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Gout

By

Brian F. Mandell

, MD, PhD, Cleveland Clinic

Last full review/revision Oct 2020| Content last modified Oct 2020
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Gout is a disorder caused by hyperuricemia (serum urate > 6.8 mg/dL [> 0.4 mmol/L]) that results in the precipitation of monosodium urate crystals in and around joints, most often causing recurrent acute or chronic arthritis. The initial attack (flare) of gout is usually monarticular and often involves the 1st metatarsophalangeal joint. Symptoms of gout include acute, severe pain, tenderness, warmth, redness, and swelling. Definite diagnosis requires identification of crystals in synovial fluid. Treatment of acute flares is with anti-inflammatory drugs. The frequency of flares can be reduced by regular use of nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or both and by persistently lowering the serum urate level with allopurinol, febuxostat, or uricosuric drugs such as probenecid.

Gout is more common among men than women. Usually, gout develops during middle age in men and after menopause in women. Gout is rare in younger people but is often more severe in people who develop the disorder before age 30. Gout often runs in families. Patients with metabolic syndrome are at risk of gout.

Pathophysiology

The greater the degree and duration of hyperuricemia, the greater is the likelihood that gout will develop. Urate levels can be elevated because of

  • Decreased renal (most common) or gastrointestinal excretion

  • Increased production (rare)

  • Increased purine intake (usually in combination with decreased excretion)

Why only some people with elevated serum uric acid (urate) levels develop gout flares is not known.

Decreased renal excretion is by far the most common cause of hyperuricemia. It may be hereditary and also occurs in patients receiving diuretics and in those with diseases that decrease the glomerular filtration rate (GFR). Ethanol increases purine catabolism in the liver and increases the formation of lactic acid, which blocks urate secretion by the renal tubules, and ethanol may also stimulate liver urate synthesis. Lead poisoning and cyclosporine, usually in the higher doses given to transplant patients, damage renal tubules, leading to urate retention.

Increased production of urate may be caused by increased nucleoprotein turnover in hematologic conditions (eg, lymphoma, leukemia, hemolytic anemia) and in conditions with increased rates of cellular proliferation and cell death (eg, psoriasis, cytotoxic cancer therapy, radiation therapy). Increased urate production may also occur as a primary hereditary abnormality and in obesity, because urate production correlates with body surface area. In most cases, the cause of urate overproduction is unknown, but a few cases are attributable to enzyme abnormalities; deficiency of hypoxanthine-guanine phosphoribosyltransferase (complete deficiency is Lesch-Nyhan syndrome) is a possible cause, as is overactivity of phosphoribosylpyrophosphate synthetase.

Increased intake of purine-rich foods (eg, liver, kidney, anchovies, asparagus, consommé, herring, meat gravies and broths, mushrooms, mussels, sardines, sweetbreads) can contribute to hyperuricemia. Beer, including nonalcoholic beer, is particularly rich in guanosine, a purine nucleoside. However, a strict low-purine diet lowers serum urate by only about 1 mg/dL (0.1 mmol/L).

Urate precipitates as needle-shaped monosodium urate (MSU) crystals, which are deposited extracellularly in avascular tissues (eg, cartilage) or in relatively avascular tissues (eg, tendons, tendon sheaths, ligaments, walls of bursae) and skin around cooler distal joints and tissues (eg, ears). In severe, long-standing hyperuricemia, MSU crystals may be deposited in larger central joints and in the parenchyma of organs such as the kidney. At the acid pH of urine, urate precipitates readily as small platelike or diamond-shaped uric acid crystals that may aggregate to form gravel or stones, which may obstruct urine outflow. Tophi are MSU crystal aggregates that most often develop in joint and cutaneous tissue. They are usually encased in a fibrous matrix, which prevents them from causing acute inflammation.

Acute gouty arthritis may be triggered by trauma, medical stress (eg, pneumonia or other infection), surgery, use of thiazide diuretics or drugs with hypouricemic effects (eg, allopurinol, febuxostat, probenecid, nitroglycerin), or indulgence in purine-rich food or alcohol. Flares are often precipitated by a sudden increase or, more commonly, a sudden decrease in serum urate levels. Why acute flares follow some of these precipitating conditions is unknown. Tophi in and around joints can limit motion and cause deformities, called chronic tophaceous gouty arthritis. Gout increases the risk of developing secondary osteoarthritis.

Symptoms and Signs

Acute gouty arthritis usually begins with sudden onset of pain (often nocturnal). The metatarsophalangeal joint of a great toe is most often involved (called podagra), but the instep, ankle, knee, wrist, and elbow are also common sites. Rarely, the hip, shoulder, sacroiliac, sternoclavicular, or cervical spine joints are involved. The pain becomes progressively more severe, usually over a few hours, and is often excruciating. Swelling, warmth, redness, and exquisite tenderness may suggest infection. The overlying skin may become tense, warm, shiny, and red or purplish. Fever, tachycardia, chills, and malaise sometimes occur.

