The differences contained in the last percent - this is what makes each person unique. In some cases, assessing the inherited characteristics of parents and other relatives can predict in what form the disease will become more likely. It is assumed that the child will be more or less similar to his parents, that is, they have approximately the same height and physique and, in many cases, a similar hair color and appearance. There are many characteristics that a child can inherit from his parents, including talents or abilities in different areas and physical qualities. For a man, the risk of gout is 8 times higher than for women who before the menopause rarely suffer from this disease. The most frequent age of the first attack is from 30 to 60 years. Other risk factors:
• High consumption of alcohol. By itself, alcohol does not cause gout, but causes an exacerbation in patients.
• High-protein diet.
• Race - for example, in Maori and Polynesians, the level of uric acid in the blood is initially higher than that of other people, so they are more prone to gout.
• Obesity.
• Diseases that cause a high rate of cell renewal, such as erythremia (increased erythrocyte concentration), as well as lymphomas and other cancers.
• Presence of gout in a family history.
• Taking diuretics or small doses of salicylic acid derivatives.
• Kidney disease.
Persons suffering from gout have an increased risk of developing lipid metabolism disorders and hypertension. In 25% of patients, even before the first attack of gout, there are cases of renal colic associated with the deposition of uric acid crystals in the kidneys. With an acute attack of gout for in vitro articular deposition, non-steroidal anti-inflammatory drugs (NSAIDs) are very effective. They should be given in high doses in the early stages of an attack; Most gout sufferers keep them at hand. For those who can not take NSAIDs, one of the oldest known drugs - colchicine remains.
disadvantages
The main disadvantages of colchicine are a very narrow range of therapeutic effect and a high risk of side effects. NSAIDs based on salicylic acid derivatives in small doses increase gout, and although in large doses they are effective against this disease, apparently, their use is still best avoided. Paradoxically, the primary use of allopurinol, a drug widely used to prevent seizures with gout, may actually provoke an articular attack. Diagnosis of gout is made on the basis of clinical symptoms, the presence in the patient's history of predisposing factors and a blood test for the content of uric acid. If doubts remain, the diagnosis can be confirmed by the detection of sodium urate crystals in a synovial fluid sample. In chronic gout, joints can be destroyed, and an X-ray examination will show typical changes. In addition, urates are deposited in tissues in the form of easily detectable gouty nodules around the joints, articular bags, tendon shells and cartilaginous ear shells.
Differential diagnostics
An acute attack can last from several hours to several weeks. Acute gout is often very similar to purulent arthritis, and hospitalization may be required to exclude this more serious disease. Similarly, inflammatory arthropathy can begin with a monoarthritis similar to gout. Increased uric acid level by itself should not be the basis for drug treatment. The vast majority of patients with elevated uric acid levels throughout their life will not experience any gout symptoms. Only some of them will suffer from recurrent seizures. But even in these cases, taking high doses of NSAIDs and then following the diet and other precautions will be more helpful than life-long preventive treatment. It is desirable to avoid food with a high content of purines, dehydration, especially in hot weather, and unusual strenuous workouts.
Diuretics and acetylsalicylic acid in low doses should be administered with caution. Drug preventive treatment should be given only to patients at high risk of developing long-term effects of gout, such as arthritis or a rare complication of chronic kidney disease. Most often these are young patients with a high level of uric acid in the blood, people with chronic nodular gout or frequent gouty attacks, and people with kidney disease. One of the most common preventive drugs is allopurinol. It is very effective and safe even for long-term use. However, some patients complain of a rash, but after discontinuing the drug, it disappears. The drug inhibits the enzyme xanthine oxidase, which converts xanthine into uric acid. Other prophylactic drugs are probenecid and sulfin-pyrazone, which increase the excretion of uric acid through the kidneys. Gout is a relatively common disease affecting about 1% of the population. It causes painful joint pain. Previously, it remained a "privilege" of the higher circles of society, whose representatives consumed more food rich in purines and whose lives were often poisoned by periodic seizures and the destruction of joints. Today, the acute pain caused by the disease can be successfully treated with anti-inflammatory drugs, in addition, gouty attacks can be prevented with drugs that reduce the level of uric acid in the blood.