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Gout is the most prevalent inflammatory arthritis in men. Several epidemiologic studies from different countries suggest that the prevalence of gout has increased over the past few decades.
Disability Adjusted Life Years (DALYs) are an estimate of the burden a disease poses. They are the sum of years of potential life lost due to premature mortality and the years of productive life lost due to disability.
According to a study published in the Annals of the Rheumatic Diseases (ARD), a European journal, the global prevalence of gout was 0.08 % in 2010. DALYs amounted to 114000 in 2010, an increase from 76000 in 1990.
Gout is a type of arthritis cause by monosodium urate (urate/ uric acid) crystal deposition. These crystals precipitate into many tissues, often in and around joints. The disease can be classified into two types, primary gout and secondary gout. Primary gout is related to underexcretion or overproduction of uric acid. Secondary gout is secondary to other diseases, particularly those that lead to high cell turn over (hemolytic anemia) and genetic diseases that causes high blood uric acid level like Lesch–Nyhan syndrome.
Gout develops when the body excessively stores uric acid in the form of monosodium urate. This happens either due to overproduction or underexcretion of uric acid. This leads to hyperuricemia (elevated serum levels or uric acid), causing monosodium urate to crystallize and deposit in soft tissues and joints2.
Overproduction of uric acid may be caused by a genetic disorder, such as Lesch-Nyhan syndrome, as a result of disorders that cause high cell turnover such as psoriasis (a skin disorder). Elevated uric acid levels may also be caused by cell destruction as a result of chemotherapy for certain diseases.
Secondary gout as a result of underexcretion of uric acid may be caused by renal insufficiency (poor kidney function), starvation or dehydration and some medication used to treat high blood pressure.
Individual gout flares are often caused by sharp increases or decreases in urate levels. These changes may be caused as a result of acute alcohol ingestion, sudden excessive consumption of foods high in purines (red meat, shellfish), or dehydration.
Risk factors for gout include eating a diet that's high in purines, which are found in food such as red meat and shellfish. Alcohol consumption, particularly beer and a family history of gout are also risk factors.
An increase in the activity of phosphoribosyl pyrophosphate synthase enzyme which promotes purine synthesis or a decrease in the amount or activity of hypoxanithine guanine phosphoribosyl transferase enzyme which leads to uric acid break down leads to hyperuricemia.
Signs and Symptoms of gout include: joint pain, swelling of the joint, stiffness of the joint and joint inflammation.
Gout is diagnosed by the presence of urate crystals in the synovial fluid or soft tissues8. Methods used to ascertain that may include synovial fluid analysis, serum uric acid levels, 24-hour urate excretion, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and white blood cell count (WBC) and an X-ray.
The treatment is divided into three types according to the aim of the treatment. Treatment of acute gout with NSAIDs, Colchicine and Glucocorticoids. Prevention of a recurrent gout attack with colchicine daily and treatment of chronic gout which includes allopurinol .This medicine should not be used in acute attacks.
Complications of gout can include small lumps forming under the skin as a result of crystal deposition (tophi), joint damage and kidney stones.
In order to prevent future gout attacks lifestyle modifications such as maintaining high levels of fluid intake and limiting consumption of high purine foods such as red meats and shellfish.
Treatment of acute gout attacks and reducing serum levels of uric acid allows patients to live a normal life. If left untreated, acute gout may develop into chronic gout.
Gout is the most common inflammatory arthritis in men. Several epidemiologic studies from different countries suggest that the prevalence of gout has increased over the past few decades.
According to a study published in the Annals of the Rheumatic Diseases (ARD), a European journal, the global prevalence of gout was 0.08 % in 2010.
Definition of gout It is a type of arthritis cause by monosodium urate (urate/uric acid) crystal deposition. These crystals precipitate into many tissues, often in and around joints. It is also known as podagra disease.
The disease can be classified into two types, primary gout and secondary gout.
Primary gout is associated with underexcretion or overproduction of uric acid. It is usually related to unhealthy dietary habits, alcohol abuse and metabolic syndrome.
Secondary gout is secondary to other diseases, particularly those that lead to high cell turn over. These diseases include psoriasis (a skin disorder), hemolytic anemia and genetic diseases that causes high blood uric acid level like Lesch–Nyhan syndrome.
Gout develops when the body excessively stores uric acid in the form of monosodium urate. This happens either due to overproduction or underexcretion of uric acid. This leads to hyperuricemia (elevated serum levels or uric acid), causing monosodium urate to crystallize and deposit in soft tissues and joints2.
Most gout patients suffer from a surplus in urate stores as a result of underexcretion (an inability to excrete enough quantities of uric acid in the urine). Of the remaining patients, some consume too much purines (found in foods such as red meat and seafood), while others produce excessive quantities of uric acid endogenously (inside the body). A few suffer from impaired intestinal elimination of uric acid.
Overproduction of uric acid may be caused by a genetic disorder, such as Lesch-Nyhan syndrome and von Gierke disease. It may also occur as a result of disorders that cause high cell turnover such as myeloproliferative (diseases of the blood cells) and lymphoproliferative disorders (abnormal proliferation of lymphocytes), psoriasis (a skin disorder), and hemolytic anemias.
Cell destruction as a result of chemotherapy for certain malignancies, particularly those of the hematopoietic (blood stem cells) or lymphatic systems, may cause an increase in uric acid levels2. Excessive exercise and obesity may also lead to an increase in uric acid levels.
Secondary gout due to underexcretion of uric acid may be caused by renal insufficiency (poor kidney function), starvation or dehydration, lead nephropathy (also called saturnine gout, kidney damage from lead exposure), chronic alcohol abuse (particularly beer and hard liquor) and some medication such as diuretics and beta-blockers (medication used to treat high blood pressure).
