What is gout, why does it occur, what evokes seizures, and what is the treatment?

What is gout, why does it occur, what evokes seizures, and what is the treatment?
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Gout is one of the oldest documented diseases in human history. There are reports of it dating back to antiquity. It is the only disease so described in detail by ancient physicians. Despite the known treatment, it does not belong to the past, its incidence has even increased in recent years.


Gout (Latin arthritis uric) is a chronic metabolic disease characterized by a high level of serum uric acid, so-called hyperuricemia, which is caused by pathological changes in purine metabolism.

Uric acid (2, 6, 8 - trioxypurine, urate) is a colorless crystalline substance that is formed as an end product of purine metabolism (part of nucleic acids).

  • normal value of uric acid in men - 180 - 420 μmol / l
  • increased value of uric acid in men - > 420 μmol / l
  • normal value of uric acid in women - 180 - 360 μmol / l
  • increased value of uric acid in women - > 360 μmol / l

Urates settle mainly in the synovial fluid of the joints, where their microcrystals accumulate and create a mechanical barrier - tofus, which grows into the environment and is lined by a local inflammatory reaction.

Larger tophi and inflammatory deposits are the cause of pain. The largest ones can even limit mobility, even disrupt and deform the subchondral bone.

Any of the joints in the upper and lower limbs can be affected, with minor joint disease predominating. The metatarsophalangeal joint of the big toe is most often affected.

Prevalence of days in the world

The disease occurs mainly in developed countries and affects about 1% of the population.

As many as 90% of all patients are middle-aged men (mainly over 40 years). The remaining 10% are women aged 55 and over (the disease occurs mostly after menopause).

In Europe, gout affects only 0.3% of the population, representing 95% of men and 5% of women.

Interesting: The
large difference in the incidence of gout in men and women is due to a hormonal imbalance that is likely to affect purine fusion de novo.
The researchers explain this inequality by decreased levels of 17-beta-estradiol and increased levels of testosterone .  

The reason for the increased prevalence of gout in developed countries is the increased production and consumption of purines in food (meat, offal, alcohol), and lower physical activity.


Gout is caused by hyperuricaemia, an increased level of uric acid. If we want to look for the causes of gout, we must look for the causes of hyperuricemia.

And there are not many of them.

Hyperuricemia is caused by a number of internal and external factors and their combination.

The essence of the disease is increased production of uric acid, which the body does not manage to excrete, and thus accumulates, or impaired renal function and its retention in the body (uric acid is excreted exclusively by the kidneys).

Breakdown of days by cause:

  • Primary gout/hyperuricemia (90%) - is caused by impaired renal tubules, excessive urate production, and at the same time their reduced uric acid excretion
  • Secondary gout/hyperuricemia (10%) - is caused by excessive production of uric acid due to the increased breakdown of nucleoproteins

The most common causes of gout/hyperuricemia

  • Genetic predisposition causes gout in up to 60% of cases (according to various statistics 20% to 80%), while the problem lies in the variation of the structure and mutation of three genes - SLC2A9, SLC22A12, and ABCG2. Abnormalities of these genes lead to increased production, and at the same time to reduced urate absorption. If there is gout in the family in the direct line (mother, sibling), it is appropriate to have the uric acid level checked at regular intervals (preventive examination).
  • Some other diseases, by their very nature, evoke the origin of gout. Such diseases preferably include metabolic syndrome (75%), renal failure, diabetes mellitus, dyslipidemia, arterial hypertension, ischemic heart disease, obesity, psoriasis, polycythemia, hemolytic anemia, myxedema, Lesch-Nyhan syndrome, and others. It also occurs after lead intoxication (kidney damage) or transplantation of some solid organs.
  • Some drugs are often associated with the development of this disease. The primacy belongs to diuretics, ie drugs that are used for dehydration - the elimination of excess water from the body through the kidneys. Another risk is immunosuppressive drugs. Niacin, cyclosporine, and acetylsalicylic acid are also likely to cause side effects and gout.
  • Eating habits are an important factor in the onset of gout. Although it may seem strange, it is the diet and its composition that are responsible for the high incidence of this disease, and increase it by 12%. The danger lies in consuming food high in purines. Their highest concentration is in meat, in some internal organs (liver, heart), in seafood, or in mackerel. The most dangerous beverages are alcoholic beverages, especially beer (it has a diuretic effect), and sweetened beverages (high in fructose content).

