Blood test for gout

Tests for gout

If you think you might have gout, it is important to get tested and diagnosed by a doctor, so that you can get the treatment you need. The tests for gout are:

Synovial fluid test

Synovial fluid is a liquid found in your body’s joints. This test looks at whether you have urate crystals in the joint fluid, which could mean you have gout. This is considered the most accurate test for diagnosing gout.
A synovial fluid test only takes a few minutes to complete. You may first be given anesthesia, a medicine to numb the area, through a shot using a small needle. Once the area is numb, your doctor or nurse will place a larger needle in the affected joint, and take a sample of the fluid. If you have received anesthesia, you should not feel much pain.

Uric acid blood test

A blood test can check the level of uric acid in your blood. A high level of uric acid could mean you have gout.

  • A uric acid level in the blood between 3.5 and 7.2 milligrams per deciliter (mg/dl) is considered normal for most people.
  • When you have gout, doctors recommend your uric acid level stay below 6.0 mg/dl.

Uric acid blood tests should not be used alone when diagnosing gout. This is because some people with high uric acid will never get gout, and some people with low uric acid do get gout. Doctors use the results of other tests together with the uric acid test to confirm whether you have gout or not.

Uric acid urine test

A urine test can check the level of uric acid in your body. A high level of uric acid could mean you have gout. The urine sample should be taken over 24 hours.

  • A uric acid level in the urine between 250 and 750 mg is considered normal for most people.

Like a uric acid blood test, a uric acid urine test will not be used alone when diagnosing gout. Instead, doctors use the results of other tests together with the uric acid test to confirm whether you have gout or not.

Joint x-ray

Your doctor may take an X-ray of your joint to make sure your joint pain is not being caused by an injury or something other than gout. If you have chronic gout, your doctor may suggest a joint X-ray to see if you have any joint damage caused by gout.


An ultrasound machine uses sound waves to create images of the muscles and joints inside your body. Your doctor may use an ultrasound to look for urate crystals or tophi in your joints.

Dual-energy CT (DECT) scan

A DECT scan uses two types of X-rays to take pictures of the inside of your body. A DECT scan can find urate crystals that other tests cannot. This test is useful when the other tests cannot tell for sure if you have gout.

Gout Diagnosis

How is gout diagnosed?

Reviewed By Floranne C. Ernste, MD

Gout is diagnosed when uric acid is found in the synovial fluid. Diagnosing gout usually takes place when an attack is occurring. Your doctor must remove synovial fluid from the inflamed area and order tests to determine the levels of uric acid.

Uric acid is a waste product that occurs naturally when your body breaks down certain proteins. Too much of it causes needle-like crystals to form that can inflame cartilage, bones, ligaments and other joint tissues. Evidence of this build up shows in the synovial fluid, which is why it is collected as part of the diagnostic process.

While the procedure to collect fluid only takes seconds, it can be painful. The skin surrounding a gout-inflamed joint is often very sensitive.

The gold standard of diagnosing gout requires removing synovial fluid from the joint with a needle. (Source: 123RF)

Other Diagnostic Options for Gout

Testing synovial fluid is the standard for diagnosing gout, but another option for getting a gout diagnosis is through a blood test. Your doctor would get a sample of blood to have the levels of creatinine and uric acid tested. While a viable alternative to joint fluid collection, this option does have its downsides. Some people can have high levels of uric acid but not enough to experience gout. At the same time, people with physical signs of gout may not have high levels of uric acid in their blood. In some academic centers with appropriate expertise, ultrasonography of the joint with guided aspiration may help to diagnose; a dual-energy CT scan (DECT) of the affected joint is also available in some centers to diagnose gout.

Some physicians may use other methods based on criteria developed by the American College of Rheumatology and adopted by the American Academy of Family Physicians.

For instance, doctors are likely to diagnose gout if you have six or more of the following symptoms:

  • lopsided joint swelling on an x-ray
  • blood test showing high uric acid levels
  • joint fluid culture negative for organisms during a gout attack
  • maximum joint inflammation developed within a day
  • arthritis in only one joint
  • more than one attack of acute arthritis
  • painful/swollen first big toe joint
  • redness over joints
  • x-rays that identify subcortical cysts without erosions
  • tophi (bumps caused by uric acid deposits)
  • a gout-like attack of on both big toe joints at the same time
  • a gout-like attack on both ankle joints at the same time.

The Importance of Obtaining an Official Diagnosis of Gout

Gout shares many common symptoms with joint infections and other types of arthritis, and it requires special treatment. By getting an accurate diagnosis of gout, you and your doctor can start working on effective treatments to stop the gout attack and recover.

Updated on: 02/12/19 View Sources


Continue Reading: Gout Treatments


Treatments for gout are incredibly successful. There are two main parts to treating gout, which are:

  • treating the acute attack
  • treatments to prevent future attacks.

Treating a gout attack

Treating an attack of gout doesn’t lower your urate levels or stop future attacks. The treatment helps you to manage your symptoms when an attack happens.

The most commonly used drug treatments for attacks of gout are:

  • non-steroidal anti-inflammatory drugs (NSAIDs)
  • colchicine
  • steroids.

Some people will be better suited to NSAIDS, while others will be suited to colchicine. But your preference is also taken into consideration – many people with gout quickly learn what works best for them.

