The diagnosis and treatment of gout

The essentials 

- Gout is more common than rheumatoid arthritis.

- Male sufferers outnumber female sufferers by 9:1.

- Risk factors should be managed to try to reduce recurrence risk.

- Gout causes problems in organs remote from joints.

- Long-term control of uric acid levels prevents recurrent attacks of gout.

1. EPIDEMIOLOGY AND DIAGNOSIS

Gout is not an uncommon condition in general practice. As levels of obesity grow, we live longer as a population, and diuretics are regularly prescribed for heart failure, the incidence of gout will continue to rise.

The condition probably affects between 1 and 2 per cent of the population, so an average GP practice list of 5,500 patients will probably have about 55 patients with gout. Many GPs might be surprised by this, but a scrutiny of notes might well reveal that you have more patients with gout than you thought.

The problem is that patients with this condition usually present in crisis, and are treated for the pain on an acute basis. They then fail to re-attend for a proper management plan after their symptoms have subsided.

The incidence of gout is greater than that of rheumatoid arthritis (RA), but patients with RA appear more numerous because they attend more frequently, and the condition has a higher profile.

The size of the problem Males with gout outnumber females with gout by about 9:1, and men are frequently poor attenders unless they are in trouble. It is therefore important to solve the problem of gout and its repercussions at the first presentation.

According to national statistics from the Department for Work and Pensions, 1.2 million working days were lost because of gout in 1999-2000, although in reality this could be far higher, because only those people who were off work for more than a week were documented.

The disease usually declares itself as a sudden onset of pain, redness and swelling in a joint. Typically it is the first interphalangeal joint of the foot, but it might be any joint. The ankles and wrists are common sites.

It is described by sufferers as extremely painful and often patients are very reluctant to allow anyone to touch the affected joint. The pain is usually said to be throbbing and the joint is invariably hot.

The joint might be stiff and occasionally might be the source of a chalky white discharge. There might also be a generalised fever. Resolution occurs after seven to 10 days, and is often associated with desquamation of the skin over the affected joint.

Differential diagnosis An infected joint can be confused with gout. If there is any doubt, it might be necessary to refer the case urgently for joint aspiration. The synovial fluid can then be sent for culture and examined under polarised light for the typical needle-shaped crystals of uric acid.

There might have been previous undiagnosed or unreported episodes of gout for some time before presentation, and so taking a careful history is important. Attacks might be separated in time by many years.

KEY POINTS

- The incidence of gout is predicted to rise.

- Problems arise because patients with this condition usually present in crisis, and then fail to re-attend for a proper management plan.

- The most important condition that can be confused with gout is an infected joint.

2. PATHOPHYSIOLOGY AND INVESTIGATIONS

Uric acid is the end product of purine metabolism and is excreted primarily in the urine. Most patients with gout are under-excretors of urate, although smaller percentages are overproducers. There is a strong genetic component in early-onset gout, so patients should always be asked about a family history.

Some people with very high serum uric acid levels have a partial enzyme deficiency. In its severest form, this presents as the Lesch-Nyhan syndrome in children.

Affected infants appear normal at birth, but dystonia and choreoathetosis develop towards the end of the first year. The condition may be misdiagnosed as athetoid cerebral palsy, and intellectual development is impaired.

Urate and renal function Uric acid readily crystallises in acid urine and results in the formation of urate stones. Thiazide diuretics and low-dose aspirin both reduce the renal excretion of urate, and anti-mitotic drugs increase urate production.

The high purine content of certain foods can contribute to hyperuricaemia, as can excessive alcohol intake, especially binge drinking. High serum uric acid levels often occur in chronic renal failure.

At acute presentation it is important to check the serum uric acid level.

Most cases of gout will have an elevated uric acid of over 500mu mol/l or 7mg/dl. Statistically, the upper limits of normal uric acid levels for men and women are 416mu mol/l and 357mu mol/l respectively.