Vegetarians whose diet is poor in purines are at low risk.
Although some vegetables contain many of them (peas, beans, lentils, artichokes), they have been considered risky in the past, but recent studies have ruled out this myth.

  • A lifestyle in which passivity predominates results in obesity, which also figures in the onset of gout.
    BMI (body mass index) higher than 35 triples the risk of gout!


Gout begins with an increase in uric acid in the blood. At this time, there are no clinical manifestations of the disease.
It can be detected during blood sampling.

If a patient has diagnosed hyperuricaemia with no gout, it is most likely a natural aging process or other illness.
In humans, it occurs with increasing age, gradually increasing. In most cases, however, gout will never develop.

Prodromal manifestations of the disease appear before the onset of the disease and the onset of specific symptoms.
The main representatives are inflation and meteorism (increased flatulence) to a high degree.

Sometimes patients also suffer from muscle and joint pain, loss of appetite, stomach upset, unpleasant taste in the mouth.
Mentally, they are often irritable, nervous, or often change their mood.

The first manifestations appear at the time when uric acid begins to accumulate in the joints.
The primary symptom is pain. The first attack of pain comes from full health, occurs suddenly, unexpectedly, typically at night or in the early morning, escalating over several hours.
It disappears without a week without treatment, with adequate therapy it disappears within 24 to 36 hours.

The affected joints are swollen, shiny at the site of swelling, under the swelling they are warmer to the touch, red to purple, sensitive to touch and pressure, painful, resp. acute bouts of intense jerky pain occur - arthritis.

As the condition progresses, tofu overgrows and the joint degenerates, which is also visible from the outside.
Degenerative joint changes lead to a restriction of his mobility.

The first metatarsophalangeal joint of the big toe is most often affected (monoarthritis). 
Later, the tendency of oligoarticular to the polyarticular form of disability (involvement of several joints) increases.
Inflammation accompanying the disease, together with an attack of pain, can be the cause of fever and general exhaustion of the patient. However, fever occurs only sporadically.

Disorders of purine metabolism are also associated with disorders of lipoprotein and carbohydrate metabolism, which also causes other diseases (dyslipoproteinemia, diabetes mellitus, obesity, hypertension, nephropathy).

Seizure-evoking factors:

  • injury/microtrauma
  • joint overload
  • cold / infection
  • alcohol
  • dietary error
  • some medicines
  • stress


The primary problem that leads the patient to the doctor is the spontaneous acute pain of the affected joint without an injury mechanism. However, most patients do not see a doctor until the pain recurs.

The basic examination by a general practitioner is the collection of urine and blood, where hyperuricemia, ie an increased level of uric acid, is detected.

In addition to hyperuricemia, the presence of salt and leukocytes (white blood cells) is usually detected in the laboratory, which narrows the differential diagnosis by confirming the ongoing inflammation in the body, so the doctor knows that it is an inflammatory disease.

Interesting :
In recent years, the clinical picture of gout has deviated from standard symptomatology.
At certain points and in individual patients, there may not be manifestations, resp. evocative factors identical to the textbook example of the disease.
Normal serum uric acid levels are also determined in the laboratory. They remain elevated in the urine.

If any gout is suspected, it is necessary to puncture the synovial fluid from the joint as part of the diagnosis. The presence of sodium urate crystals confirms the diagnosis.

