The body forms uric acid as a degradation product from purines. Purines are essential components of all cells and are found in particularly high quantities in the cell nuclei. Uric acid is therefore produced during the digestion of purine-rich food and the breakdown of the body's own cells. Most of the uric acid is excreted in the urine via the kidneys.
If the level of uric acid in the blood is higher than 6.5 mg/dl, this is known as hyperuricemia. 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 form preferentially in the synovial fluid.
Long-term elevated uric acid levels in the blood can lead to gout via this deposition of uric acid crystals.
A gout attack is a severe inflammatory reaction. The body tries to fight the uric acid crystals, which manifests itself as inflammation.
The human scavenger cells (phagocytes) play a decisive role in this process. They try to break down the uric acid crystals and cause acute inflammation in the process.
Gout is a common cause of joint pain.
Gout can affect various joints © Henrie | AdobeStock
Causes of an elevated uric acid level
The causes of increased uric acid levels and therefore gout are
- either increased formation or
- reduced excretion of uric acid.
Increased formation is found in various congenital purine metabolism defects. One example of this is Lesch-Nyhan syndrome. Tumor diseases with high cell turnover, e.g. leukaemia or chemotherapy, can also lead to increased uric acid production.
In around 99% of cases, reduced excretion via the kidneys is the cause of the increased uric acid level. Reduced excretion can occur in acute or chronic kidney disease.
However, the most common cause of typical gout is restricted uric acid excretion in the case of otherwise normal kidney function due to a specific disorder.
Triggering an acute attack of gout
Alcohol and certain medications can further reduce the excretion of uric acid via the kidneys.
It is problematic if you eat a lot of purines and purine precursors at the same time. This can lead to an acute increase in the uric acid level in the blood. This can lead to an attack of gout due to an acute build-up of uric acid crystals.
This explains why gout attacks often occur after a party (lots of food and alcohol). At the same time, gout attacks are reduced in times of famine (e.g. during and after the Second World War).
Gout is therefore considered a disease of affluence. Gout occurs disproportionately often with metabolic syndrome diseases such as
on.
Acute attack of gout
The metatarsophalangeal joint of the big toe is affected in 60 % of cases. The joint is
- reddened,
- overheated,
- swollen and
- very painful.
Those affected are often unable to bear even the covers. This is referred to as podagra = stirrups. The term "Zipperlein" was coined as a synonym for gout due to the tripping gait of those affected.
Other joints can also be affected by gout:
The gout attack usually subsides within a few days.
The risk of a gout attack increases with age.
Chronic gout
If no treatment is carried out, the clinical picture of chronic gout can develop. Chronic gout is rather rare today.
Urate crystals are deposited as tophi. This can be observed as deposits in the skin or bone, for example. If left untreated, these tophi can progress to joint and bone destruction.
Urate crystals can also manifest themselves 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
- an increase in the uric acid level in the blood and
- the loss of crystals in joints or soft tissue.
In some cases, the uric acid level in the blood is elevated, but there are no other typical gout symptoms. There is also no evidence of tophi. This is referred to as hyperuricemia.
Gout is only diagnosed when symptoms occur, usually joint inflammation. Repeated measurements are often necessary, as the blood level of uric acid can fluctuate.
In the case of acute joint inflammation and uncertainty in the clinical diagnosis, a puncture of the joint fluid can be helpful. Under a polarizing microscope, it provides evidence of phagocytes with the typical crystals.
This detection of gout is the gold standard for diagnosis. However, it is not absolutely necessary if the symptoms are typical.
In the case of chronic gout, typical joint defects can be detected on an X-ray. Gouty tophi were first described radiologically in 1896. An ultrasound of the affected joint can also provide further information.
Magnetic resonance imaging(MRI) can also provide a very good image of the joint. However, this is rarely necessary.
Gout is a typical disease of affluence. It can therefore be influenced by lifestyle changes.
What should the diet for gout look like? Which foods promote an attack of gout?
Avoid purine-rich foods if you suffer from gout. Purine-rich foods are
- Offal,
- sardines,
- meat extract,
- soup cubes,
- grilled chicken and
- legumes.
In addition to "festive meals", fasting cures can also provoke the development of a gout attack. In these situations, the body breaks down more of its own cells and produces uric acid in the process. Weight reduction should therefore be moderate.
Limit your alcohol consumption. Alcohol reduces the excretion of uric acid via the kidneys.
Beer not only inhibits uric acid excretion, but also contains purines due to the yeast content, which are converted into uric acid. Cola also contains up to 10 mg of purines per 100 ml.
Drug treatment of gout
When treating gout with medication, a distinction is made between long-term treatment and acute attack treatment.
In acute attacks of gout, non-steroidal painkillers such as diclofenac are the first choice. Steroids (cortisone) can also dampen the inflammatory reaction. Colchicine, the poison of the autumn crocus, is available as a reserve medication: It inhibits the phagocytes and thus ultimately the acute joint inflammation.
In long-term gout therapy, an attempt is made to reduce the uric acid level in the blood to a normal value (around 6 mg/100 ml). This can be achieved with allopurinol or the newly approved drug febuxostat, which reduces uric acid formation.
Alternatively, diuretic medication can be used to increase uric acid excretion by the kidneys. These drugs include the so-called uricosurics such as benzbromarone or probenecid.
Most mammals and birds break down uric acid chemically into the water-soluble allantoin. The corresponding enzyme (rasburicase) can be used in an emergency (e.g. in a chemotherapy situation).
