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Gout: common and curable?

Published on 01 January 2008
Source: Arthritis Today

If gout is supposedly curable why are so many affected people still suffering? Although new guidelines are available on how to treat this common form of inflammatory arthritis, recent research has shown that many patients are not getting the right advice or treatment. Experts Edward Roddy and Mike Doherty explain what gout is all about.

GoutA 19th century print of a typical gout sufferer is a common cause of inflamed joints and arthritis. It is much more common in men than women, affecting about one per cent of adults in the UK. Some research suggests that it is becoming more common. Effective treatment exists and gout is considered to be one of the few curable forms of arthritis.

Recently, bodies such as the European League Against Rheumatism (EULAR) and the British Society for Rheumatology (BSR) have produced recommendations advising doctors how to treat gout. The recommendations cover a wide range of areas including treatment of acute attacks of gout, the importance of life-style factor measures such as diet, alcohol and weight, and how gout should be treated in the longer term. However, recent research shows that these recommendations are frequently not followed.

What is gout?

Gout develops when levels of uric acid (which we all have in our blood) build up so high that it combines with sodium to form sodium urate crystals in and around joints (figure 1). Uric acid is produced in the body from chemicals called purines, which come either from the diet or from the breakdown of our own genetic material such as DNA. Once crystals have formed, the joints can become very inflamed, leading to acute attacks of severe pain, swelling and redness of an affected joint, most commonly the 'bunion' joint at the base of the big toe. Pain usually comes on very rapidly, often overnight, and is often so severe that bedclothes are too heavy or wearing shoes is too painful to bear. Even without treatment, attacks will settle by themselves over two to three weeks. However, treatment leads to more rapid improvement. Crystals can more rarely deposit at other sites such as the skin, known as tophi, and kidneys.

Microscope slide of fluid withdrawn from a joint
Figure 1 – Microscope slide of fluid withdrawn from a joint showing bright needle-shaped yellow and blue sodium urate crystals.

What causes gout?

Several factors are known to increase the risk of developing gout. It is more common in men in whom it may also run in families. Several life-style factors such as drinking alcohol (particularly beer) excessively, a high intake of purines in the diet, and being overweight raise uric acid levels and predispose to gout. Foods that are rich in purines include red meat, offal such as liver and kidneys, shellfish, and dark fish such as sardines and tuna. Gout is also more common in people with medical problems such as high blood pressure, diabetes, high levels of cholesterol or fats in the blood, and heart or kidney problems. Finally, certain medicines can predispose to gout, most importantly, diuretics, or 'water tablets', which treat high blood pressure or fluid retention associated with heart or kidney problems.

How is gout diagnosed?

Edward RoddyThe only way to be certain that a patient has gout is to insert a needle into a joint in order to withdraw some synovial fluid which can be examined under a microscope for the bright needle-shaped urate crystals that cause the disease (figure 1). However, this test is not possible at most GPs’ surgeries and the diagnosis is often based on the dramatic, characteristic clinical features. A blood test may be taken to measure the level of uric acid in the blood. However, uric acid levels can be normal during an attack of gout, and many people with raised levels never get gout, so the blood test itself does not make the diagnosis.

How is gout treated?

Professor Michael DohertyThe treatment of acute attacks of gout is very different from longer term treatment.

Acute attacks of gout
Acute gout is one of the most painful conditions known. Treatment aims to reduce pain, swelling and inflammation quickly. The most commonly used drugs are non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or diclofenac, although they cannot be used in patients with a history of stomach ulcers or kidney problems. Another commonly used drug is colchicine, which is a naturally occurring compound derived from the autumn crocus. Colchicine is very effective but can cause diarrhoea when used in high doses. The most effective treatment for acute gout is the insertion of a needle into the affected joint to withdraw some fluid and to inject a steroid into the joint although this is not often performed by GPs. Applying an ice-pack (or a packet of frozen peas wrapped in a towel!) to the joint can also relieve pain, swelling and inflammation.

Long-term treatment
Long-term treatment of gout is usually considered once the acute attack has settled down. There are two strategies for long-term treatment:

  1. changing diet and losing weight
  2. changing drug treatment

Changing adverse life-style factors is an important part of treatment. Losing weight and reducing consumption of alcoholic drinks (particularly beer) and purine-rich foods (such as red meat, offal and dark fish) can all help to reduce uric acid levels. Various foods have been suggested to specifically reduce uric acid levels. A small amount of research evidence supports the consumption of dairy products such as low-fat yogurts and skimmed milk, or cherries.

A hand affected by goutLong-term drug treatment of gout aims to lower uric acid in order to prevent new crystals from forming and dissolve existing crystals. Once all the crystals have gone the gout has been “cured”. The most commonly used drug in the UK is allopurinol which reduces the amount of uric acid produced by the body. Other drugs, such as sulphinpyrazone and benzbromarone, increase the elimination of uric acid into the urine. When starting one of these drugs, the sudden drop in uric acid levels may partially dissolve some urate crystals which shake loose into the joint cavity triggering an acute attack. Therefore, an anti-inflammatory or colchicine is often prescribed for the first 3–6 months of therapy. Allopurinol is often started at a low dose and slowly increased (every 4 weeks or so) until the right dose is achieved – this slower change in uric acid levels is less likely to trigger an acute attack. Allopurinol is usually taken for life once started. Side-effects are uncommon but very rarely a severe allergic reaction can occur. New drugs are in development. Febuxostat, like allopurinol, reduces the amount of uric acid produced by the body and appears to be as effective as allopurinol. It is not available in the UK at the moment.

Gout treatment and the EULAR recommendations

A recent study from Nottingham examined how well gout treatment follows the EULAR recommendations. Less than half of patients questioned could recall advice to restrict consumption of alcoholic drinks or purine-rich foods or to keep their weight down. Only 30 per cent were taking medications such as allopurinol to lower their uric acid levels. Even those taking allopurinol were often not on enough to lower their uric acid sufficiently. The reason for such unsatisfactory treatment is almost certainly inadequate education. Doctors often do not realise that:

  • the aim of treatment of gout is cure
  • uric acid levels need to be reduced below a certain level to be effective (not just into the normal range)
  • the dose of allopurinol needs to be increased above 300 mg if necessary to achieve this

These important principles are not often accurately communicated to patients so they are not aware how important it is to reduce uric acid levels, or that gout can be cured. Also they often do not appreciate how bad gout can get if they remain untreated. Further research is needed into the reasons behind poor treatment of this common but totally curable disease.

Edward Roddy is a Clinical Lecturer and Honorary Consultant Rheumatologist at the Primary Care Musculoskeletal Research Centre, Keele University, and Michael Doherty is Professor of Rheumatology at the University of Nottingham.

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