It is a very common arthritis that occurs when there is too much uric acid in the blood.
This is called hyperuricemia . Uric acid is a breakdown product of normal metabolism in the body and is excreted through the urine.
The buildup of uric acid produces needle-like crystals that form in joints, soft tissues, and organs.
The rise in gout cases today is likely due to an aging population, changes in diet and lifestyle, the increasing incidence of obesity, and increased use of medications, such as diuretics, all of which may cause a high level of uric acid in the body.
Development of hyperuricemia and gout
The process that leads to hyperuricemia and gout begins with the metabolism or breakdown of purines.
The purines are compounds that are important for energy. They are part of the nucleic acids (DNA and RNA) that are present in all cells of the body.
They can be divided into two types:
Endogenous purines are produced within human cells and exogenous purines are obtained from food.
The process of breaking down purines results in the formation of uric acid in the body. Most mammals, except humans, have an enzyme called uricase.
The enzyme urate oxidase breaks down uric acid so that it can be easily removed from the body.
Because humans lack urate oxidase, uric acid is not easily removed and can accumulate in body tissues.
Uric acid and hyperuricemia
Purines in the liver are converted to uric acid. Uric acid enters the bloodstream.
Most of the uric acid passes through the kidneys and is excreted in the urine. The remaining uric acid travels through the intestines where bacteria help break it down.
The enzyme responsible for the production of uric acid from purines is xanthine oxidase.
This enzyme is the target of urate-reducing treatments such as allopurinol.
This process keeps the uric acid level in the bloodstream at levels below 6.8 mg / dL.
But sometimes the body makes too much uric acid or eliminates too little.
In any case, the level of uric acid increases in the blood. This condition is known as hyperuricemia.
If uric acid reaches a blood level of 7 mg / dL or more, it becomes insoluble and needle-like crystals of a salt called monosodium urate can form.
As the crystals build up in the joints, they can trigger inflammation, redness, swelling, and pain.
However, most people with hyperuricemia do not have gout symptoms.
The higher the uric acid level, the greater the risk of crystal formation.
About 0.5% of people with a uric acid level between 7.0 and 8.9 mg / dL develop gout and about 5% of people with a uric acid level greater than 9 mg / dL develop gout.
The symptoms of gout depend on the stage of the disease.
When gout remains untreated, the periods between acute gout attacks become shorter and shorter and the attacks, although sometimes less intense, can last longer.
In about 10 to 20 years, gout becomes a chronic disorder with constant low-grade pain and mild or acute inflammation.
Gout can subsequently affect several joints, including those that may have been symptom-free at the onset of the disorder.
In rare cases, the shoulders, hips, or spine are affected.
Gout can be divided into four stages:
- Asymptomatic hyperuricemia.
- Acute gouty arthritis.
- Intercritical drop.
- Chronic tophaceous gout.
Symptoms of Asymptomatic Hyperuricemia
Asymptomatic means there are no symptoms. Increased uric acid in the blood (hyperuricemia) is the first stage of gout. This stage can last 30 years or more.
Hyperuricemia does not always lead to gout. Less than 20% of people with hyperuricemia develop gout.
However, there is an association between hyperuricemia and the risk of hypertension, heart disease, and kidney disease.
This association should be carefully studied as it might be possible to lower uric acid and reduce the risk of developing these diseases.
Currently, treating asymptomatic hyperuricemia is not recommended.
Symptoms of acute gouty arthritis
Acute gouty arthritis occurs when the first symptoms of gout appear.
Sometimes the first signs of gout are brief stabs of pain (small attacks) in an affected joint.
These attacks can occur for several years before the full condition occurs.
Symptoms of acute gouty arthritis often begin in one joint and include any of the following:
- Severe pain in and around the joint. It may feel like “crushing” pain or a dislocated bone; physical activity and even the weight of the sheets can be excruciating.
- Heat on the skin of the joint. Tight, shiny, red skin over the affected area, which may peel off after a few days.
- Chills and mild fever, loss of appetite, general malaise.
Gout that occurs in a joint is called monoarticular gout.
About 60% of all first-time monoarticular gout attacks in middle-aged adults occur in the big toe.
This is known as podagra. Symptoms can also occur in other places, such as the ankle or knee.
If more than one joint is affected, the condition is known as polyarticular gout.