In cases where one drug doesn’t seem to be working on its own, your doctor might suggest a combination of NSAIDs with either colchicine or steroids.

Non-steroidal anti-inflammatory drugs (NSAIDs)

Attacks of gout are often treated with NSAID tablets, which can help with pain and reduce some of your inflammation. Ibuprofen, Naproxen and diclofenac are three NSAIDs you could be given.

If you’ve been prescribed NSAIDs to treat an attack, you should start taking them as soon as you notice signs of one coming on. Your doctor may let you keep a supply so you can start taking them at the first signs of an attack.

The earlier you start treatment, the better.

NSAIDs aren’t suitable for everyone, so talk to your doctor about them first if you have any other conditions. They can also interact with other drugs, so make sure you talk to a doctor before starting on any new medication.

NSAIDs aren’t usually prescribed for a long period of time, as they can cause problems with your digestive system. To reduce the risk of this happening and to protect your stomach, your doctor will also prescribe a proton pump inhibitor.


Colchicine isn’t a painkiller, but can be very effective at reducing the inflammation caused by urate crystals.

As with NSAIDs, colchicine tablets should be taken as soon as you notice an attack coming on, or it may not work as well. Your doctor will probably recommend keeping a supply at home.

Colchicine can interact with several other drugs, including statins taken for high cholesterol. Your doctor will advise whether you’d be better off using an NSAID instead, or adjusting your other medications while you’re taking colchicine.

You should avoid taking colchicine if you have chronic kidney disease.

Colchicine tablets can cause diarrhoea or stomach aches.


If colchicine or NSAIDs haven’t worked for you, or if you’re at risk of side effects from these drugs, your doctor may prescribe steroids.

They are usually taken as a short course of tablets, lasting a few days.

However, they can also be taken as an injection into a muscle or joint affected by gout. This can be particularly helpful if gout is affecting only one joint.

Check out our steroids and steroid injection pages for more information.

Tips for managing an attack at home

  • Keep the area cool – an ice pack, or a bag of frozen peas wrapped in a tea towel, can be particularly good at reducing some of the pain and swelling.
  • Rest the affected joint.
  • Think about getting yourself a bed cage. These support the bedsheets above your feet so that your affected joint can rest without the strain of the sheets.

Treatments to prevent gout attacks

There are drugs available that can lower urate levels, prevent new crystals from forming and dissolve away the crystals in your joints. They are called urate lowering therapies or ULTs for short.

Treatment with ULTs is generally started after an attack of gout has completely gone.

There’s no single fixed dose of a ULT, and different people need different doses to get to the right blood urate level.

It can take a few months or years for the drugs to completely clear your body of urate crystals. But once they’re gone, you will no longer have attacks of gout, tophi or risk of joint damage due to gout.

It’s important to remember that ULTs won’t stop attacks of gout straight away. You could actually have more attacks within the first six months of starting them.

Don’t stop taking your ULTs if this happens to you, as this is actually a sign that the drugs are working. As the drugs start dissolving the crystals, they become smaller and are more likely to get into the joint cavity, triggering an attack.

Your doctor might suggest taking a low dose of colchicine or NSAID as a precaution against attacks during the first six months of starting ULTs.

ULTs are usually life-long treatments and require yearly check-ups to monitor your urate levels. If your symptoms aren’t getting under control, talk to your doctor about your urate level, as you might need to be on a higher dose.

Try not to miss or skip any of your doses, especially in the first year or two of starting treatment. This could cause your urate levels to go up and down, which could trigger an attack.


Allopurinol is the most commonly used ULT. It’s a very effective treatment for most people with gout.

It works by reducing the amount of urate that your body makes.

You’ll start on a low dose of allopurinol, which can be gradually increased until you are on the right dose.

Gradually building up the dose means it’s less likely to trigger an attack and also makes sure you’ll have the lowest dose needed to get your gout under control.

Allopurinol is broken down and removed from the body through your kidneys, so if you have a problem with your kidneys, it may not be suitable for you. Your doctor might decide to start you on an even lower dose and increase slowly, or suggest that you try febuxostat instead.


Febuxostat is a newer drug that reduces the amount of urate made in the body in the same way that allopurinol does.

You won’t be prescribed febuxostat as your first ULT, unless your doctor has said that you can’t take allopurinol.

It works in a similar way to allopurinol but, instead of being broken down by the kidneys, it’s broken down by your liver. It’s useful if you have kidney problems and can’t take a high enough dose of allopurinol.

Febuxostat is more likely to trigger gout attacks than allopurinol when you first start treatment. So, as a precaution, it’s likely you’ll be prescribed a low-dose NSAID or colchicine to take on a daily basis for the first six months of starting febuxostat.

There are just two doses of febuxostat, so if your urate levels haven’t lowered enough after a month on the low dose, you may need to go on to the higher dose.

Uricosuric drugs

Uricosuric drugs, which include sulfinpyrazone, benzbromarone and probenecid, work by flushing out more urate than normal through your kidneys.

They’re not used much in the UK, as they’re not widely available. They’ll only be prescribed by a rheumatologist if allopurinol and febuxostat haven’t worked or aren’t suitable for you.

