Generality
Gout is a disorder of purine metabolism, characterized by:
- Elevated serum urate levels ( hyperuricemia );
- Formation of uric acid deposits in various locations ( tophi );
- Acute articular inflammatory attacks ( monoarticular arthritis ), with deposits of urates in the cartilages;
- Kidney disease ( gouty nephropathy ):
Gout is an almost exclusive prerogative of the male sex (about 95% of the cases) and begins, on average, between 30 and 50 years.
A blood test or taking a sample of liquid from the swollen joint can help confirm the diagnosis.
A change in life habits, together with adequate therapy, is able to keep the symptoms under control.
Hyperuricemia
Gout is the consequence of chronic hyperuricemia .
Hyperuricemic is considered to be the person who, after 5 days of hypopuric diet and without taking drugs that affect uricemia (vitamin C, vitamin PP, salicylic, diuretic), has uric acid values in the blood higher than:
- 7 mg / dl if man
- 6.5 mg / dl if female
- After 9 mg / dl, the gout risk becomes high and specific drugs are administered
Hyperuricemia is classified as:
- Primitive : if it is not consequent to acquired disease;
- Secondary : when it derives from a morbid alteration of another type or from the taking of specific drugs.
What's this
GOTTA is one of the main depositions of uric acid . The latter represents the final product of the purines and is formed in the body starting from the metabolism of both endogenous purines (de novo synthesis) and exogenous (deriving from the diet).
Various conditions can cause an increase in the serum level of uric acid, such as: alcoholism, obesity, states of high metabolic turn-over (tumor lysis and myeloproliferative diseases), some drugs (including salicylates and diuretics) and diets rich in purines (eg . meat).
Even rare genetic diseases can cause EUREUREMEMIA, with and without urate deposit.
Chronic hyperuricemia is a harmful condition for the body, as it is the pathogenetic basis for the development of monosodium urate (UMS) deposits in various organs and tissues.
If left untreated, the consequences associated with this situation can be disabling, especially when cardiovascular, renal and joint complications arise.
Gout can result from excessive production of uric acid and / or decreased excretion .
In addition to an increase in uricemia, clinical evidence of gout includes attacks of acute inflammatory arthritis with redness, swelling and joint pain. In the most serious cases, the formation of nodules is observed - called tofi - due to the deposition of monosodium crystals of uric acid, surrounded by an amorphous matrix.
The triggers of arthritis attacks are alcohol abuse and overeating, prolonged fasting and joint trauma, as well as prolonged intense efforts.
Causes
Gout can be caused, basically, by:
- Exalted synthesis of purines with consequent overproduction of uric acid;
- Decreased renal excretion of uric acid *.
* Purines are nitrogenous substances that enter into the composition of DNA. They can be endogenous (produced by body metabolism) or exogenous (derive from food degradation). Their catabolism gives rise to uric acid, whose persistent increase in plasma in turn gives rise to gout.
The first condition (1) is often hereditary and can however be aggravated by an increased introduction of purine compounds with the diet. In the second case (2) the hyperuricemia is due to the decreased efficiency of the kidney in the elimination of uric acid.
Traditionally the onset of gout is blamed for exaggerated food intake. Although this factor, together with alcoholism, a sedentary lifestyle and the abuse of certain drugs, is nevertheless predisposing, its contribution tends to be marginal.
Symptoms
To learn more: Gout symptoms
The patient suffering from gout complains of intermittent joint pain ( monoarticular arthritis ), generally associated with swelling, erythema and heat. Painful episodes mainly involve the joints of hands and feet and, in about 90% of cases, the metatarsal-phalangeal joint of the big toe is primarily affected.
In the chronic forms can appear nodules of variable size called tophi . These deposits of uric acid are initially formed around the interphalangeal and metacarpal and / or metatarsal-phalangeal joints. Later they appear also in the extrarticular site, as in the Achilles tendon and in the external part of the ear. Their initially salmon-pink color then becomes yellowish-white.
Gout also facilitates the formation of urinary calculi and lithiasis up to compromising, in an advanced stage, the entire renal function.
Gout: Clinical Features
- Involvement of a joint at a time (monoarticular arthritis), which often originates from the joint of the big toe;
- Sudden onset;
- The affected joint appears warm, red and shiny;
- Excruciating pain;
- Possible malaise and fever;
- Recurrent attacks involving other joints, with possible duration of about a week;
- Subcutaneous formation of gouty tophi, nodules that collect crystals of uric acid.
Diagnosis
The diagnosis of chronic hyperuricemia with deposits of urate (gout) should be suspected in the presence of factors that favor the increased production and / or reduced excretion of uric acid.
The evaluation includes:
- Anamnesis : involves the collection of information related to the levels of uricemia resulting from previous tests, presence of concomitant diseases, family history, use of drugs, food and beverages.
- Physical examination : must look for evidence of arthritis with redness, swelling and pain in the joints; the attacks begin mainly affecting the big toe, with a subsequent extension to other parts of the body, such as ankles, knees, wrists and elbows, causing burning and redness.
- Laboratory analysis (uricemia) : hyperuricemia is the major risk factor for gout and can also be used as a diagnostic marker, although some gouty patients demonstrate a normal serum concentration of uric acid.
In addition to these investigations, the doctor can indicate the execution of an arthrocentesis to search for the presence of crystals and a radiograph of the joints involved in the search for deposits or signs of joint pain.
Treatment
To learn more: Gout treatment drugs and Gout remedies
Gout therapy is based on the control of uric acid metabolism.
In case of acute attack of monoarticular arthritis, it is good to immobilize the joint by resting it and uncovering the painful area.
drugs
Furthermore, under medical supervision it is possible to take:
- NSAIDs ;
- Colchicine (a toxic antimitotic alkaloid that promotes the excretion of uric acid, equipped, among other things, with good analgesic and anti-inflammatory properties).
In case of gout, the intake of some drugs, such as certain diuretics, cortisone drugs, aspirin and derivatives must be suspended. On the other hand, chronic hyperuricemia will be treated with medicines capable of inhibiting the synthesis of uric acid (ie allopurinol ) or favoring their elimination (uricosuric drugs: probenecid or sulfinpyrazone). The administration of these drugs should never be started during an acute gout episode.
Dietary measures and lifestyle
To learn more, read: Diet for Gout and Example Diet for Gout
The exaggerated intake of purines with food is an extremely rare but still possible cause, especially in those predisposed. For this reason, drug therapy is accompanied by dietary therapy which involves the elimination of foods rich in purines and alcohol, combined with a caloric moderation necessary to promote weight loss.
In case of gout, an adequate supply of water is also essential, in order to prevent the formation of kidney stones.
