Gout

Gout is a metabolic disease in which an increased concentration of uric acid in the blood (hyperuricemia) can lead to the deposition of uric acid crystals in certain joints (especially in the metatarsophalangeal joint). The body's immune response to these crystal deposits triggers a so-called gout attack, which manifests itself with sudden severe pain and swelling in the affected joint.

Men are far more likely to suffer from gout than women. It is estimated that about 20 percent of the male population in industrialized countries has high uric acid levels. The higher the uric acid concentration in the blood, the greater the risk of a gout attack. In women, gout usually occurs after menopause (menopause).

In most cases, the metabolic disease becomes noticeable between the ages of 40 and 60. Patients often also suffer from obesity, diabetes mellitus (diabetes), hyperlipidemia (elevated blood fat levels) and hypertension (high blood pressure). The combination of these diseases is called metabolic syndrome.

Gout is the result of an increased uric acid level in the blood (hyperuricemia). Uric acid is a breakdown product of the metabolism of purine bases and is produced during the breakdown of nucleic acids (components of DNA) or during food digestion and then excreted via the kidneys. If the concentration in the blood rises above a certain level, uric acid crystals form, which can be deposited in the joints. The cells of the immune system try to eliminate these uric acid crystals, causing inflammation in the joint, which triggers the characteristic symptoms of gout.

Two causes of elevated uric acid levels are distinguished:

• The primary form is the most common cause of hyperuricemia. This is a congenital metabolic disorder in which the kidneys do not excrete enough uric acid due to an excretory disorder. In very rare cases, the cause may also be an overproduction of uric acid.
• In the secondary form, the increased uric acid level is caused by other diseases or by certain medications. Examples of this can be anaemia (anaemia of the blood), tumour diseases or cancer therapy (radiation, cytostatics).

The reason why the kidneys can only excrete insufficient uric acid is often due to diabetes mellitus (increased blood sugar), other kidney diseases, diuretic medication or excessive alcohol consumption.

If the uric acid level in the blood is only slightly elevated (hyperuricemia), those affected usually live free of symptoms for years before the first occurrence of a gout attack.

Characteristic symptoms of a gout attack are:

• severe pain in the affected joint, lasting up to three days
• the joint is swollen, reddened and overheated
• movements of the joint cause pain
• fever may occur during an acute gout attack

In about 60 percent of cases, the gout attack manifests itself in the metatarsophalangeal joint. In about 10 to 15 percent, the knee joint, the ankle joint or the tarsus are also affected. In rare cases, the symptoms can also occur in the finger, hand or elbow joints.

After several acute attacks of gout, chronic gout may develop, causing irreversible changes and damage to the affected joint. As a result, joint deformities and frequent attacks of pain occur.

The increased uric acid level can also lead to the formation of kidney stones or a complete failure of kidney function.

A distinction is made between four phases of gout:

• symptom-free hyperuricemia (elevated uric acid level in the blood without symptoms)
• acute gout attack
• intercritical phase (the symptom-free period between two acute gout attacks)
• chronic gout

There can sometimes be several symptom-free years between two gout attacks (intercritical phase). Nowadays, the chronic gout stage only occurs in patients in whom gout has not been treated or has been treated poorly.

If the symptoms characteristic of gout occur, a blood test can determine whether the uric acid level is within the normal range or elevated. A normal uric acid level cannot, however, exclude gout with certainty, as the blood level fluctuates depending on food intake and the uric acid concentration can therefore already be in the normal range again when the blood is taken, despite the gout attack. During an acute attack of gout, increased inflammation values (e.g. CRP or blood sedimentation rate) can also frequently be detected. If uric acid crystals can be detected in the joint fluid, this is considered a reliable diagnosis of gout.

In chronic cases, the disease-related changes in the joints can be detected on an X-ray. In some cases, the kidneys are also checked, as kidney function can be severely impaired by long-standing, untreated gout.

In therapy, a distinction is made between the treatment of the acute gout attack and the reduction of the elevated uric acid level:

Acute gout attack

The goal in the treatment of an acute gout attack is to reduce the pain as much as possible. For this purpose, anti-inflammatory painkillers from the class of NSAIDs (non-steroidal anti-inflammatory drugs, such as diclofenac, indometacin) are used. In addition, cooling joint compresses and immobilisation of the joint alleviate the symptoms. In the case of a severe attack of gout, cortisone preparations can also be used, as these have a much stronger anti-inflammatory effect than the NSAID painkillers. If the previous therapy has no effect, colchicine can also be administered, which improves the symptoms within a short time - however, due to the stronger side effects, colchicine is only a second-choice remedy.

Hyperuricemia (elevated uric acid level)

To avoid further acute attacks of gout, it is particularly important to keep the uric acid level within the normal range. This can be well achieved by avoiding foods with a high purine content (are metabolised to uric acid) such as offal, fish and pulses. Alcohol consumption should also be greatly reduced, as this also increases uric acid levels. An elevated uric acid concentration can be normalised by maintaining a healthy body weight. Furthermore, care should be taken to drink enough fluids every day (especially water or unsweetened herbal teas).

In addition to lifestyle changes, various medications are available to increase uric acid excretion (uricosurics) or reduce uric acid formation (uricostats).

The individual tendency to an increased uric acid level cannot be treated, but it can be kept within the normal range by a conscious diet (avoidance of foods that increase uric acid) and by means of drug therapy. This greatly reduces the risk of a gout attack. Long-term damage such as joint deformities or kidney damage can also be effectively avoided in this way.

To prevent a gout attack, it is particularly important to keep the uric acid level within the normal range. This can usually be easily achieved by completely avoiding certain purine-containing foods (which increase the uric acid level) in the diet or at least greatly reducing their consumption.

Examples of foods with high purine levels would be:

• Offal (liver, kidney, sweetbreads).
• Fish (especially trout, herring)
• Legumes
• Meat

Since being overweight increases the risk of a gout attack, reducing body weight also has a positive effect on the risk of gout disease. In addition, foods with a high fat content and alcohol should only be consumed in small quantities.