It’s unlikely you’ll be able to take these drugs if you’ve had severe problems with your kidneys or had kidney stones. This is because, by encouraging your kidneys to filter more urate, they also increase the risk of developing kidney stones.

Uricosuric drugs are usually used on their own. But in rare cases, where you’ve tried several ULTs and none have worked for you, uricosurics can be used in combination with other ULTs, like allopurinol or febuxostat.

If you’re unable to take allopurinol, febuxostat or a uricosuric, or if they don’t work for you, you’ll need to see a rheumatologist for advice.

Treatment for joint damage

If your gout has caused damage to your joints, then the treatments available will be the same as those used for osteoarthritis. They include:

  • exercising regularly
  • reducing the strain on your affected joints
  • staying at a healthy weight
  • taking painkillers
  • in more severe cases, joint replacement surgery.

Visit our osteoarthritis page to find out more about treatments available for joint damage.

US Pharm. 2009;34(5):40-47.

Clinical literature has recently reported that gout is the most common inflammatory arthritis in the United States, with 3 to 5 million sufferers.1,2 Both the incidence and the prevalence of gout appear to be increasing worldwide.3 Gout is perhaps the oldest known type of arthritis; it has been colorfully depicted in art and literature along with commentaries on the moral character of the gout sufferer (FIGURE 1). Literature accounts have referred to gout’s association with rich foods and excessive alcohol consumption—thus the description, “the disease of kings.”

Gout is a monosodium urate, monohydrate crystal deposit disease with a very rich history mirroring the evolution of medicine itself.4,5 It was among the earliest diseases to be recognized as a clinical entity. Since gout has been recognized for so many centuries, its diagnosis and treatment generally have not elicited much interest; thus, the management of gout is a challenge for the clinician caring for the patient with this disease.6

Recent medical literature recognizes that most patients with gout visit a primary care physician for disease management, but there are challenges to diagnosing and treating gout in this setting.7 Further, Weaver et al stated that the arrival of newer investigational agents in the market has prompted rheumatologists to consider how they can share current information to improve gout management.7 It is this concept of sharing current information on the management of gout that is the main impetus for the preparation of this review. It is hoped that pharmacists will be empowered with this knowledge to assist the prescribing clinician to maximize patient outcomes when treating gout. First, to serve as a foundation, new insights into the pathogenesis of hyperuricemia and gout will be discussed. Second, risk factors, typical presentation of symptoms, and key diagnostic parameters will be reviewed so that the pharmacist may achieve an appreciation of the disease. Finally, nonpharmacologic treatment modalities and both current as well as newer investigational therapeutics will be offered so that the pharmacist may facilitate greater patient adherence through medication counseling.


Biologically significant hyperuricemia occurs when serum urate levels exceed solubility (~6.8 mg/dL). Hyperuricemia is a common serum abnormality that does not always progress to gout. Humans generate about 250 to 750 mg of uric acid per day. The uric acid comes from dietary purines and the breakdown of dying tissues. The exact cause of gout is not yet known, although it may be linked to a genetic defect in purine metabolism. Uric acid, the most insoluble of the purine substances, is a trioxypurine containing three oxygen groups. The pathogenesis of gout starts with the crystallization of urate within the joint, bursa, or tendon sheath, which leads to inflammation as a result of phagocytosis of monosodium urate crystals; the disease is usually associated with an elevated concentration of uric acid in the blood.2,8 Specifically, uric acid is a breakdown product of the purines adenine, guanine, hypoxanthine, and xanthine. Adenine and guanine are found in both DNA and RNA. Hypoxanthine and xanthine are not incorporated into the nucleic acids as they are being synthesized, but they are important intermediates in the synthesis and degradation of the purine nucleotides. Both undissociated uric acid and monosodium salt, which is the primary form found in the blood, are only sparingly soluble.

The amount of urate in the body depends on the balance between dietary intake, synthesis, and excretion.9 In people with primary gout, defects in purine metabolism lead to hyperuricemia, or high levels of uric acid in the blood. This can be caused by increased production of uric acid, abnormal retention of uric acid, or both. Urate in the blood can accumulate either through an overproduction or an underexcretion of uric acid. Hyperuricemia results from the overproduction of urate found in 10% of gout patients and from underexcretion of urate found in the remaining 90%.9 The majority of patients with endogenous overproduction of urate have the condition as a result of salvaged purines arising from increased cell turnover in proliferation and inflammatory disorders, from pharmacologic intervention resulting in increased urate production, and from tissue hypoxia.9

The renal mechanism for handling urate is one of glomerular filtration followed by partial tubular reabsorption.10 The final fractional excretion of uric acid is about 20% of what was originally filtered. Uric acid levels independently predict renal failure in patients with preexisting renal disease. Hyperuricemia causes interstitial and glomerular changes that are independent of the presence of crystal, and the changes very much resemble what hypertensive changes would look like chronically. In addition, serum hyperuricemia is epidemiologically linked to hypertension and seems to be an independent factor for the development of hypertension. Finally, hyperuricemia is defined as a serum uric acid level greater than 6.8 mg/dL. Serum uric acid can be normal, especially during the gout attack. The target goal for uric acid treatment is to achieve a level less than 6.0 mg/dL.