Causes of gout flares
Individual gout flares are often caused by sharp increases or decreases in urate levels. These changes may be caused as a result of acute alcohol ingestion, sudden excessive consumption of foods high in purines (red meat, shellfish), rapid weight loss, dehydration, or trauma. Gout flares may also be caused by additions of or changes in dosage of medications that raise or lower uric acid levels, such as loop and thiazide diuretics and xanthine oxidase inhibitors.
Eating a diet that's high in purines found in food such as red meat, seafood, particularly shellfish and animal entrails (internal organs). Consumption of large quantities in beverages with fructose may also increase the levels of uric acid in the body. Alcohol consumption, particularly beer, also increases the risk of gout.
Obesity increases the risk of gout.
Medical conditions such as untreated high blood pressure, anemia and chronic illnesses such as diabetes, metabolic syndrome, and heart (such as hypertension, hypercholesterolemia, hypertriglyceridemia) and kidney diseases (such as renal insufficiency).
Medications such as thiazide diuretics (hypertension medication) and anti-rejection drugs used by recipients of an organ transplant.
Family history of gout.
Age and gender. Men between the ages of 30-50 and women after menopause are the most likely to develop gout.
Recent surgery or trauma.
The disease is the result of an increase in uric acid levels in the blood which can be caused by either of these mechanisms
1. Underexcretion of uric acid. There will be a defect in the renal tubules excretion of uric acid.
2. Overproduction of uric acid.So either an increase in the activity of phosphoribosyl pyrophosphate synthase enzyme which promotes purine synthesis or a decrease in the amount or activity of hypoxanithine guanine phosphoribosyl transferase enzyme which leads to uric acid break down.
As a result there will be a disorder in purine metabolism resulting in crystallized uric acid and monosodium urate crystals that will be deposited in avascular tissues like cartilage or relatively vascular tissues like tendons, tendon sheaths and walls of bursae. Other locations for crystal deposition also include the ear helix, kidney parenchyma, eye lid, olecranon, and Achilles tendon.
In a gout attack, the tophi (deposit of crystalline uric acid) breaks down as a result of the triggering factor. It then induces an immune mediated inflammatory reaction by either an increase in the level of interleukin 1 beta or a decrease in the level of urate oxidase (uricase) enzyme.
The patient usually presents complaining of the following:
1. Joint pain
This pain is sudden and is accompanied by a burning sensation. It usually occurs at night and may be severe enough to wake the patient from their sleep. It usually affects the joint of the big toe, but it may happen in the feet, ankles, knees, hands and wrists. The pain is usually most severe within the first four to 12 hours after it begins6.
2. Swelling of the joint
3. Signs of joint inflammation which include hotness, redness, tenderness and loss of function.
4. Stiffness of the joint with a decrease in joint motion.
5. Possible fever and chills with a generalized feeling of fatigue.
6. The patient may also be able to feel tophi which is a hard, painless deposition of urate crystals. May be single or multiple.
Fluid is collected from the afflicted joint using a needle. The fluid is then examined under the microscope to look for the presence of urate crystals. The crystals will aid in ruling out a diagnosis of infectious arthritis and their shape will confirm a diagnosis of gout or pseudogout.
Patients may present with hyperuricemia but an absence of symptoms, this is not diagnostic of gout. Furthermore many patients with gout symptoms may have normal serum uric acid levels at the time of a gout attack8. Consequently, an elevated serum uric acid level does not indicate or predict gout8.
A 24-hour urinary uric acid evaluation is performed if uricosuric therapy (medications that increase the excretion of uric acid in the urine) is being considered. If more than 800 mg of uric acid are excreted in 24 hours while the patient is consuming a regular diet, this patient’s body produces too much uric acid. These patients require allopurinol instead of probenecid to reduce uric acid levels.
The treatment is divided into three types according to the aim of the treatment.
Includes the use of NSAIDs (other than aspirin), colchicine and glucocorticoids. Other treatments include rest, ice and fluid intake more than 3 liters per day and lifestyle modifications (such as reduce consumption of purines).
With colchicine daily
Which includes allopurinol which leads to a decrease in the levels of uric acid by blocking its production. This medicine should not be used in acute attacks.
Stopping or altering any medication that may have caused the gout attack such as thiazide diuretics.
Since allopurinol, febuxostat, and probenecid alter serum and tissue uric acid levels, they may cause acute gout attacks of gout. To reduce the possibility of the attack, colchicine or low-dose NSAID treatment is provided for at least 6 months.
Dietary modifications, which include:
Reducing the consumption of foods high in purines such as organ meats, sardines, shellfish, trout, haddock, salmon and turkey.
Drinking at least 8 glasses of water or liquids per day
Limiting alcoholic beverages and fructose sweetened drinks.
Drugs that promote uric acid excretion.
Complications of gout can include small lumps forming under the skin as a result of crystal deposition (tophi), joint damage and kidney stones.
In order to prevent future gout attacks lifestyle modifications are necessary.
Lifestyle modifications include:
Treatment of acute gout attacks and reducing serum levels of uric acid allows patients to live a normal life. If left untreated, acute gout may develop into chronic gout.
Gout is the most prevalent inflammatory arthritis in men. Several epidemiologic studies from different countries suggest that the prevalence of gout has increased over the past few decades.
Disability Adjusted Life Years (DALYs) are an estimate of the burden a disease poses. They are the sum of years of potential life lost due to premature mortality and the years of productive life lost due to disability.
According to a study published in the Annals of the Rheumatic Diseases (ARD), a European journal, the global prevalence of gout was 0.08 % in 2010. DALYs amounted to 114000 in 2010, an increase from 76000 in 1990.
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