Multiple joints are affected only in 10% to 20% of the first attacks.
Older people are more likely to have polyarticular gout.
The most commonly affected joints are the foot, ankle, knee, wrist, elbow, and hand.
The pain usually occurs in the joints on one side of the body, and usually, but not always, in the legs and feet.
People with polyarticular gout are more likely to have slower-onset pain and a longer delay between attacks.
People with polyarticular gout are also more likely to experience a low-grade fever, loss of appetite, and a general feeling of poor health.
An untreated attack peaks 24 to 48 hours after symptoms first appear and disappears after 5 to 7 days.
Some attacks last only a few hours, while others last for several weeks.
Although the symptoms may disappear, the crystals are still present and future attacks are likely to occur.
Symptoms of intercritical gout
Intercritical gout is the term used to describe the periods between attacks.
The first attack is usually followed by a complete disappearance (remission) of symptoms.
But, without treatment, gout almost always returns. More than two-thirds of patients have at least one more attack within 2 years of the first attack.
In 10 years, more than 90% of patients who had a seizure are likely to have more seizures.
Symptoms of chronic tophaceous gout
After several years, patients with high uric acid can develop uric acid deposits called tophi.
These are solid deposits of uric acid crystals that form in joints, cartilage, bones, and elsewhere in the body.
In some cases, tophi break through the skin and appear as white or yellowish calcareous nodules that have been described as crab eyes.
Without treatment to lower uric acid, tophi develop about 10 years after disease onset, although tophi can also occur 3 to 42 years later.
Risk factors for the appearance of tophi are:
Tophi are more likely to appear early in the course of the disease in older people.
Women have a higher risk of developing tophi than men.
People who have undergone an organ transplant and take the drug cyclosporine are also at high risk of developing tophi.
Location of tophi
A tophus can form in the following locations:
- Curved ridge along the edge of the outer ear.
- Elbow or knee.
- Hands or feet: Older patients, particularly women, are more likely to have gout in the small joints of the fingers.
- Around the heart and spine (rare).
Tophi are generally painless. But they can cause pain and stiffness in the affected joint. Over time, they can also damage cartilage and bone and destroy the joint.
Large tophi under the skin of the hands and feet can cause serious deformities.
Properly treated gout by reducing uric acid to less than 6.0 mg / dL is indeed “curable” and rarely poses a long-term health threat, although pain can be disabling during an attack.
Pain and disability
If left untreated, gout can become a painful and disabling chronic disorder.
Persistent gout can destroy cartilage and bone. This causes deformed joints and loss of movement.
If gout is not treated, tophi can grow to the size of golf balls and destroy bone and cartilage in joints.
This is similar to the process in rheumatoid arthritis . In very severe cases, joint destruction results in complete disability.
Gout and heart disease
Gout is found at higher rates in people with high blood pressure, coronary artery disease, or heart failure.
A high uric acid level has been linked to a high risk of death from heart disease.
Studies have also found an association between gout and metabolic syndrome.
This is a collection of health problems, such as abdominal obesity, high blood pressure, high triglycerides, and low (good) cholesterol.
This syndrome increases a person’s risk of developing heart disease and diabetes.
Studies are underway to determine whether it is beneficial to treat asymptomatic hyperuricemia in these people.
Uric acid nephrolithiasis (kidney stones)
People who have kidney stones that are formed from uric acid are more likely to have hyperuricemia, which suggests that hyperuricemia is responsible for this type of kidney stone.
Uric acid stones can also form in a person who does not have gout or hyperuricemia.
Not all kidney stones in gout patients are made of uric acid.
Some are made from calcium oxalate, calcium phosphate, or substances combined with uric acid.
Uric acid stones can also form in a person who does not have gout or hyperuricemia.
Chronic uric acid interstitial nephropathy
Chronic interstitial uric acid nephropathy occurs when crystals slowly form in the structures and tubes that carry fluid from the kidney.
Chronic kidney disease
For many years, hyperuricemia was not thought to cause kidney disease, but hyperuricemia was considered to be a consequence of kidney disease.
Acute kidney failure
Sudden overproduction of uric acid can sometimes block the kidneys and cause them to fail.
This occurrence is very rare but can develop after any of the following:
- Chemotherapy for leukemia or lymphoma, particularly acute forms of the disease.