Risk Factors for Gout

A number of references by Choi et al have identified, explained, and reviewed the risk factors for the development of gout.11-13 Nonmodifiable risk factors include being a male or a postmenopausal female, genetic influences, end-stage renal disease, and resulting major organ transplantation. Its prevalence increases with age, from 1.8/1,000 in people under the age of 45 years to 30.8/1,000 in those over age 65.8 Elevated serum urate levels are also associated with increased risk.8 Hypertension is a definite risk factor, as a significant percentage of patients with hyperuricemia will develop hypertension. Hyperuricemia and gout have been linked to other disease states including metabolic syndrome, cardiac disease, stroke, and renal disease.8 The risk of gout correlates with truncal obesity, as measured by body mass index and waist-to-hip ratios.8,11

Avoidable risk factors include diet and medications. Foods that have been implicated in causing gout are red-organ meats, seafood, and foods containing high-fructose corn syrup. Fructose has been recognized as a cause of hyperuricemia.8,14-16 Choi et al conducted a small prospective study that investigated the ability of diets high in fructose to induce higher serum urate levels relative to diets high in glucose or low in carbonates.16 High alcohol intake, especially beer, is also a risk factor. The presence of guanosine in beer has been identified as the cause of gouty attacks.

Certain drugs used to treat gout, particularly thiazide diuretics and the cyclosporine administered to transplant patients, have been implicated with gouty attacks. Despite the cardioprotection offered by low-dose 81-mg aspirin, this drug may be associated with the precipitation of gout.8,17 Commonly, the use of cyclosporine has been reported to cause a rapidly occurring type of gout, swiftly ascending and polyarticular in many cases. Roubenoff validates that these risk factors are increasing by reporting that gout incidence and prevalence have increased by twofold from 1970 to 1990.18 Furthermore, Wallace et al have reported that the prevalence of gout has increased by two cases per 1,000 patients during the 1990s because of lifestyle changes.19

Typical Presentation of Gout

Gouty attacks are usually associated with a precipitating event.6,20 These attacks consist of intense pain involving the lower extremity, with 80% of first attacks involving a monoarticular joint; however, after long periods of time, gout attacks may become polyarticular.6,20,21 This pain and inflammation is a result of a dramatic inflammatory response. Some authors have estimated that between 50% to 90% of the initial attacks occur in the first metatarsophalangeal joint (podagra).6,21-23 In postmenopausal women, the distal interphalangeal joints may be involved.6 Attacks often occur at night and are associated with a precipitating event.6,20 Acute gouty arthritis may be accompanied by low-grade fever, chills, and malaise.6,21,23 The majority of patients experience a second acute gout attack within 1 year of the first episode.24 Untreated initial acute gout attacks resolve completely within 3 to 14 days.6,20,23

There are four clinical stages of gout.23 At serum urate concentrations greater than 6.8 mg/dL, urate crystals may start to deposit. Hence, the first stage of gout is known as asymptomatic hyperuricemia. During this first period, urate deposits may directly contribute to organ damage. After sufficient urate deposits have developed around a joint and some traumatic event triggers the release of crystals into the joint space, a patient will suffer an acute gout attack and move into the second stage, known as acute gouty arthritis. During this second stage, acute inflammation in the joint caused by urate crystallization and crystal phagocytosis is present. This episode is known as a “flare” and is self-resolving and likely to recur. The interval between acute flare gout attacks with persistent crystals in the joints is the third stage and is known as an intercritical period. When crystal deposits continue to accumulate, patients develop chronically stiff and swollen joints leading to the final stage—advanced gout, which includes the long-term complications of uncontrolled hyperuricemia characterized by chronic arthritis and tophi. The nodular mass of uric acid crystals is described as a tophus and is characteristically deposited in different soft tissue areas of the body in gout. This advanced stage of gout is uncommon because it is avoidable with interventional therapy.23


The diagnosis of gout can be straightforward. The only way to establish the diagnosis with certainty is to demonstrate uric acid crystals in synovial fluid or tophi.7 Polarizing microscopic examination of synovial fluid reveals negatively birefringent crystals, confirming the diagnosis of gout. It must be recognized that normal uric acid levels are observed in approximately 50% of acute gouty flares.7

Dalbeth and McQueen’s review summarizes recent advances in plain radiography and advanced imaging for gout, calcium pyrophosphate dihydrate crystal arthropathy, and basic calcium phosphate crystal arthropathy.24 They suggest that high-resolution ultrasonography may improve noninvasive diagnosis of the crystal-induced arthropathies and allow for monitoring of intra-articular tophi. They also determined that computed tomography provides excellent definition of tophi and bone erosion, and three-dimensional computed tomography assessment of tophus volume is a promising outcome measure in gout.24 Finally, they state that magnetic resonance imaging is also a reliable method for assessment of tophus size in gout and has an important role in detection of complications of the disease in clinical practice.

