A Hyperuricemia denotes a increased uric acid concentration in the serum. From concentration values ​​of over 6.5 mg / dl one speaks of an increased uric acid level. The limit depends on the solubility of the sodium salt of uric acid. At concentrations above this, the uric acid is no longer uniformly dissolved in the serum, but can be in the form of Uric acid or urate crystals fail. These are deposited in the blood and tissue and cause symptoms over time. Typical complaints take the form of acute ones Gout attacks with severe joint pain and signs of inflammation. A chronic gout and a Gouty arthritis can develop as they progress.

Basically, you can two causes distinguish.
The primary hyperuricemia is familial. In the vast majority of cases it is a clear one reduced uric acid excretion via the kidneys.
In the secondary form the cause of the hyperuricemia is different. These include the increased uric acid attack as a result of a disturbed purine metabolism or increased uric acid production and the reduced excretion due to chronic kidney disease, the use of certain diuretics, alcohol abuse and a so-called Ketoacidosis. Furthermore, the increased breakdown or remodeling of cells in the context of malignant tumor diseases can also act as a cause. A common trigger in the western world is that increased uptake of proteins with the food.

ICD 10 classification

According to ICD-10, the international Classification of diseases, the hyperuricemia is under the number E79.0 coded. The code E79 summarizes disorders of the purine and pyrimidine metabolism. ICD-10 is the most important diagnostic system for classifying diseases. It is accepted worldwide and is published by the World Health Organization, WHO.

The number E79.0 stands for asymptomatic hyperuricemia. With this form, there are no signs of inflammation of the joints (arthritis) or the formation of nodules on bones and soft tissues (tophic gout) in front.

The hyperuricemia manifests itself in the form of falling out Urate crystals and if symptomatic, one speaks of gout. She receives the coding M10 according to ICD-10.



Among the causes of a secondary hyperuricemia count certain Diuretics. The effect of diuretic substances is based on promoting water excretion via the kidneys. They are used, among other things, in the treatment of heart failure, high blood pressure, edema and connective tissue transformation of the liver (cirrhosis of the liver).

A significantly increased uric acid level is often observed during therapy with a diuretic. Patients are usually symptom-free, although the concentration is higher than in many cases of an acute gout attack. A drug therapy recommendation for diuretic-induced hyperuricemia is currently not made.


One of the most common causes of secondary hyperuricemia in the western world is the intake of purine-rich foods.
The "disease of affluence" is often associated with meat-rich diet, Alcohol consumption and little physical activity to observe. In addition to the risk factors mentioned, it also appears Fructose to play a vital role in the development of elevated uric acid levels. Fruit sugar or fructose is not only found in fruits and vegetables, but is increasingly being used in a concentrated, artificially produced form in the food industry. A high concentration of fructose is found in sweet drinks, sweets, baked goods and ready-made dressings and sauces. A rise in the uric acid level in both blood and urine can be observed just a short time after ingestion of fructose. The metabolism of fructose in the body not only causes an increased purine synthesis, but also a reduced uric acid excretion via the kidneys.

The effect of fructose on the uric acid concentration in the serum is similar to the effect of alcohol. Especially people with proven hyperuricemia are exposed to a significantly increased risk of a gout attack. Healthy people are also affected by an increased risk. For this reason, finished products containing fructose, which contain few other nutrients in addition to a high concentration of fructose, should be avoided.


In many cases the Hyperuricemia clinically normal. If the hyperuricemia manifests itself in the form of complaints, it is gout. Typical manifestations are the acute gout attack, the chronic gout and morbid Kidney changes. Hyperuricemia without arthritis is also a possible course. Elevated uric acid levels are usually in the initial stages no symptoms to observe. However, an increased uric acid concentration can be the basis for the development of gout. Symptoms only appear after five to ten years on. In the intermediate phase, the phase between two gout attacks, there are no symptoms. However, the freedom from symptoms is limited in time and simulates the appearance of a cure.

A acute gout attack is associated with typical signs of inflammation and severe, sudden pain. The start of the complaint is usually at night. The gout attack is in many cases associated with a particularly lush, high purine meal and occurs most often Big toe joint on. These are other locations Metacarpophalangeal joint, the Finger joints and the knee- such as Ankle joint. The skin near the joints is swollen and red. Those affected complain of severe joint pain, which usually reaches its maximum after six to twelve hours. Fever is also observed. The symptoms of an acute gout attack can last up to a week.

If the acute gout attacks are left untreated for a long time, the frequency of the attacks and the affected joints increases. One speaks of one Chronification the gout. This corresponds to a creeping progression of the deposition of uric acid crystals, which the Increasingly destroying joints. The symptom-free intervals decrease, while the painful phases increase. The permanent inflammation of the joints doesn't just affect the joints cartilage, but also the bone on. Typically, tophi or gout nodules appear. Their most common location is that ear, but they are also found on Hands, Feet and Bursa such as Tendon sheaths.