- Other cancers, such as breast cancer and lung cancer.
- Seizures of epilepsy.
- Preeclampsia o eclampsia.
- Use of medications to prevent kidney transplant rejection, such as cyclosporine.
- Kidney conditions.
Causes and risk factors
Gout is considered primary or secondary, depending on the causes of the high uric acid level in the blood (hyperuricemia).
Almost all cases of primary gout are idiopathic. This means that the cause of hyperuricemia cannot be determined.
Primary gout is most likely the result of a combination of genetic, hormonal, and dietary factors.
Secondary gout is caused by medications or medical conditions other than a metabolic disorder.
People with gout are at a higher risk of having metabolic syndrome.
Metabolic syndrome is a collection of health problems, such as abdominal obesity, high blood pressure, and low (good) cholesterol.
This syndrome increases a person’s risk for heart disease and stroke.
Therefore, lifestyle changes are an important aspect of preventing gout and improving overall health.
The following factors increase the risk of developing gout:
Gout generally occurs in men in their mid-40s.
Men in this age group who have gout are often obese, have high blood pressure, unhealthy cholesterol levels, and drink large amounts of alcohol.
In the older age group, the risk of developing gout is equal in men and women.
In this group, gout is more often associated with kidney problems and the use of diuretics.
Less frequently it is associated with alcohol consumption.
Gout in children is rare except for rare inherited genetic disorders that cause hyperuricemia.
Men have a much higher risk of developing gout than women.
In men, the uric acid level normally increases at puberty.
In some men, the level is higher than normal, which means they have hyperuricemia.
Gout symptoms appear after 20 to 40 years of persistent hyperuricemia.
Men who develop gout generally experience their first attack between the ages of 30 and 50.
Before menopause, women have a much lower risk of developing gout than men.
This may be because estrogen causes the kidneys to excrete more uric acid.
Only about 15% of gout cases in women occur before menopause.
After menopause, the risk increases. At age 60, the risk of developing gout in men and women is equal.
After age 80, gout occurs more often in women.
Family History and Genetics
About 20% of people with gout have a family history of this condition.
Several genes are related to uric acid metabolism and gout.
Some people have a faulty protein (enzyme) that interferes with the way the body breaks down purines.
Scientists have found a clear link between body weight and uric acid level.
The higher a person’s body mass index, the greater the chance of developing gout.
As a result, the risk of developing gout in many countries is increasing due to the increasing incidence of obesity.
Children who are obese may be at higher risk of developing gout as adults.
Thiazide diuretic medications are used to control high blood pressure.
These medications are closely related to the development of gout.
Many older patients who develop gout take diuretics.
Other medications can also increase uric acid levels and increase the risk of developing gout.
- Aspirin: Low doses reduce uric acid excretion and increase the chances of hyperuricemia. This can be a problem for older people who take low doses of aspirin to protect against heart disease.
- Niacin: This medicine is used to treat cholesterol problems.
- Pyrazinamide: it is used to treat tuberculosis.
- Cyclosporine and Tacrolimus : Two drugs used to control the body’s immune response.
- Levodopa: commonly used to treat Parkinson’s disease.
- Beta-blockers and angiotensin converting enzyme inhibitors: Other medicines used to treat high blood pressure.
Drinking excessive amounts of alcohol can increase the risk of developing gout.
Beer is more strongly linked to gout. Alcohol consumption is highly associated with gout in young adults.
Excessive alcohol consumption particularly increases uric acid level.
It appears that alcohol plays a minor role among older patients, especially among women with gout.
Alcohol increases uric acid level in the following ways:
- Provides an additional dietary source of purines (the compounds from which uric acid is formed).
- It intensifies the production of uric acid in the body.
- The kidneys’ ability to excrete uric acid decreases.
Long-term exposure to lead is associated with the accumulation of uric acid and a high incidence of gout.
People who have had a kidney transplant are at high risk of developing gout.
Other organ transplants, such as heart and liver, also increase the risk of developing gout.
This is because the surgery itself increases the risk of developing gout, as does the drug cyclosporine used to prevent rejection of the transplanted organ.
Cyclosporine also interacts with indomethacin, a common drug for gout.
Treatment of other conditions can cause a high level of uric acid in the blood, which can lead to a gout attack.