Treatment of Gout

Key elements necessary to improve clinical outcomes in gout management include enhancing health professional and patient education as well as exploring novel urate-lowering agents. One of the most valuable health care professionals when assisting clinicians in the treatment of gout is the pharmacist. Pharmacists can appreciate that the optimal treatment for gout requires both adjunctive nonpharmacologic as well as pharmacologic interventional therapies (TABLE 1). A practicing pharmacist is directed to read the Becker and Chohan editorial, which suggests that successful gout management is possible by embracing the 12 evidence-based recommendations from the European League Against Rheumatism (EULAR) (TABLE 2).25,26 Treatment and prevention of acute gout flares, as well as the management of hyperuricemia and gout, can best be appreciated by patients with a brief narrative and be accentuated graphically through easy-to-read tables that the pharmacist may access quickly when a question arises.

A treatment regimen must be individually tailored to each patient. The treatment of gout has three main components: therapy of the acute attack, prophylaxis against gout flares, and management of hyperuricemia.8 Several aspects must be independently considered when planning to treat a patient with gout. Given that gout is a reversible urate crystal deposit disease, the main objective is to eliminate the urate crystals from the joints and other structures.27 Li-Yu et al determined through a 10-year prospective investigation that serum urate levels should be reduced to below 6.0 mg/dL in order to eliminate crystals.28

Pharmacotherapy for Acute Gout Attacks: Medications used to treat an acute gout attack include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids. A combination of these may also be necessary. A summary of the pharmacologic agents used to treat acute gout is shown in TABLE 3.6-8,25-27 These medications have no effect on the serum uric acid level. The classic antidote for gouty arthritis is colchicine. The most common associated adverse drug event reported with colchicine use is diarrhea.6 However, even low-dose colchicine may be associated with severe adverse effects and toxicity such as myopathy and myelosuppression.6,8,27 Monitoring of serum troponin levels during an acute colchicine overdose may help avoid vascular collapse.29

Guidelines indicate that fast-acting oral NSAIDs should be used during acute attacks if there are no contraindications.6-8,26 Since there are no significant clinical differences among NSAIDs, the choice of agent should be based on the agent’s side-effect profile, it’s cost, and patient’s ability to adhere to the prescribed agent.6,8,25,27 Suppressive therapy to prevent flares usually involves colchicine or NSAIDs.8 An important factor in choosing therapeutic agents for an acute attack is the presence of comorbidities. The most common therapy for acute gout in the setting of acute or chronic renal or hepatic failure is corticosteroids.8 If NSAIDs and colchicine are contraindicated because of patient comorbidities, intra-articular aspiration and injection of a corticosteroid is an effective treatment of an acute attack of gout once the possibility of a septic joint has been eliminated.6

Urate-Lowering Therapy: The therapeutic goal of urate-lowering therapy is to promote dissolution of the urate crystals and to prevent crystal formation.6,28 In addition, urate-lowering therapy is used to prevent disease progression, reduce the frequency of acute attacks, and maintain and improve quality of life. Treatments for chronic gout are aimed at reducing serum urate levels to less than 6.0 mg/dL in order to dissolve existing crystals and prevent formation of new ones.8 Dore recommends that patients who overproduce urate should be treated with allopurinol, as this drug has the advantage of being effective for both overproducers and underexcretors.6 Patients who underexcrete urate despite near-normal creatinine clearance levels should be treated with uricosurics. Urate-lowering therapy should be lifelong. If an acute flare occurs when urate-lowering therapy is initiated, therapy should not be discontinued, because doing so will result in fluctuating urate levels.30 Initiating urate-lowering therapy can mobilize urate deposits, which may precipitate an attack because of rapid serum uric acid lowering.7 The practice of using concomitant gastroprotectant NSAID and colchicine prophylaxis with the initialization of urate-lowering therapy has been suggested.7,25

Pharmacists can be a tremendous resource by informing the clinician about potential drug interactions and side effects of urate-lowering agents to maximize therapeutic outcomes. Finally, pharmacists must remember that treatment of asymptomatic hyperuricemia is not recommended.7

Since 1965, one traditional approach to the treatment of gout has been the drug allopurinol, an isomer of hypoxanthine. Allopurinol is a substrate for xanthine oxidase. The product binds so tightly that the enzyme is now unable to be oxidized in its normal substrate. Uric acid production is diminished, and xanthine and hypoxanthine levels in the blood rise. These are more soluble than urate and are less likely to deposit as crystals in the joints. The allopurinol dose must be adjusted in patients with renal impairment.6 Allopurinol is often started at 100 mg per day, and the daily dosage is increased in 100 mg increments every 2 to 4 weeks.8,25,26 The usual dosage range for allopurinol is 200 to 300 mg/day for mild gout and 400 to 600 mg/day for cases of moderate and severe gout. Up to 5% of patients are unable to tolerate allopurinol due to adverse effects such as rash, nausea, and bone marrow suppression.31 If a severe rash occurs, the pharmacist should advise discontinuation of allopurinol. Allopurinol has fewer drug interactions than uricosuric agents.6 Despite allopurinol’s limitations, it is used extensively for most gouty patients and is considered safe and effective.27

Emerging Therapies: Uricosurics are considered second-line therapy for patients who are intolerant to allopurinol. Of all the older urate-lowering drugs, probenecid or sulfinpyrazone may be used in patients refractory to allopurinol therapy.27 In the U.S., probenecid is the only potent uricosuric agent available.8 Probenecid is most useful in patients with mild gout and normal renal function. Its mechanism of action is inhibition of the uric acid transporter (URAT1) involved in the reabsorption of uric acid.8 Uricosuric therapy is contraindicated in patients with a history of nephrolithiasis and is not effective in patients with a creatinine clearance of less than 50 mL/min. Finally, both losartan and fenofibrate have slight uricosuric properties and may be useful as adjunctive therapy in gout patients with comorbidities of hypertension and hyperlipidemia.6,32

