The uric acid is a substance produced in the liver derived from the purine metabolism, a type of protein present in foods ingested daily, the more purine eat more uric acid is produced by the body.

During the evolution of species, humans lost the ability to produce an enzyme called uricase, which transforms uric acid into allantoin, a much more soluble substance in the blood. Humans have much higher uric acid levels than most other mammals. Our blood uric acid levels do not reach toxic levels just because most of us manage to eliminate the excess through the kidneys.

Symptoms of elevated uric acid levels

The usual blood levels of uric acid are very close to the solubility limit, causing small increases in its concentration to cause crystallization of it in the tissues. Uric acid is deposited in the tissues in the form of sodium urate.

When there is a deposition of uric acid crystals in the joints, they cause an intense inflammatory reaction, which leads to a very painful arthritis called gout. Importantly, it takes years of elevated uric acid to develop gout disease.

The drop is typically one monoarthritis, ie arthritis that affects just one joint in each crisis. The joints most affected are those of the feet, mainly the first toe and the knees. The clinical manifestation of gout is arthritis, that is, inflammation of a joint characterized by pain, redness, swelling, and local heat.

The gouty arthritis is so painful that some people fail to even cover their feet, for the simple contact of the inflamed area with the sheet causes a very strong pain. There may be chills and fever, simulating an infectious picture.

The gout attack lasts a few days and then disappears spontaneously. The time interval between the first and second seizures can last up to two years. If left untreated, gout attacks become more frequent and intense, affecting more than one joint at a time. Over the years, untreated gout leads to the formation of tophi in the joints, caused by chronic deposition of urate crystals. Tophi can be single or multiple, and can cause deformations.

The excess uric acid can also lead to the formation of kidney stones uric acid. There is also the risk of urate deposition and formation of tophi in the kidneys, causing chronic renal failure.

Gout is caused by high levels of uric acid in the blood. Although, not everyone with high uric acid develops gout. Gout is much more common in men, occurring between the ages of 35 and 45. In women, it usually occurs only after menopause.

The main risk factors for gout are:

· Obesity.

· Hypertension.

· Trauma to the joints.

· Long periods of fasting.

· Alcohol consumption

· High intake of foods rich in purine.

· Uses of medications that increase uric acid, such as diuretics.

Foods rich in purine (uric acid) are:

· Meats: bacon, pork, vellum, goat, lamb, giblets (liver, heart, kidney, tongue).

· Fish and seafood: salmon, sardines, trout, cod, fish eggs, caviar, shellfish, oyster, shrimp.

· Birds: turkey and goose.

· Alcoholic drinks.

Foods with moderate amounts of purines or uric acid:

· Meats: cow, calf and rabbit.

· Birds: chicken and duck.

· Fruits of the sea: lobster and crab.

· Legumes: beans, chickpeas, peas, lentils, asparagus, mushrooms, cauliflower, spinach.

Foods with low or no levels of purine or uric acid:

· Milk

· tea

· coffee

· chocolate

· yellow cheese

· boiled egg

· cereals such as bread, pasta, corn cake

· potato

· White rice

· corn

· vegetables cabbage, cabbage, lettuce, chard and watercress.

· nuts, sweets and fruits even acidic ones.

How to diagnose gout

The diagnosis of gout is made when there is a typical clinical picture associated with high levels of uric acid. When there is doubt about the cause of arthritis, the doctor usually punctures the fluid from the inflamed joint looking for deposits of urate crystals.

How to treat it

The treatment of gout is divided into two stages: seizure treatment and seizure prophylaxis. Gout has no cure but it can be controlled. During the gout attack, treatment is carried out with common anti-inflammatory drugs (NSAIDs) and / or colchicine.

Colchicine, being less toxic than anti-inflammatories, effectively controls gout, but it can cause unpleasant side effects, such as nausea, vomiting, and diarrhea.

Aspirin should be avoided as far as possible, because despite having an anti-inflammatory effect, it reduces the excretion of uric acid through the kidneys, once the gout attack has stopped, treatment is focused on reducing it. of uric acid levels.

Since most patients with high uric acid do not develop a gout attack or kidney stone, drug treatment is started if a first episode of a gout attack, a kidney stone, occurs. In the cases of patients with asymptomatic hyperuricemia, only an alteration of the diet is indicated, in order to avoid foods rich in purines.

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