Course

The first few flares usually affect only a single joint and last only a few days. Later flares may affect several joints simultaneously or sequentially and persist up to 3 weeks if untreated. Subsequent flares develop after progressively shorter symptom-free intervals. Eventually, multiple flares may occur each year.

Tophi

Palpable tophi develop in patients with gout and can rarely occur in patients who have never had acute gouty arthritis. They are usually firm yellow or white papules or nodules, single or multiple. They can develop in various locations, commonly the fingers, hands, feet, and around the olecranon or Achilles tendon. Tophi can also develop in the kidneys and other organs and under the skin on the ears. Patients with osteoarthritic Heberden nodes may develop tophi in the nodes. This development occurs most often in older women taking diuretics, and these can become dramatically inflamed and misdiagnosed as inflammatory osteoarthritis. Normally painless, tophi, especially in the olecranon bursae, can become acutely inflamed and painful, often after mild or inapparent injury. Tophi may erupt through the skin, discharging chalky masses of urate crystals. These sinus tracts can become infected. Tophi in and around joints may eventually cause deformities and secondary osteoarthritis.

Complications of gout

Gouty arthritis can cause pain, deformity, and limited joint motion. Inflammation can be flaring in some joints while subsiding in others. Patients with gout may develop urolithiasis with uric acid stones or calcium oxalate stones.

Complications of gout include renal obstruction and infection, with secondary tubulointerstitial disease. Untreated progressive renal dysfunction, most often related to coexisting hypertension or, less often, some other cause of nephropathy, further impairs excretion of urate, accelerating crystal deposition in tissues.

Diagnosis

  • Clinical criteria

  • Synovial fluid analysis

The diagnosis of gout should be suspected in patients with acute monoarticular arthritis or oligoarticular arthritis, particularly older adults or those with other risk factors. Podagra and recurrent instep inflammation are particularly suggestive. Previous flares that began explosively and resolved spontaneously are also characteristic. Similar symptoms can result from the following:

Palindromic rheumatism is characterized by acute, recurrent flares of inflammation in or near one or occasionally several joints or tendon sheaths with spontaneous resolution; pain and erythema can be as severe as in gout. Flares often subside spontaneously and completely in 1 to 3 days. Such flares may herald the onset of RA, and rheumatoid factor tests can help in differentiation; they are positive in about 50% of patients (these tests are positive in 10% of gouty patients also).

Synovial fluid analysis

If acute gouty arthritis is suspected, arthrocentesis and synovial fluid analysis should be done at the initial presentation. A typical recurrence in a patient with known gout does not mandate arthrocentesis, but it should be done if there is any question of the diagnosis or if the patient’s risk factors or any clinical characteristics suggest infectious arthritis.

Synovial fluid analysis can confirm the diagnosis by identifying needle-shaped, strongly negatively birefringent urate crystals that are free in the fluid or engulfed by phagocytes. Synovial fluid during flares has inflammatory characteristics (see Table Microscopic Examination of Crystals in Joints), usually 2,000 to 100,000 white blood cells/mcL, with > 80% polymorphonuclear white blood cells. These findings overlap considerably with infectious arthritis, which must be excluded by Gram stain (which is insensitive) and culture.

Table
icon

Microscopic Examination of Crystals in Joints

Crystal Type

Birefringence

Elongation*

Shape

Length (micrometer)

Monosodium urate

Strong

Negative

Needle- or rod- shaped

2–15

Weak or often not birefringent

Positive

Rhomboid- or rod- shaped

2–15

Calcium oxalate (rare)†

Weak or strong

Positive or indeterminate

Bipyramidal

5–30

Not birefringent with polarized light

Shiny, coinlike, or slightly irregular (often too small to delineate)

3–65 (aggregates)

* Elongation is determined by inserting an additional red plate or compensator between the two polarizing plates in the microscope and aligning a crystal with an orienting arrow denoting the axis of slow vibration. Crystals that have negative elongation are yellow parallel to the axis of slow vibration marked on the compensator; positive elongation appears blue in the same direction. Clinically, these have previously been called negative or positive birefringence.

† These crystals occur primarily in patients with renal failure.

Serum urate level

An elevated serum urate level supports the diagnosis of gout but is neither specific nor sensitive; at least 30% of patients have a normal serum urate level during an acute flare in part due to the uricosuric properties of the proinflammatory cytokine, interleukin-6 (IL-6). However, the baseline serum urate level between flares reflects the size of the extracellular miscible urate pool. The level should be measured on 2 or 3 occasions in patients with newly proven gout to establish a baseline. Quantitation of urinary uric acid excretion to differentiate between overproduction and underexcretion is no longer recommended; it does not predict a patient's response to allopurinol or febuxostat (which decrease uric acid production).