X-rays of the affected joint are usually an additional examination, but at the same time, they can tell a lot. Inflammatory changes in the joint and urate deposits are evident in the image.
In the later stage of the disease, limited osteoporotic changes in the vicinity of sediments, cysts to bone erosions, extensive osteolytic deposits with joint deformity can be detected.

Since 1977, doctors, especially orthopedists, have used ARA diagnostic criteria . They were developed by the American Society of Rheumatology in order to differentiate gout from other rheumatological or inflammatory joint diseases as reliably as possible.

ARA diagnostic criteria:

  1. Evidence of uric acid crystals in synovial fluid or topha
  2. Presence of at least 6 of the symptoms listed below:
  3. maximum joint inflammation on the first day
  4. at least two seizures for days
  5. monoarticular arthritis (inflammation of one joint)
  6. reddening of the skin above the affected joint
  7. joint pain and swelling I.MTP joint
  8. unilateral involvement of I.MTP joint
  9. unilateral involvement of the tarsal joint
  10. the suspected presence of tofu or its confirmation
  11. hyperuricemia (increased serum uric acid)
  12. asymmetric (uneven) swelling of the joint
  13. present cysts on the leg on X-ray
  14. the negative result of culturing on bacteria in synovial fluid


Gout occurs in four basic stages, from the asymptomatic period to the chronic form of the disease with frequent gout attacks.

Stage days:

  1. The period of asymptomatic hyperuricemia is the stage when the patient has no problems, but an increased uric acid concentration may be detected by random examination. This period can last several years.
  2. The period of an acute attack of gout is typically manifested by an arthritic episode. It is characterized by joint pain, swelling, redness, in elderly patients often the only edema in the beginning. Seizures first occur as monoarthritis (isolated involvement of one joint), mostly affecting the first metatarsophalangeal joint. They are becoming more common and the symptoms are getting worse.
  3. The inter-seizure period begins after the acute seizure period. This is a temporary regression of symptoms. Gradually the inflammation subsides, the joint ceases to be painful, and slowly swells. This interval varies from a few weeks to years.
  4. The period of chronic gout is manifested by repeated seizures, while changes in the form of the presence of tophi to deformities are already noticeable on the joints. These changes cause a reduction in momentum.

What are the regimen measures for a patient with gout?

In addition to drug treatment, regimen measures that improve the course of the disease and reduce the number of daily attacks also contribute to improving the patient's condition.

These measures mainly concern eating habits (a varied diet low in purines), but also lifestyle (prevention of obesity, hypertension, treatment of diabetes, physical activity) 

Regular physical activity has a gentle and moderate effect on the joints. It perfuses them, improves their mobility, and thus alleviates the consequences of days.

Conversely, unilateral loading, whether the excessive or incorrect movement can cause a painful attack.

The patient should consult with their doctor or physiotherapist before starting the nature of the exercise or the degree of load.

Changing eating habits should focus not only on food but also on drinks.

Low purine diets and beverages improve the patient's condition by reducing serum uric acid and thus its deposition in the joints.

Adequate fluid intake must again be maintained due to its faster excretion from the body.

Table with suitable and unsuitable food and beverages:

Suitable food Restricted foods Unsuitable food
  • vegetables
  • fruit
  • rice
  • cereals
  • milk products
  • cooked poultry meat
  • fresh fish
  • legumes
  • meat products
  • entrails
  • fish in oil
Suitable drinks Limited drinks Unsuitable drinks
  • clearwater
  • alkaline mineral water
  • weaker tea
  • fruit juices
  • alcohol, mainly distilled
  • sweetened beverages

Spa treatment is recommended only during the intervertebral period. The patient undergoes various spa procedures, which are associated with monitoring his drinking regime and daily diuresis (amount of urine per day).

Mineral waters with diuretic (diuretic) effects are preferred, which by their effect increase the daily amount of urine, change its pH, and at the same time increase the excretion of uric acid.

How it is treated: Gout

How is gout treated? Medication, diet or rehabilitation

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