Gout: Information & Gout Specialists

The body produces uric acid as a breakdown product of purines. Purines are essential components of all cells and are found in particularly high concentrations in cell nuclei.

Uric acid is therefore produced during the digestion of purine-rich foods and 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 hyperuricemia. At this level, 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 primarily in the synovial fluid.

Long-term elevated uric acid levels in the blood can lead to gout through 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 seen in various congenital purine metabolism disorders. Lesch-Nyhan syndrome is one example.

In cases of cancer with high cell turnover, such as leukemia, or during chemotherapy, increased uric acid production may also occur.

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

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

Triggers of an Acute Gout Attack

Alcohol and certain medications can further reduce uric acid excretion by the kidneys.

The problem arises when you simultaneously consume large amounts of purines and their precursors in your diet. This can lead to an acute increase in blood uric acid levels. This, in turn, can result in an acute deposition of uric acid crystals, leading to a gout attack.

This explains why gout attacks often occur after a celebration (involving copious amounts of food and alcohol). At the same time, gout attacks decrease during times of famine (e.g., during and after World War II).

Gout is therefore considered 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% of cases, the metatarsophalangeal joint of the big toe is affected. 

The joint is:

• red
• warm
• swollen, and
• very painful

Often, those affected can no longer even tolerate the weight of the bedspread. This is referred to as “Podagra” (from the Latin for “stirrup”). The term “Zipperlein,” used as a synonym for gout, derives from the shuffling or hopping 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 today.

In this condition, urate crystals are deposited as tophi. Doctors can identify these deposits in the skin or bones, among 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 kidney tissue can further impair kidney function. In severe cases, this can lead to chronic kidney failure.

The basis for a diagnosis of gout is:

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

In some cases, the uric acid level in the blood is elevated, but no other symptoms are present. There is also no evidence of tophi. This condition is referred to as hyperuricemia.

Only when symptoms—usually joint inflammation—appear is the condition referred to as gout. Repeated measurements are often necessary, as blood uric acid levels can fluctuate.

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

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

On an X-ray, typical joint defects are visible in cases of chronic gout. An ultrasound of the affected joint may also be performed.

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

Gout is a classic disease of affluence. It can therefore be influenced by lifestyle changes.

What should your diet look like if you have gout? Which foods can trigger a gout attack?

Avoid foods high in purines if you suffer from gout.

Foods high in purines include:

• Organ meats
• Sardines
• Meat extract
• Bouillon cubes
• Grilled chicken and
• legumes

In addition to “feast meals,” fasting regimens can also trigger a gout attack. In these situations, the body breaks down more of its own cells, thereby producing uric acid. Weight loss should therefore be moderate.

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

Beer inhibits uric acid excretion 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, nonsteroidal anti-inflammatory drugs (NSAIDs) such as diclofenac are considered the first-line treatment. Steroids (cortisone) can also help 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 lower blood uric acid levels to a normal range (around 6 mg/100 ml). This can be achieved with allopurinol or the newly approved medication febuxostat, which reduces uric acid production.

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

 

Most mammals and birds chemically break down uric acid into the water-soluble compound allantoin. The enzyme responsible for this (rasburicase) can be used in emergency situations (e.g., chemotherapy).