Among the pathological changes in the kidney count the so-called Urate nephropathy and the formation of Kidney stones. Both sequelae are based on the deposition of uric acid crystals. The urate nephropathy refers to this acute failure of the kidney as a result of a blocked duct system of the kidney tubules.


The primary diagnosis of hyperuricemia is the Laboratory value used. There are other diagnostic tests to clarify the cause.

If a high uric acid level is suspected, the Uric acid level in blood serum certainly. From values ​​greater than 6.5 mg / dl one speaks of an increase in the value above the normal range.

Furthermore, the excretion of the uric acid concentration in the urine can be measured. This plays an important role in distinguishing between one primary, so a hereditary uremia, and one secondary Hyperuricemia. If there is a genetic cause, uric acid excretion via the kidneys is restricted in the vast majority of cases. In about one percent of cases, it is an enzyme defect that is associated with overproduction of uric acid. Determining the Uric acid clearance differentiates between overproduction and decreased excretion. For this purpose, in addition to the uric acid concentration in the serum, the concentration in the 24-hour urine collection is also measured. The uric acid to creatinine ratio serves the same purpose, but is less precise.

Symptomatic hyperuricemia in the form of unspecific joint problems is diagnosed with the help of a joint puncture. For this you remove with a needle Synovial fluid and examines them for uric acid crystals. The uric acid level is not necessarily elevated in an acute gout attack.


As long as hyperuricemia does not cause any symptoms, one is sufficient conservative therapy recommendation mostly off. The measures include Low-purine, low-meat food as possible, low alcohol consumption and Weight loss if you are overweight. In addition, the daily fluid intake should be at least two liters. This applies up to a uric acid level of 9 to 10 mg / dl. If the concentration is higher or the first clinical symptoms can be observed, medicinal measures are initiated. It will be as permanent as possible Lowering of the serum uric acid concentration controlled to 5.0 to 5.5 mg / dl. In the context of secondary hyperuricemia, the underlying disease should first be treated. Uricostatics and uricosurics are also used. Febuxostat and Allopurinol inhibit uric acid production. Benzbromaron acts on the kidneys and in this way reduces the reuptake of uric acid. Uricostatics, as well as uricosurics, are used in the Therapy of gout used.

Diet for hyperuricemia

If there is an elevated uric acid level, some should Avoided food become. This also applies if there are no manifest symptoms. High purine foods are broken down into uric acid in the body and contribute to a further increase in the value. A high percentage of purines is especially in flesh and Bowels contain. These include in particular Pork, goose and beef. Some Types of fish such as trout, herring and sardines also have a high purine concentration. Some Vegetables like peas, cabbage, and beans should be consumed in small quantities. One clearly reduced alcohol consumption also plays an important role in lowering uric acid levels.

You don't have to do without products with a high protein content such as dairy products. Fruit and most of the vegetables can also be consumed without hesitation.


The gout is defined as Manifestation of hyperuricemia with different symptoms. The development of symptomatic gout can be divided into four stages. Not all stages are characterized by symptoms. Symptoms-free phases alternate with acute forms.

  • The first stage of gout is clinically normal. Hyperuricemia is present in the laboratory alone. Its duration can be between five and ten years.
  • In the second stage, gout becomes symptomatic for the first time through an acute gout attack. This is accompanied by severe joint pain and usually occurs at night. It is often seen as a result of a large, purine-rich meal. The metatarsophalangeal joint of the big toe is the most common place of manifestation.
  • The third stage is also known as the intermediate phase. It is the period between two acute gout attacks. It is characterized by freedom from symptoms and can last between six months and two years. In a proportion of those affected, around eight percent, no new seizure can be observed.
  • The fourth stage describes the chronic course of gout with typical manifestations. These include degenerative joint changes and the appearance of characteristic nodules, so-called Tophie, on bones and soft tissues.


Podagra denotes the acute gout attack at the metatarsophalangeal joint of the big toe. The first attack of gout occurs on this joint in more than half of the cases. Those affected complain of sudden, severe pain, which occurs mainly at night. The joint is swollen, the skin feels warm and has a reddish discoloration. It is about a arthritis, an acute inflammation of the metatarsophalangeal joint of the big toe. There is a close connection between the localization and the occurrence of the first acute attack of gout. Joints that are furthest from the warm core of the body are lower in temperature. An increased uric acid level in the blood, changes in the pH value and a lower temperature in the peripheral joints promote the precipitation of urate crystals.