Febuxostat is a potent, new selective xanthine oxidase inhibitor that received FDA approval in February 2009 for the management of hyperuricemia in patients with gout.8,33,34 This agent is not a purine analog and has a mechanism similar to that of allopurinol. The recommended starting dose of febuxostat is 40 mg once a day. For patients who do not achieve a serum uric acid less than 6 mg/dL after 2 weeks with 40 mg, increasing the dose to 80 mg is recommended.34 Febuxostat has demonstrated efficacy superior to allopurinol.27,34 It is primarily metabolized by the liver and may be an alternative agent for patients with renal insufficiency. The adverse-effect profile for febuxostat includes elevation in liver enzymes, rash, diarrhea, and headache.8 The manufacturer has reported that febuxostat has a higher rate of risk of cardiovascular thromboembolic events compared to allopurinol.34 Finally, febuxostat is contraindicated in patients treated with azathioprine, mercaptopurine, or theophylline.34

Uric acid oxidase, also known as uricase, is an enzyme that catalyzes the conversion of uric acid to allantoin and is present in all mammals except humans and higher primates.27 There is interest in using uricase therapies to lower serum uric acid. Rasburicase, a recombinant uricase IV product indicated for tumor lysis syndrome, might be successfully used in unusually severe cases of gout.35 Rasburicase has a black box warning for anaphylaxis, hemolysis, and methemoglobin. Pegloticase (pegylated recombinant porcine uricase) has also shown urate-lowering efficacy.14,36 Adding polyethylene glycol (PEG) prolongs the half-life of uricase and decreases the antigenicity. Intravenous administration of PEG-uricase has been investigated for the potential treatment of severe tophaceous gout in patients who are hypersensitive to allopurinol.37

Pharmacists should appreciate the relative contraindications to both NSAIDs and corticosteroids as symptomatic therapies. Therefore, attention has been directed to the recent advances in the understanding of gouty inflammation and the proinflammatory role of several cytokines in the pathophysiology of acute gout.25,38 Early small clinical trials have identified interleukin-1B as the most prominent in acute gout. The practice of inhibiting interleukin-1 may be efficient and safe in terminating the symptoms of acute gouty arthritis.25


Gout is a monosodium urate, monohydrate crystal deposit disease. It was among the earliest diseases to be recognized as a clinical entity. Clinical pharmacists need to be empowered with knowledge to assist prescribing clinicians in order to maximize therapeutic outcomes when treating gout. To achieve this goal, a foundation of new insights into the pathogenesis of hyperuricemia and gout has been reviewed. Risk factors, typical presentation of symptoms, and key diagnostic parameters have been offered so that pharmacists can achieve an appreciation of gout as a significant disease. Both nonpharmacologic modalities and pharmacologic therapies have been discussed so that greater patient adherence through medication counseling can be achieved.

