Gout: Information, symptoms & treatment of gouty arthritis

The body produces uric acid as a breakdown product of purines. If the body produces too much uric acid or excretes too little, the level in the blood rises. Purines are essential components of all cells and are found in particularly high quantities in cell nuclei.

Uric acid is therefore produced during the digestion of purine-rich food and during the breakdown of the body’s own cells. The kidneys excrete most of the uric acid in the urine.

If the level of uric acid in the blood is higher than 6.5 mg/dl, this is referred to as hyperuricaemia. Above this value, the solubility product for uric acid in the blood is exceeded. 

This can lead to the deposition of uric acid crystals (urates) in the body’s tissues. They tend to form in the synovial fluid.

Long-term elevated levels of uric acid in the blood can lead to gout via this deposition of uric acid crystals.

A gout attack is a severe inflammatory reaction. The body attempts to combat the uric acid crystals, which manifests as inflammation.

Human phagocytes play a crucial role in this process. They attempt to break down the uric acid crystals, thereby triggering acute inflammation.

Gout is a common cause of joint pain.

Gout can affect various joints © Henrie | AdobeStock

Causes of elevated uric acid levels

Causes of elevated uric acid levels, and thus of gout, include:

• either increased production or
• reduced excretion of uric acid

Increased production is found in various congenital purine metabolism disorders. Lesch–Nyhan syndrome is one example.

In tumour diseases characterised by high cell turnover, such as leukaemia, or during chemotherapy, increased uric acid production may also occur.

In approximately 99 per cent of cases, reduced excretion via the kidneys is the cause of elevated uric acid levels. Reduced excretion can occur in acute or chronic kidney disease.

However, the most common cause of typical gout is impaired uric acid excretion in the presence of otherwise normal kidney function, due to a specific disorder.

Triggers of an acute gout attack

Alcohol and certain medicines can further reduce the excretion of uric acid via the kidneys. A diet high in purines is one of the most common triggers of a gout attack.

The problem arises when you consume large amounts of purines and their precursors in your diet at the same time. This can lead to a sudden rise in blood uric acid levels. This, in turn, can result in an acute deposit of uric acid crystals, leading to a gout attack.

This explains why a gout attack often occurs after a celebration (involving copious amounts of food and alcohol). At the same time, gout attacks are less frequent during times of famine (e.g. during and after the Second World War).

Gout is therefore regarded as a disease of affluence.

Gout occurs disproportionately often alongside conditions associated with metabolic syndrome, such as:

• Obesity
• High blood pressure (hypertension)
• Diabetes mellitus and
• Heart disease (coronary heart disease)

Acute gout attack

In 60 per cent of cases, the base of the big toe is affected. 

The joint is:

• red
• overheated
• swollen and
• causes severe pain

Often, sufferers cannot even bear the weight of the duvet. This is known as ‘podagra’ (from the Latin for ‘stirrup’). The term ‘Zipperlein’ – a synonym for gout – derives from the shuffling or shuffling gait of those affected.

Other joints can also be affected by gout, such as:

• the knee joint (gonagra)
• the thumb joint (chiragra)

A gout attack usually subsides within a few days.

The risk of a gout attack increases with age.

Chronic gout

If left untreated, the clinical picture of chronic gout may develop. Chronic gout is relatively rare nowadays.

In this condition, urate crystals are deposited as tophi. Doctors can identify these as deposits in the skin or bones, amongst other places. If left untreated, these tophi can progress to the point of joint and bone destruction.

Urate crystals can also manifest as kidney stones and cause renal colic. The deposition of crystals in the kidney tissue can further impair kidney function. In severe cases, this can lead to chronic kidney failure.

The basis of gout is:

• elevated levels of uric acid in the blood and
• the formation of crystals in joints or soft tissues

The diagnosis and treatment of gout often require several steps, as uric acid levels can fluctuate. This elevated concentration of uric acid in the blood can be detected by a simple blood test. In some cases, the level of uric acid in the blood is elevated, but no other symptoms are present. Nor is there any evidence of tophi. This condition is referred to as hyperuricaemia.

It is only when symptoms – usually joint inflammation – occur that the condition is referred to as gout. Repeated measurements are often necessary, as blood uric acid levels can fluctuate.

In the event of acute joint inflammation and uncertainty regarding the clinical diagnosis, a joint fluid aspiration may be helpful. Under a polarising microscope, this reveals phagocytes containing the characteristic crystals.

This detection of uric acid crystals is the gold standard for diagnosis. However, it is not strictly necessary if the clinical presentation is typical.

On an X-ray, typical joint damage is visible in cases of chronic gout. An ultrasound scan of the affected joint may also be carried out.

Magnetic resonance imaging (MRI) also provides excellent visualisation of the joint. However, its use is rarely necessary.

Gout is a classic disease of affluence. It can therefore be effectively managed by making changes to diet and lifestyle. People with gout also benefit from a healthy diet low in purines.

What should the diet for gout look like? Which foods trigger a gout attack?

Avoid foods high in purines if you suffer from gout.

Foods high in purines include:

• offal
• Sardines
• Meat extract
• Stock cubes
• Grilled chicken and
• pulses

However, as well as ‘feast meals’, fasting regimens can also trigger a gout attack. In these situations, the body breaks down its own cells at an increased rate, thereby producing uric acid. Weight loss should therefore be achieved gradually.

Limit your alcohol consumption. Alcohol reduces the excretion of uric acid via the kidneys.

Beer inhibits the excretion of uric acid and contains purines, which in turn are converted into uric acid. Cola also contains up to 10 mg of purines per 100 ml.

Medication for gout

Medical professionals distinguish between the following approaches to the pharmacological treatment of gout:

• long-term treatment and
• treatment of acute attacks

During an acute gout attack, non-steroidal anti-inflammatory drugs such as diclofenac are considered the first-line treatment. Steroids (cortisone) can also help to reduce the inflammatory response. 

Colchicine, the toxin found in autumn crocus, is available as a reserve medication: it inhibits phagocytes and thus ultimately reduces acute joint inflammation.

In long-term gout management, doctors aim to reduce the level of uric acid in the blood to a normal level (around 6 mg/100 ml). This can be achieved using allopurinol or the newly approved drug febuxostat, which reduces uric acid production.

Alternatively, diuretic medicines can increase the excretion of uric acid by the kidneys. These medicines include uricosurics such as benzbromarone or probenecid.

Most mammals and birds metabolise uric acid further into the water-soluble compound allantoin. The enzyme required for this (rasburicase) can be used in emergencies (e.g. during chemotherapy).