abolic disease whose clinical manifestations are due to the precipitation of monosodium urate crystals in the tissues. The characteristic manifestation is the episodes of joint inflammation, generally self-limited and recurrent, due to the deposit of monosodium urate crystals in the synovial fluid. They can also be deposited extarticularly, forming easily palpable aggregates called tophi. To all this can be associated kidney disease and uric acid urinary stones.
It is usually accompanied by hyperuricemia, although during the acute attack it is not uncommon for the uricaemia to be normal.
Causes of gout
More than 95% of gout cases are primary. Although some enzyme alterations have been identified, in most cases of primary gout it has not been possible to find the metabolic defect.
3-5% of cases are secondary. The most important causes are neoplasms, especially of hematological origin, and the administration of some drugs (diuretics, low-dose salicylates, pyrazinamide).
Before puberty, uric acid levels in the blood are very low, and children, except for rare enzyme defects, do not suffer from gout. Upon reaching puberty, boys reach levels that will be maintained throughout life, although these levels tend to increase over the years. In women, the main increase in uricaemia occurs after menopause .
It is common to find several members of the family affected by hyperuricemia and gout, presumably due to the existence of genetic predisposition, although common eating habits may also play a role.
Uric acid levels in the blood increase by two possible mechanisms:
- Increased uric acid synthesis, which is usually accompanied by increased renal excretion and increased incidence of renal uric acid stones. This increase in synthesis may be due to:
– Enzyme defects, which are genetically transmitted.
– Increased catabolism of purines, which is more frequent. It is observed in neoplasms and
- Decreased renal excretion, which is the most common mechanism. This mechanism appears in states of malnutrition, diabetic ketoacidosis, lactic acidosis in alcoholics, drug intake, thyroid diseases, kidney failure, etc.
What symptoms appear?
Arthritis gouty acute : occurs after many years of sustained asymptomatic hyperuricemia. Appears between 30 and 50 years. It is less common in women. A number of triggers have been defined as major trauma, repeated microtrauma, excessive alcohol intake, dietary violation, fasting, stress, or surgery.
It is characterized by the sudden onset of monoarticular pain, frequently of nocturnal onset. The pain is spontaneous but is exacerbated by any friction or attempted movement. The spontaneous duration is variable but remits between a few days and a few weeks without leaving sequelae.
In 50% of patients, the joint initially affected is the foot. It is followed in frequency: knee, tarsus, wrist, elbow, shoulder and other distal metatarsophalangeal and interphalangeal of the foot. The periarticular area is usually affected with redness and swelling of soft tissues. Occasionally it is accompanied by a fever of 38º. In the healing phase, the skin that covers the joint usually peels off.
After an initial attack there is an asymptomatic period that can go from weeks to years. These asymptomatic periods shorten over time.
In advanced disease, polyarticular episodes (involvement of several joints) are not uncommon.
Chronic gouty arthritis or tophaceous gout : it is the consequence of the body’s progressive inability to eliminate urate crystals as they are deposited. The presence of tophi is correlated with the time of evolution of the disease and the severity of hyperuricemia. The most common location for tophi is the pinna, elbow, hands, wrists, feet, knees, and the Achilles tendon.
The deposition of monosodium urate in the joints produces a picture of continuous pain with marked functional impotence .
Renal manifestations :
- Renal lithiasis: appears in 30% of gouty patients. Although these stones are usually uric acid, these patients present with mixed uric acid and calcium or pure calcium stones more frequently than the general population. Sometimes they precede joint manifestations by years.
- Uratic nephropathy: Some degree of renal failure usually appears in 50% of patients with gout. Evolution is slow and progressive, but it does not by itself slow down life expectancy. However, gouty disease is frequently associated with other diseases that affect kidney function, such as high blood pressure and diabetes mellitus.
Diagnosis of gout
The suspected diagnosis can be made by the symptoms, but with the exception of very typical cases, the margin of error is very important.
In the blood test, uric acid may be normal in gout attacks, since joint inflammation is due to monosodium urate crystals in synovial fluid and not to increased uric acid in the blood.
Radiography has no role in diagnosing gout attacks. Some alterations may appear on the radiograph in late phases.
The treatment of the acute attack of gout is done with NSAIDs or colchicine. NSAIDs are a very effective treatment. In general, indomethacin is recommended at high doses by mouth. Treatment should be maintained until symptoms disappear. Colchicine is used orally. It is given until the acute attack of gout disappears or side effects appear (nausea, vomiting, diarrhea). Clinical improvement after administration is a diagnostic criterion. Its effectiveness decreases with the time elapsed since the start of the attack.
In the event that the gout attack coincides with a pathology that prevents the use of NSAIDs or colchicine, there are other alternative treatments such as intra-articular corticosteroid injection.
The term treatment is treatment of hyperuricemia to prevent disease progression. The drugs used are:
- Allopurinol, which is the treatment of choice. Its intolerance is rare and a daily intake is sufficient.
- Uricosuric drugs, which increase the renal excretion of uric acid and are indicated when the excretion is less than 600 mg / day. They are contraindicated in kidney failure and kidney stones. It should be accompanied by an intake of 2 liters of water a day and make the urine alkaline to avoid the formation of stones.
Hypouricemic treatment should not be started until 2 weeks after the acute attack of gout and should be associated with colchicine for 6-12 months. Isolated asymptomatic hyperuricemia does not require treatment.
How to avoid it?
It is not recommended to follow any strict diet, as its effectiveness is very limited. However, it is advisable to moderate the intake of alcohol as well as some foods (game, shellfish, organ meats). Concomitant ingestion of hyperuricemic drugs (diuretics, pyrazinamide, nicotinic acid, and low-dose salicylates) should also be considered.
As it is frequently associated with obesity, a reduction in weight is beneficial.
To prevent further attacks, colchicine is prescribed after the last attack at low doses for 6-12 months. The aim is to prevent new gout attacks from appearing while reducing urate deposits with hypouricemic treatment.
You should see a doctor before any episode of inflammation of a joint with swelling and pain, to make a differential diagnosis of causes of arthritis.
Hello Readers, I am Nikki Bella a Psychology student. I have always been concerned about human behavior and the mental processes that lead us to act and think the way we do. My collaboration as an editor in the psychology area of Well Being Pole has allowed me to investigate further and expand my knowledge in the field of mental health; I have also acquired great knowledge about physical health and well-being, two fundamental bases that are directly related and are part of all mental health.