1. Helmick CG, Felson DT, Lawrence RC, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part I. Arthritis Rheum. 2008;58:15-25.
2. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis Rheum. 2008;58:26-35.
3. Weaver AL. Epidemiology of gout. Cleve Clin J Med. 2008;75(suppl 5):S9-S12.
4. Pillinger MH, Rosenthal P, Abeles AM. Hyperuricemia and gout. Bull NYU Hosp Jt Dis.
5. Nuki G, Simkin PA. A concise history of gout and hyperuricemia and their treatment. Arthritis Res Ther. 2006;8(suppl 1):S1.
6. Dore RK. Gout: what primary care physicians want to know. J Clin Rheumatol. 2008;14(suppl 5):S47-S54.
7. Weaver AL, Cheh MA, Kennison RH. How PCP education can impact gout management: the gout essentials. J Clin Rheumatol. 2008;14(suppl):S42-S46.
8. Mandel DA, Simkin PA. Gout: update on pathogenesis, diagnosis, and treatment. New Develop Rheum Dis. 2007;20-25. 2007;65:215-221. Simkin.pdf. Accessed February 26, 2009.
9. Choi HK, Mount DB, Reginato AM. Pathogenesis of gout. Ann Intern Med. 2005;143:499-516.
10. Wyngaarden JB. The role of the kidney in pathogenesis and treatment of gout. Arthritis Rheum. 1958;1:191-203.
11. Choi HK, Atkinson K, Karlson EW, et al. Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the health professionals follow up study. Arch Intern Med. 2005;165:742-748.
12. Choi HK, Atkinson K, Karlson EW, et al. Alcohol intake and risk of incident gout in men: a prospective study. Lancet. 2004;363:1277-1281.
13. Choi HK, Atkinson K, Karlson EW, et al. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004;350:1093-1103.
14. Pillinger MH, Keenan RT. Update on the management of hyperuricemia and gout. Bull NYU Hosp Jt Dis. 2008;66:231-239.
15. Emmerson BT. Effect of oral fructose on urate production. Ann Rheum Dis. 1974;33:276-280.
16. Choi JW, Ford ES, Gao X, Choi HK. Sugar-sweetened soft drinks, diet soft drinks, and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2008;59:109-116.
17. Schlesinger N, Schumacher HR. Update on gout. Arthritis Rheum. 2002;47:563-565.
18. Roubenoff R. Gout and hyperuricemia. Rheum Dis Clin North Am. 1990;16:539-550.
19. Wallace KL, Riedel AA, Joseph-Ridge N, Wortmann R. Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population. J Rheumatol. 2004;31:1582-1587.
20. Hawkins DW, Rahn DW. Gout and hyperuricemia. In: DiPiro JT, Talbert RL, Yee GC, et al, eds. Pharmacotherapy: A Pathophysiologic Approach. 5th ed. New York, NY: McGraw-Hill; 2002:1659-1664.
21. Becker MA, Jolly M. Clinical gout and the pathogenesis of hyperuricemia. In: Koopman WJ, Moreland LW, eds. Arthritis and Allied Conditions. 15th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005:2303-2339.
22. Worthmann PL, Kelly WN. Gout and hyperuricemia. In: Harris ED Jr, Budd RC, Genovese MC, et al, eds. Kelly’s Textbook of Rheumatology. 7th ed. Philadelphia, PA: WB Saunders Company; 2005:1402-1429.
23. Mandell BF. Clinical manifestations of hyperuricemia and gout. Cleve Clin J Med. 2008;75(suppl 5):S5-S8.
24. Dalbeth N, McQueen FM. Use of imaging to evaluate gout and other crystal deposition disorders. Curr Opin Rheumatol. 2009;21:124-131.
25. Becker MA, Chohan S. We can make gout management more successful now. Curr Opin Rheumatol. 2008;20:167-172.
26. Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65:1312-1324.
27. Pascual E, Sivera F. Therapeutic advances in gout. Curr Opin Rheumatol. 2007;19:122-127.
28. Li-Yu J, Clayburne G, Sieck M, et al. Treatment of chronic gout. Can we determine when urate stores are depleted enough to prevent attacks of gout? J Rheumatol. 2001;28:577-580.
29. van Heyningen C, Watson ID. Troponin for prediction of cardiovascular collapse in acute colchicine overdose. Emerg Med J. 2005;22:599-600.
30. Schumacher HR Jr, Chen LX. The practical management of gout. Cleve Clin J Med. 2008;75(suppl 5):S22-S25.
31. Schlesinger N. Management of acute and chronic gouty arthritis: present state-of-the-art. Drugs. 2004;64:2399-2416.
32. Eggebeen AT. Gout: an update. Am Fam Physician. 2007;76:801-808.
33. Becker MA, Schumacher HR, Wortmann RL, et al. Febuxostat compared with allopurinol in patients with hyperuricemia and gout. N Engl J Med. 2005;353:2450-2461.
34. Uloric (febuxostat) package insert. Deerfield, IL: Takeda Pharmaceuticals North America; February 2009. Accessed April 13, 2009.
35. Vogt B. Urate oxidase (rasburicase) for treatment of severe tophaceous gout. Nephrol Dial Transplant. 2005;20:431-433.
36. Biggers K, Scheinfeld N. Pegloticase, a polyethylene glycol conjugate of uricase for the potential intravenous treatment of gout. Curr Opin Investig Drugs. 2008;9:422-442.
37. Terkeltaub R, Bushinsky DA, Becker MA. Recent developments in our understanding of the renal basis of hyperuricemia and the development of novel antihyperuricemic therapeutics. Arthritis Res Ther. 2006;8(suppl 1):S4.
38. Martinon F, Petrilli V, Mayor A, et al. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature. 2006;440:237-241.
To comment on this article, contact [email protected]

What is gout?

Gout is a common form of inflammatory arthritis that is very painful. It usually affects one joint at a time (often the big toe joint). There are times when symptoms get worse, known as flares, and times when there are no symptoms, known as remission. Repeated bouts of gout can lead to gouty arthritis, a worsening form of arthritis.

There is no cure for gout, but you can effectively treat and manage the condition with medication and self-management strategies.

What are the signs and symptoms of gout?

Gout flares start suddenly and can last days or weeks. These flares are followed by long periods of remission—weeks, months, or years—without symptoms before another flare begins. Gout usually occurs in only one joint at a time. It is often found in the big toe. Along with the big toe, joints that are commonly affected are the lesser toe joints, the ankle, and the knee.

Symptoms in the affected joint(s) may include:

  • Pain, usually intense.
  • Swelling.
  • Redness.
  • Heat.

Top of Page

What causes gout?

Gout is caused by a condition known as hyperuricemia, where there is too much uric acid in the body. The body makes uric acid when it breaks down purines, which are found in your body and the foods you eat. When there is too much uric acid in the body, uric acid crystals (monosodium urate) can build up in joints, fluids, and tissues within the body. Hyperuricemia does not always cause gout, and hyperuricemia without gout symptoms does not need to be treated.

Top of Page

What increases your chances for gout?