These conditions include:
Triggers are events or conditions that can trigger a gout attack. Triggers include:
- Too much alcohol or foods rich in purines.
- Serious illness or infection.
- Sudden weight loss, crash diet.
- Radiation therapy
- Use of certain drugs.
The first step in diagnosing gout is determining which joints are affected.
A physical exam and medical history can help confirm or rule out gout. For example, gout is more likely if arthritis first appears in the big toe.
The speed of the onset of pain and swelling is also important.
Symptoms that take days or weeks (rather than hours) to develop are likely pointing to a problem other than gout.
Unusual enlargements in joints that have been affected by a previous injury or osteoarthritis are possible signs of gout.
This is especially true of older women taking diuretics.
Synovial fluid examination is the most accurate method of diagnosing gout.
Synovial fluid is the lubricating fluid that fills the joint space (synovium).
This is the membrane that surrounds a joint and creates a protective pocket.
The fluid cushions the joints and supplies nutrients and oxygen to the cartilage surface that lines the bones.
This test also helps detect gout between attacks.
A procedure called arthrocentesis is also done. The doctor removes fluid from the affected joint, using a procedure called aspiration.
The fluid sample is sent to a laboratory for analysis. If uric acid crystals, also called monosodium urate, are found, this points to the diagnosis of gout.
These crystals are very distinctive under the microscope using special polarizing filters.
Aspiration sometimes relieves symptoms by reducing swelling and pressure on the tissue around the joint.
A blood test may be done to measure the level of uric acid in the blood.
Since uric acid can drop during an attack, uric acid may not be elevated at that time.
Some doctors can wait until several days after the attack to order a blood test.
Almost all people with gout have high uric acid in this case, although not all people with high uric acid have gout.
Therefore, uric acid in the blood is only part of making the diagnosis.
Sometimes a urine test is done to check the amount of uric acid in a patient’s urine.
If uric acid in the urine is greater than a certain value, more tests will be ordered to detect an enzyme defect or other cause of gout.
A high level of uric acid in the urine means that the patient is more likely to develop uric acid kidney stones.
Some available medications increase uric acid excretion and can alter the result of this test.
It is possible that the doctor to make a differential diagnosis requires imaging tests.
X-rays usually show no problems during the early stages of gout.
X-rays are most often used in chronic gout. X-rays can help find other problems with symptoms similar to gout.
Tophi can be seen on x-rays before they can be found during a physical exam.
In very rare cases, advanced imaging techniques are used to identify tophi.
These techniques include computed tomography, magnetic resonance imaging, and Doppler ultrasound.
As part of the diagnosis, other disorders that cause gout-like symptoms or that cause hyperuricemia should be ruled out.
In general, it is easy to distinguish acute gout that occurs in a joint from other arthritic conditions.
At some point in its course, other conditions may resemble gout.
The two disorders that can confuse this diagnosis are pseudogout and septic arthritis.
Pseudogout is a condition that is likely to be mistaken for gout.
Chronic gout can often resemble rheumatoid arthritis.
Pseudogout or calcium gout
Pseudogout is also called calcium gout or calcium pyrophosphate dihydrate deposition disease.
It is a very common type of inflammatory arthritis in older adults.
It is similar to gout. Like gout, pseudogout is caused by crystal deposits in and around the joints.
But the type of pseudogout crystals is calcium pyrophosphate dihydrate.
These are quite different under the microscope compared to uric acid crystals.
The symptoms of pseudogout resemble gout in some ways, but there are differences:
- The first attack usually affects the knee. Other commonly affected joints are the shoulders, wrists, and ankles.
- At least two-thirds of cases affect more than one joint during a first attack.
- Pseudogout can involve any joint, although the small joints in the fingers and toes are not commonly affected.
- The symptoms of pseudogout also appear more slowly than those of gout, taking days, rather than hours, to develop.
- Pseudogout is more likely to develop first in older people, particularly those with osteoarthritis.
- Conditions that are at high risk for pseudogout in older patients include acute medical conditions, trauma, or surgery.
- Medical conditions related to pseudogout include hypothyroidism, diabetes, gout, and osteoarthritis .
- X-rays often show calcium deposits in the articular cartilage. This is not seen in uric acid gout.
- There is no cure for removing the calcium deposits that cause pseudogout.
