prophylaxis.

• Asymptomatic
• Hyperuricaemia
• Acute gout
• Intercritical gout and chronic tophaceous gout

Classification

The condition can be classified into primary or secondary gout depending on the cause of hyperuricaemia:

• Primary gout occurs mainly in men age 30-60 years presenting with acute attacks.
• Secondary gout normally is due to chronic diuretic therapy. It occurs in older subjects, both men and women, and is often associated with osteoarthritis.

Pathogenesis

It affects both upper and lower limbs with acute attacks. Less often it presents with painful, tophaceous deposits (± discharge) in Heberden's and Bouchard's nodes.

• Most patients with hyperuricaemia never develop gout and gouty patients may not have hyperuricaemia at presentation.
• Patients can be over-excreters of uric acid, normo-excreters or under-excreters.
• Most cases of primary gout are due to undersecretion.²
• Fewer than 10% are due to overproduction.³

Epidemiology

• Research using the UK General Practice Database reported the incidence of gout to be 11.9 -18.0 cases per 10,000 patient-years and a prevalence of 1.4% (years 1990-1999).⁴ In men the prevalence increased with age and was approximately 7% over the age of 65.⁴
• Asian populations and people of the Pacific Islands have a much higher prevalence and more severe disease.⁵
• The male to female ratio is 9:1, although prevalence increases in women after the menopause.^5,6

Risk factors

The European League Against Rheumatism (EULAR) produced evidence-based guidelines in 2006.² It identified the following risk factors:

• Male sex
• Meat
• Seafood
• Alcohol (10 or more grams per day)
• Diuretics
• Obesity
• Hypertension
• Coronary heart disease
• Diabetes mellitus
• Chronic renal failure
• High triglycerides

Chemotherapeutic drugs are also precipitants of gout. The presence of previous joint morbidity and trauma may influence which joint is affected.⁵

Presentation⁶

• The EULAR guidelines for diagnosis suggest that the development of acute pain in a joint which becomes swollen, tender and erythematous and which reaches its crescendo over a 6-12 hour period is highly suggestive of crystal arthropathy, though not specifically of gout.²
• 50% of all attacks and 70% of first attacks affect the first metatarsophalangeal joint.
• Other sites often affected are:
  • Knee
  • Midtarsal joints
  • Wrists
  • Ankles
  • Small hand joints
  • Elbows
• The inflammation reaches its peak within 24 hours, often with fever and malaise.

Signs

• There is florid synovitis and swelling and extreme tenderness with overlying erythema. Untreated, the attack resolves spontaneously over 5-15 days, usually with itching and desquamation of overlying skin.
• Atypical attacks can occur with tenosynovitis, bursitis and cellulitis, with mild discomfort without swelling lasting a day or two.
• Chronic tophaceous gout - in this condition large crystal deposits produce irregular firm nodules mainly around extensor surfaces of fingers, hands, forearms, elbows, Achilles tendons and ear.
• Typically, tophi are asymmetrical with a chalky appearance beneath skin. Damage is usually found in the 1st metatarsophalangeal joints, mid foot, small finger joint and wrist, with restricted movement, crepitus and deformity.

Differential diagnosis

• Acute attacks - sepsis and other forms of crystal-related synovitis.
• Chronic tophaceous - rheumatoid arthritis, generalised nodal osteoarthritis, xanthomatosis with arthropathy, multicentric reticulohistiocytosis.

Investigations²

The EULAR guidelines recommend the following evidence-based approach:

• For typical presentations such as inflammation of the first metatarsophalangeal joint (also known as podagra) with hyperuricaemia, a clinical diagnosis can be made with reasonable accuracy, but is not definitive unless the presence of uric acid crystals can be demonstrated.
• Demonstration of monosodium urate (MSU) crystals in synovial fluid or tophi confirms the diagnosis of gout.
• Since gout can present atypically, an opportunity should be taken to examine all samples of synovial fluid aspirated from joints for MSU crystals, even if not inflamed at the time.
• Gram staining and culture of synovial fluid should be arranged, even if MSU crystals are found, since gout and sepsis can co-exist.
• Although a raised serum uric acid level is an important risk factor for gout, the use of serum uric acid as a diagnostic test is limited. It can be normal during acute gout, whilst patients with hyperuricaemia may never develop an attack. Studies suggest that the cut-off point above which a level can be considered raised is 360 μmol/l.²
• Renal uric acid secretion (as detected by a 24-hour urine sample) may be helpful in diagnosis, particularly in patients with a family history of young onset gout, patients whose first attack of gout was under the age of 25, and patients with renal stones. Such patients are likely to be over-excreters of uric acid.
• Radiographs may be useful in chronic gout, when punched out lesions, areas of sclerosis and, in the latter stages, tophi may be seen. The first lesions usually occur in and around the first metatarsophalangeal joint. CT scanning may be helpful in less accessible areas.³ Radiography is less helpful in early gout or during an acute attack.²
• Fasting glucose and lipids should be performed to rule out hyperglycaemia and hyperlipidaemia as gout is commonly associated with metabolic syndrome.

Management

See Management of Acute Gout record.

Complications

• Renal disease
  • Renal colic is seen in 10-25% of patients and uric acid stones represent 5-10% of all kidney stones in UK.⁷
  • Chronic urate nephropathy results from widespread deposition of urate crystals in the interstitium of medulla and pyramids causing inflammation and fibrosis. End stage renal failure occurs in up to 25% of cases of untreated chronic tophaceous gout.⁸
  • Gout patients who have a 24-hour urinary excretion of uric acid above 1100 mg have a 50% risk of developing urate and oxalate kidney stones. Those with a measured urate excretion greater than 800 mg per 24 hours may benefit from allopurinol prophylaxis to prevent urate nephropathy.
• Severe degenerative arthritis
• Secondary infections
• Recurrent painful episodes
• Carpal tunnel syndrome (rare)
• Nerve or spinal cord impingement

Prognosis

Further attacks will usually occur within the first year, if at all.⁹

• Prognosis is usually good with early treatment.
• Sometimes the attacks become more frequent and involve more sites, eventually causing joint damage and chronic pain (usually after 10 years).

Prevention

See Gout Prophylaxis record.

Document references

1. Martinon F, Glimcher LH; Gout: new insights into an old disease. J Clin Invest. 2006 Aug;116(8):2073-5. [abstract]
2. Zhang W, Doherty M, Pascual E, et al; EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006 Oct;65(10):1301-11. Epub 2006 May 17. [abstract]
3. Smelser C; Gout. eMedicine, September 2007.
4. Mikuls TR, Farrar JT, Bilker WB, et al; Gout epidemiology: results from the UK General Practice Research Database, 1990-1999. Ann Rheum Dis. 2005 Feb;64(2):267-72. [abstract]
5. Chen LX, Schumacher HR; Gout: an evidence-based review. J Clin Rheumatol. 2008 Oct;14(5 Suppl):S55-62.
6. Kaplan J; Gout and Pseudogout, eMedicine, Aug 2009.
7. Kramer HM, Curhan G; The association between gout and nephrolithiasis: the National Health and Nutrition Examination Survey III, 1988-1994. Am J Kidney Dis. 2002 Jul;40(1):37-42. [abstract]
8. Gout, Clinical Knowledge Summaries (2007)
9. Bandolier; An Introduction to Gout (2007).

Acknowledgements