The following make it more likely that you will develop hyperuricemia, which causes gout:

  • Being male.
  • Being obese.
  • Having certain health conditions, including:
    • Congestive heart failure.
    • Hypertension (high blood pressure).
    • Insulin resistance.
    • Metabolic syndrome.
    • Diabetes.
    • Poor kidney function.
  • Using certain medications, such as diuretics (water pills).
  • Drinking alcohol. The risk of gout is greater as alcohol intake goes up.
  • Eating or drinking food and drinks high in fructose (a type of sugar).
  • Having a diet high in purines, which the body breaks down into uric acid. Purine-rich foods include red meat, organ meat, and some kinds of seafood, such as anchovies, sardines, mussels, scallops, trout, and tuna.

Top of Page

How is gout diagnosed?

A medical doctor diagnoses gout by assessing your symptoms and the results of your physical examination, X-rays, and lab tests. Gout can only be diagnosed during a flare when a joint is hot, swollen, and painful and when a lab test finds uric acid crystals in the affected joint.

Top of Page

Who should diagnose and treat gout?

The disease should be diagnosed and treated by a doctor or a team of doctors who specialize in care of gout patients. This is important because the signs and symptoms of gout are not specific and can look like signs and symptoms of other inflammatory diseases. Doctors who specialize in gout and other forms of arthritis are called rheumatologists. To find a provider near you, visit the database of rheumatologistsExternal on the American College of Rheumatology website. Once a rheumatologist has diagnosed and effectively treated your gout, a primary care provider can usually track your condition and help you manage your gout.

Top of Page

How is gout treated?

Gout can be effectively treated and managed with medical treatment and self-management strategies. Your health care provider may recommend a medical treatment plan to

  • Manage the pain of a flare. Treatment for flares consists of nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, steroids, and the anti-inflammatory drug colchicine.
  • Prevent future flares. Making changes to your diet and lifestyle, such as losing weight, limiting alcohol, eating less purine-rich food (like red meat or organ meat), may help prevent future attacks. Changing or stopping medications associated with hyperuricemia (like diuretics) may also help.
  • Prevent tophi and kidney stones from forming as a result of chronic high levels of uric acid. Tophi are hard, uric acid deposits under the skin. For people with frequent acute flares or chronic gout, doctors may recommend preventive therapy to lower uric acid levels in the blood using drugs like allopurinol, febuxostat, and pegloticase.

In addition to medical treatment, you can manage your gout with self-management strategies. Self-management is what you do day to day to manage your condition and stay healthy, like making healthy lifestyle choices. The self-management strategies described below are proven to reduce pain and disability, so you can pursue the activities important to you.

Top of Page

How can I manage my gout and improve my quality of life?

Gout affects many aspects of daily living, including work and leisure activities. Fortunately, there are many low-cost self-management strategies that are proven to improve the quality of life of people with gout.

For gout in particular:

  • Eat a healthy diet. Avoid foods that may trigger a gout flare, including foods high in purines (like a diet rich in red meat, organ meat, and seafood), and limit alcohol intake (particularly beer and hard liquor).

CDC’s Arthritis Program recommends five self-management strategies for managing arthritis and its symptoms. These can help with gout as well.

  • Learn self-management skills. Join a self-management education class, which helps people with arthritis and other chronic conditions—including gout—understand how arthritis affects their lives and increase their confidence in controlling their symptoms and living well. Learn more about the CDC-recommended self-management education programs.
  • Get physically active. Experts recommend that adults engage in 150 minutes per week of at least moderate physical activity. Every minute of activity counts, and any activity is better than none. Moderate, low impact activities recommended include walking, swimming, or biking. Regular physical activity can also reduce the risk of developing other chronic diseases such as heart disease, stroke, and diabetes. Learn more about physical activity for arthritis.
    • Go to effective physical activity programs. For people who worry that physical activity may make arthritis worse or are unsure how to exercise safely, participation in physical activity programs can help reduce pain and disability related to arthritis and improve mood and the ability to move. Classes take place at local Ys, parks, and community centers. These classes can help people with arthritis feel better. Learn more about CDC-recommended physical activity programs.
  • Talk to your doctor. You can play an active role in controlling your arthritis by attending regular appointments with your health care provider and following your recommended treatment plan. This is especially important if you also have other chronic conditions, like diabetes or heart disease.
  • Lose weight. For people who are overweight or obese, losing weight reduces pressure on joints, particularly weight bearing joints like the hips and knees. Reaching or maintaining a healthy weight can relieve pain, improve function, and slow the progression of arthritis.
  • Protect your joints. Joint injuries can cause or worsen arthritis. Choose activities that are easy on the joints like walking, bicycling, and swimming. These low-impact activities have a low risk of injury and do not twist or put too much stress on the joints. Learn more about how to exercise safely with arthritis.

Top of Page

Learn more about gout

  • National Institute of Arthritis and Musculoskeletal and Skin DiseasesExternal External
  • American College of RheumatologyExternal
  • National Library of Medicine—MedlinePlus—Acute GoutExternal External
  • National Library of Medicine—MedlinePlus—Chronic GoutExternal External

Top of Page

Learn more about arthritis

  • Arthritis Types
  • Physical Activity for Arthritis
  • Frequently Asked Questions (FAQs)
  • Arthritis-Related Statistics

Top of Page

About the author

Leave a Reply

Your email address will not be published. Required fields are marked *