What disorders do uric acid cause
The term gout encompasses various metabolic diseases that are caused by an increased uric acid level in the blood (hyperuricemia) and which in turn can trigger various secondary diseases:
- Primary hyperuricemia
- Secondary hyperuricemia
- Acute gout
- Chronic gout
Uric acid is produced in the human body as the end product of the breakdown of purines. On the one hand, these occur during normal cell metabolism and are converted into 300-400 milligrams of uric acid per day. On the other hand, humans also take in purines with their food, which are ultimately also broken down into uric acid (300-600 milligrams daily). In total, there is around 1 gram of uric acid in the body of a healthy person.
The human body can no longer use uric acid and therefore excretes it via the kidneys (80%) and the intestines (20%). Normally there is a physiological equilibrium between the formation and excretion of uric acid. It is therefore dissolved in a certain concentration in the blood (uric acid values). However, if the kidneys excrete less uric acid or if larger amounts of uric acid develop than are excreted, the balance is disturbed and the uric acid level rises.
In most cases, the cause of high uric acid levels is an inherited metabolic disorder called primary hyperuricemia. The uric acid excretion function of the kidneys is impaired in 99% of affected patients. In 1% of the cases, an enzyme that is involved in building up or breaking down the purines is defective, such as B. in Lesch-Nyhan syndrome (hypoxanthine-guanine-phosphoribosyltransferase deficiency).
Certain diseases or medications can also raise the level of uric acid in the blood and trigger what is known as secondary hyperuricemia. Causes can be:
- Increased cell breakdown or cell remodeling: In diseases such as blood cancer, hemolytic anemia or psoriasis, as well as in chemotherapy of a tumor, more cells die. This results in higher amounts of purine in the body, which are broken down into uric acid.
- Diseases that reduce the excretion of uric acid through the kidneys, e.g. kidney disease or type 2 diabetes
- Certain medications such as laxatives, diuretics, medicines for tuberculosis or cancer, low-dose aspirin (<1 gram / day).
- Excessive alcohol consumption: Intermediate products of alcohol breakdown increase uric acid production and reduce excretion via the kidneys.
Elevated uric acid levels, as present in primary and secondary hyperuricemia, are responsible for the development of primary and secondary gout. With such an increased uric acid concentration in the blood serum and in the tissue fluids, deposits of uric acid crystals from monosodium urate, also called urate crystals, form in the joints and tissues. With gout, the body stores up to 30 grams of uric acid in the form of urate crystals.
As uric acid levels rise, the risk of a gout attack increases:
- 0.5% of patients experience the first attack of gout at 7 to 9 milligrams / deciliter of blood
- 5% of patients experience the first attack of gout with more than 9 milligrams / deciliter of blood
- Over 90% of patients experience the first attack of gout with more than 10 milligrams / deciliter of blood
Interactions of uric acid crystals in the joint space of affected joints with immune cells trigger inflammatory and immunological reactions. These run off very quickly and can lead to a gout attack. Triggers for a gout attack in these patients can be excessive meat consumption, excessive alcohol consumption / alcohol abuse or strict fasting. Alcohol affects uric acid levels in several ways: It reduces the excretion of uric acid through the kidneys. In addition, the breakdown of alcohol causes acidification of the blood, which reduces the solubility of uric acid and uric acid crystals are more easily formed.
If a gout disease has existed for many years (chronic gout), uric acid crystals are deposited in so-called gout nodes (tophi), e.g. B. under the skin or near the joints on hands and feet. In principle, tophous deposits can develop throughout the body. Deposits in the kidney can lead to kidney gravel or stones.
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