- It is a progressive disorder that can eventually destroy the joints.
- Treatments for acute attacks of pseudogout are similar to those for gout and aim to relieve pain and inflammation and reduce the frequency of attacks.
- The use of non-steroidal anti-inflammatory drugs is effective in treating the inflammation and pain of pseudogout.
- For acute attacks in large joints, aspiration of fluids alone or with corticosteroids can help.
- Magnesium carbonate can help dissolve the crystals, but existing hard deposits can remain.
- Colchicine can be used for acute attacks. Surgery may be required for joint replacement.
Rheumatoid arthritis can deform the finger joints and cause inflammation and pain that can be similar to gout.
In older people, it is difficult to distinguish chronic gout from rheumatoid arthritis.
A proper diagnosis can be made with a detailed medical history, laboratory tests, and identification of monosodium urate crystals.
Gout can coincide and be confused with osteoarthritis in older people, particularly when it occurs in arthritic finger joints in women.
In general, gout should be suspected if the joints in the fingertips are unusually enlarged.
Joint infections can have characteristics that resemble gout.
A correct diagnosis is important for proper treatment.
A high fever and high white blood cell count help diagnose infection, while urate crystals in the joint usually point to gout.
Pie de Charcot
People with diabetes who also have problems with the nerves in the feet (diabetic peripheral neuropathy) can develop Charcot’s foot or Charcot’s joint (medically known as neuropathic arthropathy).
The first changes can resemble gout, with the foot swollen, red and warm, although it involves other parts of the foot than the big toe.
Bunion is a bony growth in the joint.
It forms when the big toe is forced towards the rest of the toes, causing the head of the first metatarsal bone to protrude and rub against the side of the shoe.
The underlying tissue becomes inflamed and a painful lump forms.
Treatment of an acute attack of gout
Acute gout attacks and long-term treatment of gout and hyperuricemia require different approaches.
Treatment generally involves medications.
After the first attack, some doctors advise patients to keep a supply of medications on hand at the first symptom of a second attack.
Treatments are prescribed for conditions associated with gout, including uric acid nephropathy and uric acid nephrolithiasis.
Supportive measures include applying ice and resting the affected joint.
Many patients do not require medication.
Lifestyle and dietary measures are often enough to prevent attacks.
Measures include not eating high-purine foods, not drinking alcohol, and maintaining a healthy weight.
Medicines for gout attacks are aimed at relieving pain and reducing inflammation.
These medications can be combined to treat a gout attack.
Non-steroidal anti-inflammatory drugs
Nonsteroidal anti-inflammatory drugs are the drugs of choice for an acute attack in younger, healthier patients without serious health problems, such as kidney, liver, or heart disease.
Many non-steroidal anti-inflammatory drugs available over the counter include ibuprofen, naproxen, and ketoprofen.
Indomethacin is a prescription non-steroidal anti-inflammatory drug.
It is often the first option for treatment.
Usually 2 to 7 days of high-dose indomethacin is enough to treat a gout attack.
Regular use of non-steroidal anti-inflammatory drugs can cause health problems, such as ulcers and gastrointestinal bleeding.
Patients must follow instructions exactly on how much to take and for how long to avoid such health problems.
Diabetes patients taking oral glucose-lowering medications may need to adjust their dosage if they also take non-steroidal anti-inflammatory medications.
This is due to possible harmful interactions between these medications.
Colchicine is a derivative of autumn saffron (meadow saffron). It has been used for gout attacks since ancient times.
It is very effective in relieving a gout attack. It should not be used by elderly patients or patients with kidney, liver or bone marrow disorders.
Colchicine can affect fertility. This medicine is contraindicated during pregnancy.
Colchicine should be started soon after the gout attack begins and currently only a total of 3 tablets are recommended (2 tablets immediately and a third tablet after 1 hour).
Certain medications can interact with colchicine, such as some antibiotics and stomach acid reducers such as H2 blockers.
Patients should inform their physician of all other medications they are taking before they are prescribed colchicine.
In those who suffer from what is called difficult gout, which is an acute attack of gout that occurs in multiple joints or in the presence of diseases of the kidneys, heart or in other conditions where the use of anti-inflammatory drugs should be avoided non-steroidal or colchicine.