If there is any doubt about the diagnosis, then aspiration and culture of the fluid for micro-organisms and microscopy for uric acid crystals is mandatory. It is important that aspirated fluid is sent to the laboratory as quickly as possible because the crystals can dissolve.

It is important to remember that some patients with gout will have a normal uric acid, so a raised level is not essential to the diagnosis.

An FBC should be done to exclude polycythaemia, as well as biochemical analysis to assess renal and liver function. This is to discover if any damage has been done to the kidneys and liver by the hyperuricaemia.

Further investigations Inflammatory markers may be raised but they do not help in confirming the diagnosis.

After the initial attack has subsided, usually about two weeks, further investigations should be done, including a repeat uric acid level, a fasting blood sugar level (because of the link with diabetes mellitus) and a fasting cholesterol.

It is at this point that the serious topic of future management should be discussed with the patient. Important areas include discussion of lifestyle and diet, future problems that may arise if the patient continues to take drugs for acute treatment, and the option and benefits of long-term prophylactic treatment.

A booklet for patients about gout is available from the UK Gout Society.

KEY POINTS

- Most patients with gout are under-excretors of urate, although smaller percentages are overproducers.

- Some patients will have a normal uric acid.

- There is a strong genetic component in early-onset gout, so family history is important.

- After the initial attack has subsided, further investigations should be done and future management discussed.

3. TREATMENT APPROACHES

Acute treatment of gout involves appropriate protection of the joint to avoid pressure.

Elevation of the bedclothes at night by enclosing an affected foot in a cardboard box might seem a crude device, but is a suggestion that is well received by patients who cannot sleep because of pain from the weight of even a single sheet. Elevation of the affected joint and (if bearable) the application of cool pads can bring relief.

Colchicine and NSAIDs

An old standby for acute treatment is colchicine, with a starting dose of 1mg, then 0.5mg every hour until either pain relief is obtained or diarrhoea prevents further dosing. For many doctors, this treatment has been superseded by the use of NSAIDs, but colchicine remains useful if NSAIDs are contraindicated, such as when the patient is on warfarin.

The ideal regime is high doses of the NSAID best tolerated by the patient.

Indomethacin 50mg three times a day was the gold standard, but the risks of producing a gastrointestinal bleed are substantial at this dose.

Other NSAIDs can be used but are less effective. Etoricoxib, a COX-2 inhibitor, has been compared directly with indometacin in gout in a large good-quality trial. It was found to be as effective as high-dose indomethacin, but with the theoretical lower risk of bleeds, making a dose of 120mg of etoricoxib ideal for acute treatment.

Prednisolone 15-20mg daily might be useful for elderly patients with chronic renal failure, and intra-articular steroid therapy is useful when the knee joint is involved.

Long-term treatment

It can be difficult deciding when to start treatment with long-term prophylactic medication.

The level of uric acid used to make this decision might be considered to be above 500mu mol/l (7mg/dl). Patients who have had more than two attacks of acute gout should be considered for prophylactic therapy. The mainstay of long-term prophylaxis is allopurinol. It should be started at a dose of 100mg a day and titrated up to 300mg over six weeks.

The purpose of this step-wise approach is to avoid provoking an acute attack.

However often the custom and practice for GPs is to start patients on allopurinol 300mg straight away.

This is because patients might not attend for follow-up and then stay on an inadequate 100mg dose in the long term.

Uric acid levels

Once allopurinol has been started, it is important, and also good practice, to check uric acid levels at three months.

During the first month of treatment with allopurinol, there is an increased risk of inducing an attack of acute gout, so an NSAID should be co-prescribed.

Some patients develop an allergic rash to allopurinol or, more rarely, a leukopenia.

Therefore you should prescribe alternative drugs, such as probenecid or sulfinpyrazone which act as uricosuric agents, but they should only be prescribed after seeking specialist advice.

KEY POINTS

- Simple measures should be taken to avoid pressure on the affected joint, especially at night so sleep is not disturbed.

