Causes
Among the causes of secondary hyperuricemia are certain diuretics. The effect of diuretically active substances is based on a promotion of water excretion via the kidneys. They are used, among other things, in the treatment of heart failure, high blood pressure, edema and a connective tissue transformation of the liver (liver cirrhosis).
A significantly increased uric acid level is frequently observed under therapy with a diuretic. Patients are usually free of symptoms, although the concentration is higher than in many cases of an acute attack of gout. A drug therapy recommendation for diuretic-induced hyperuricemia is currently not given.
One of the most common causes of secondary hyperuricemia in the western world is the intake of purine-rich food. This “disease of affluence” is often observed in connection with a diet rich in meat, alcohol consumption and little physical activity. In addition to the risk factors mentioned, fructose also seems to play a decisive role in the development of an elevated uric acid level.
Fructose or fructose is not only contained in fruit and vegetables, but is increasingly used in concentrated, artificially produced form in the food industry. A high fruit sugar concentration is found especially in sweet drinks, sweets, baked goods and ready-made dressings and sauces. A short time after fructose intake, an increase in the uric acid level in the blood and urine can be observed.
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 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 besides a high fruit sugar concentration, should be avoided.
Symptoms
In many cases hyperuricemia remains clinically unremarkable. If the hyperuricemia manifests itself in the form of symptoms, it is called gout. Typical manifestations are the acute attack of gout, chronic gout and pathological kidney changes.
Hyperuricemia without arthritis is also a possible form of the disease. In the initial stage of an elevated uric acid level, no symptoms are usually observed.However, an increased uric acid concentration can be the basis for the development of gout. Symptoms only appear after five to ten years.
In the intermediate phase, the phase between two attacks of gout, there are no symptoms. However, freedom from symptoms is limited in time and gives the appearance of a cure. An acute attack of gout is accompanied by typical signs of inflammation and severe, sudden pain.
The onset of symptoms is usually at night. In many cases, the attack of gout is associated with a particularly sumptuous, purine-rich meal and occurs most frequently at the metatarsophalangeal joint of the big toe. Further localizations are the metacarpophalangeal joint, the finger joints and the knee and ankle joints.
The skin near the joint is swollen and reddened. 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 attack of gout can last up to a week. If the acute attacks of gout remain untreated for a long time, the frequency of the attacks and the affected joints increases. This is known as the chronicity of gout.
This corresponds to a creeping progression of the deposition of uric acid crystals, which increasingly destroy the joints. The intervals between attacks decrease, while the painful phases increase. The permanent inflammation of the joints attacks not only the cartilage but also the bone.
Typically, tophi or gout nodules occur. Their most common location is the ear, but they are also found on the hands, feet, bursae and tendon sheaths. Pathological changes of the kidney include the so-called urate nephropathy and the formation of kidney stones. Both consequences are based on the deposition of uric acid crystals. Urate nephropathy is the acute failure of the kidney due to a blocked duct system of the renal tubules.