Corticosteroids can be used in patients who cannot tolerate non-steroidal anti-inflammatory drugs, such as the elderly or those with kidney disease.
Corticosteroid injections into an affected joint provide relief for many patients.
Orally administered steroids can be used for patients who cannot take non-steroidal anti-inflammatory drugs or colchicine and who have gout in more than one joint.
These are new agents that target a key chemical released during acute gout called interleukin-1.
Anakinra, given as a daily injection, has been evaluated to treat difficult gout.
Anakinra is an expensive therapy with a significant risk of developing side effects, it can be used for gout in specific circumstances.
Canakinumab is also effective for acute and difficult gout, but has risks of adverse effects.
These drugs are not approved by the FDA.
Treatment to lower the level of uric acid in the blood
People already taking urate-lowering drugs will likely continue to take this drug during an attack.
You will start a new medicine to lower the urate after the acute attack is under control.
Treatment to prevent attacks
After an acute attack, some patients remain at high risk for another attack for several weeks during the intercritical period.
Such patients include those with kidney failure or those with congestive heart failure taking diuretics.
Colchicine or non-steroidal anti-inflammatory drugs can be used for 1 to 2 months or longer to prevent another attack.
The cause of gout is hyperuricemia. Lifestyle changes should be recommended for all gout patients, including weight loss if obese, changes in diet, and reduction in alcohol consumption.
If uric acid remains elevated despite these recommendations, a medication that lowers the level of uric acid in the blood or that blocks uric acid production is usually prescribed to prevent gout attacks and other complications.
Hyperuricemia that does not cause symptoms may not need drug treatment.
Asymptomatic hyperuricemia often does not cause gout or other health problems.
Before treatment, a 24-hour urine collection sample may be ordered for patients with frequent attacks of gout.
This is to determine if they are overproducers or excretors of uric acid.
Low doses of non-steroidal anti-inflammatory drugs or colchicine are used for several months after starting drugs that lower the concentration of urates to prevent gout attacks.
It is recommended for people who have had a gout attack and any of the following:
- Tophi on exam or imaging.
- History of kidney stones.
- Chronic kidney disease of any kind.
There are several reasons why people with gout and kidney disease should start taking urate-lowering medications with just one gout attack.
They usually have hyperuricemia due to kidney disease. Treatment of acute gout is more difficult with kidney disease.
Urate-lowering medications such as allopurinol can protect the kidneys from worsening kidney disease.
Recommended first-line therapies to lower uric acid include allopurinol or febuxostat.
Allopurinol decreases uric acid production by blocking an enzyme called xanthine oxidase.
It is the most widely used drug in the long-term treatment of gout for older patients, in patients with kidney disease and in those who produce uric acid in excess.
When first started, allopurinol can trigger more gout attacks. Therefore, a low dose is used first.
For the first few months or more, the patient also takes a non-steroidal anti-inflammatory drug or colchicine to reduce that possibility.
Allopurinol is generally well tolerated, but it can cause side effects in some people, especially people of Chinese, Thai, or Korean descent.
A genetic test called HLA B-58: 01 is recommended in such individuals before starting allopurinol.
Allopurinol has positive effects on hypertension, heart, and kidney disease, so it may be better than other medications for patients with gout and these conditions.
Possible interactions with other medications and allopurinol should be discussed with your doctor before taking the medication.
Febuxostat is a newer drug and is particularly useful for patients allergic to allopurinol.
Like allopurinol, it blocks xanthine oxidase, and gout can reactivate after starting the drug.
The dose of febuxostat does not need to be adjusted in people with kidney disease.
This drug continues to be monitored for hypersensitivity reactions. It is much more expensive than allopurinol.
Uricosuric drugs are first-line alternative therapies.
These medications prevent the kidney from reabsorbing uric acid and therefore increase the amount excreted in the urine.
They can be used when the kidneys do not remove enough uric acid, which is present in about 80% of gout cases.
The doctor will check a 24-hour urine sample to diagnose this problem.
These medications are not used for patients with reduced kidney function, or those with tophaceous gout.
Other patients who may benefit from uricosuric drugs include:
- Less than 60 years of age.
- Normal kidney function.
- No risk of kidney stones.
- NSAIDs, particularly aspirin and similar medications, reduce the effectiveness of uricosuric drugs. Patients taking uricosuric drugs should avoid NSAIDs if possible.