- Colchicine can still be used, especially if NSAIDs are contraindicated, such as in patients on warfarin.

- Indometacin has always been the standard treatment, but etoricoxib has been shown to be effective and is probably safer.

- Gastrointestinal complications can limit the use of high-dose NSAIDs.

- The decision about when to start long-term treatment can be difficult.

- The mainstay of long-term prophylaxis is allopurinol.

- Once allopurinol has been started, there should be a follow-up after three months.

4. PROBLEMS WITH RECURRENT ATTACKS

Patients who experience recurrent attacks of gout due to uncontrolled hyperuricaemia might develop subcutaneous deposits of uric acid crystals in various locations. These gouty tophi commonly occur around the elbows, where they mimic rheumatoid nodules. They can also occur on the ear lobes, along the line of tendons, and can also affect the fingers.

Insidious onset in the elderly

In the elderly, and usually in females, gout can present insidiously with a chronic arthritis of the hands associated with gouty tophi.

It is invariably the case that these patients are taking long-term treatment with a thiazide diuretic. They might also be on low-dose aspirin. Both drugs cause hyperuricaemia. In these cases there is often no convincing history of an acute attack of gout.

Gout and the kidney

Besides the joints, other organs in the body can be affected by hyperuricaemia.

The kidneys are particularly vulnerable. Large and small renal stones can form, and these can eventually lead to renal failure. This is especially likely if high serum levels of uric acid are left untreated.

Regular checks of renal and liver function should be arranged at frequent intervals.

Effects on other systems

Hyperuricaemia is associated with insulin resistance and hyperlipidaemia.

There is also some evidence that it might be an independent risk factor for stroke and IHD. It is therefore necessary to take recurrent attacks of gout seriously in these circumstances, and effective treatment should be started with adequate follow-up.

It is important to keep serum uric acid levels within the normal range in order to prevent these avoidable complications. Co-morbidity should be managed accordingly.

KEY POINTS

- Gouty tophi commonly occur around the elbows, where they mimic rheumatoid nodules.

- The onset of gout is often insidious in the elderly.

- In such cases, the patient is usually taking a thiazide diuretic or aspirin.

- Urate stones can form in the kidneys, and can lead to renal failure.

- Hyperuricaemia is associated with insulin resistance and hyperlipidaemia.

5. RISK FACTORS FOR GOUT

The uric acid level might only rise at the time of an acute attack.

However, it might be permanently elevated, increasing the risk of complications.

Obesity increases the risk of gout considerably, and GPs might be able to offer some help and support in encouraging patients to lose weight.

Age - Gout rarely presents in young people and there seems to be an increasing incidence with age. There are two peaks - one in middle age and the other in the elderly.

Patients on thiazide diuretics have already been discussed as being at increased risk, and it is important to remember that many combination tablets contain a thiazide.

Gender - Males are much more commonly affected than females. This would suggest that in women there should be a lower threshold querying about the diagnosis and making sure that a septic joint is not missed. Patients with myeloproliferative disease are also more prone to gout.

Alcohol - Alcohol might be an important factor in patients with gout. Again the GP is in an ideal position to ask questions about alcohol intake, and to offer help and support to help patients stop drinking.

Diet is important, not just from a calorie point of view to prevent obesity, but also to try and limit foods rich in purines (see box).

FOODS RICH IN PURINES
Meat Fish Others
Offal Sardines Beer
Liver Mackerel Marmite and
Anchovies other yeast extracts
Herring Strawberries

KEY POINTS

- Obesity increases the risk of gout considerably.

- There is an increasing incidence with age.

- In women, there should be a lower threshold for querying the diagnosis and making sure that a septic joint is not missed.

- Alcohol might well be an important factor in patients with gout so avoidance is essential.

- Diet is important for calorie restriction and to limit foods rich in purines.

FURTHER RESOURCES

FURTHER READING

Sturrock R. Gout: easy to misdiagnose. BMJ 2000; 320: 132-3

WEBSITES

See Medicine on the Web, page 36.

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