Probenecid is an older medicine developed in the 1950s.
It can be helpful in patients who cannot take other gout medications.
Lesinurad (Zurampic) is a newer uricosuric agent.
It is used in conjunction with urate depletion therapy (such as allopurinol or febuxostat) in gout patients for whom urate depletion therapy alone was insufficient to achieve normal uric acid levels.
A combination therapy of lesinurad and allopurinol (Duzallo) is also available.
Lesinurad is not indicated in asymptomatic hyperuricemia or in patients with impaired renal function.
Pegloticase (Krystexxa, formerly Puricase) is a recombinant form of the enzyme uricase that breaks down uric acid so it is eliminated through the urine.
Pegloticase injections are given intravenously every two weeks and are reserved for patients with severe chronic gout who have not been helped by first-line treatments.
Mild to severe reactions are possible.
The FDA recommends that an antihistamine and a corticosteroid be given before injection to avoid reactions and that other urate-lowering drugs be discontinued.
Several side effects are possible, some of which can be serious.
There is no research in patients with heart failure.
Starting medications that lower uric acid can trigger a gout attack.
You should check with your doctor to find out what medications and dosages can cause gout flare-ups.
In general, it is better to increase the dose slowly over many weeks.
Also, you may need a drug like colchicine to prevent gout flares for the first few months after you start taking the urate-lowering drug.
Your uric acid should drop to less than 6.0 mg / dL, and sometimes less than 5.0 mg / dL.
Gout medications can interact with other drugs.
Most people with gout will need to take the urate-lowering medicine for the rest of their lives.
People with gout are at high risk for high blood pressure (hypertension).
Some medications for high blood pressure, such as thiazide diuretics, beta blockers, or angiotensin converting enzyme inhibitors can increase the risk of developing gout attacks.
Other medications, such as calcium channel blockers, can have beneficial effects on high blood pressure and gout.
Large tophi that drain, infect, or interfere with joint movement may need to be surgically removed.
Surgery may not be suitable for people with other medical conditions, such as infection.
In most cases, measures such as taking medications that lower uric acid should reduce the need for surgery.
There are other types of surgeries available to relieve joint pain and improve joint function.
In some cases, joint replacement is needed.
Resting and protecting the affected joint with a splint can also promote recovery.
Applying ice packs during an acute attack can help relieve symptoms.
Changes in lifestyle
The uric acid level is only slightly affected by diet. Therefore, diet therapy does not play an important role in the prevention of gout.
Still, avoiding or cutting down on foods high in purine can help.
Foods and drinks to avoid:
- Organ meat (liver, kidney, heart, gizzard).
- High fructose corn syrup (in foods and beverages, like most sugary sodas).
- Alcohol during gout attacks.
- Beef, pork, lamb.
- Seafood rich in purines (shellfish, sardines, anchovies, tuna, herring).
- Alcohol, especially beer and hard liquor.
- Fruit juices or sweet fruits.
Eating a moderate amount of purine-rich vegetables (spinach, cauliflower, mushrooms, and legumes) does not appear to increase the risk of developing gout.
Dairy products, especially low-fat products, can actually protect against gout.
Drinking coffee can also have a preventive effect against gout.
Taking folic acid and vitamin C can lower your uric acid level.
Drinking plenty of fluids helps eliminate uric acid from the body.
Consuming alcohol such as beer and hard liquor increases uric acid levels, which can lead to gout attacks.
This is the reason why many people who drink an excessive amount of alcohol have gout attacks.
Drinking wine from time to time does not appear to be related to an increase in gout attacks.
Diets high in fructose, which include soda and fruit juice, can increase the risk of developing gout.
keep a healthy weight
A supervised weight loss program can be effective in reducing uric acid levels in overweight people.
However, an explosive diet can have the opposite effect because it can increase uric acid level and cause an acute attack.
Avoid joint injuries
People with gout should avoid activities that cause repetitive trauma to the joints, such as wearing tight shoes.
Traveling can increase the risk of gout attacks.
Not only does traveling increase stress, but eating and drinking patterns can change.
Before traveling, patients should discuss preventive measures with their doctor.
Your doctor may prescribe taking a corticosteroid at the first sign of a gout attack.
In most cases, this stops the attack.