Imaging

X-rays of the affected joint may be taken to look for bony erosions or tophi, but they are probably unnecessary if the diagnosis of acute gout has been established by synovial fluid analysis and are rarely diagnostic at the time of first flares. In calcium pyrophosphate arthritis, radiopaque deposits may sometimes be present in fibrocartilage, hyaline articular cartilage (particularly the knee), or both.

Ultrasonography is more sensitive (although operator-dependent) and specific than plain x-rays for the diagnosis of gout. Urate deposition over the articular cartilage (double-contour sign) and clinically inapparent tophi are characteristic changes. These findings may be evident even before the first gout flare. Dual-energy CT scans (DECTs) can also reveal uric acid deposits and can be useful if the diagnosis is unclear based on standard clinical evaluation and testing, particularly if synovial fluid aspiration and analysis cannot be done.

Diagnosis of chronic gouty arthritis

Chronic gouty arthritis should be suspected in patients with persistent joint disease or subcutaneous or bony tophi. Plain x-rays of the 1st metatarsophalangeal joint or other affected joint may be useful. These x-rays may show punched-out lesions of subchondral bone with overhanging bony margins, most commonly in the 1st metatarsophalangeal joint; lesions must be 5 mm in diameter to be visible on x-ray. Joint space is typically preserved until very late in the course of disease. Synovial fluid findings from chronic effusions are usually diagnostic.

Diagnostic ultrasonography is increasingly used to detect a typical double-contour sign suggesting urate crystal deposition, but sensitivity is operator-dependent and differentiation from calcium pyrophosphate crystal deposits may be more difficult to do conclusively.

Prognosis

With early gout diagnosis, therapy enables most patients to live a normal life. For many patients with advanced disease, aggressive lowering of the serum urate level can resolve tophi and improve joint function. Gout is generally more severe in patients whose initial symptoms appear before age 30 and whose baseline serum uric acid level is > 9.0 mg/dL (> 0.5 mmol/L). The high prevalence of metabolic syndrome and cardiovascular disease probably increases mortality in patients with gout.

Some patients do not improve sufficiently with treatment. The usual reasons include inadequate education provided to patients, nonadherence, alcoholism, and undertreatment of the hyperuricemia by physicians.

Treatment

  • Termination of an acute flare with nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, corticosteroids, or an interleukin-1 (IL-1) antagonist

  • Prevention of recurrent acute flares with daily colchicine or an NSAID

  • Prevention of further deposition of monosodium urate (MSU) crystals, reduction in flare incidence, and resolution of existing tophi by lowering the serum urate level (by decreasing urate production with allopurinol or febuxostat, dissolving deposits with pegloticase, or increasing urate excretion with probenecid)

  • Treatment of coexisting hypertension, hyperlipidemia, and obesity and sometimes avoidance of excess dietary purines

Treatment of acute flares

Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective in treating acute flares and are generally well-tolerated. However, they can have adverse effects, including gastrointestinal upset or bleeding, hyperkalemia, increases in creatinine, and fluid retention. Older and dehydrated patients are at particular risk, especially if there is a history of renal disease. Virtually any NSAID used in anti-inflammatory (high) doses is effective and is likely to exert an analgesic effect in a few hours. Treatment should be continued for several days after the pain and signs of inflammation have resolved to prevent relapse.

Oral colchicine, a traditional therapy, often produces a dramatic response if begun soon after the onset of symptoms; it is most effective if started within 12 to 24 hours of an acute flare. A dose of 1.2 mg can be followed with 0.6 mg 1 hour later; joint pain tends to decrease after 12 to 24 hours and sometimes ceases within 3 to 7 days, but usually continued dosing is needed to achieve resolution. If colchicine is tolerated, 0.6 to 1.2 mg once/day can be continued as the flare subsides. Renal insufficiency and drug interactions, especially with clarithromycin, may warrant reduction of dosage or use of other treatments. Gastrointestinal upset and diarrhea are common adverse effects.

IV colchicine is no longer available in the US.

Corticosteroids are used to treat acute flares. Aspiration of affected joints, followed by instillation of corticosteroid ester crystal suspension, is very effective, particularly for monarticular symptoms; prednisolone tebutate 4 to 40 mg or prednisolone acetate 5 to 25 mg can be used, with dose depending on the size of the affected joint. Oral prednisone (about 0.5 mg/kg once/day), IM or IV corticosteroids, or single-dose adrenocorticotropic hormone (ACTH) 80 U IM is also very effective, particularly if multiple joints are involved. As with NSAID therapy, corticosteroids should be continued until after the flare fully resolves to prevent relapse.

If monotherapy is ineffective or doses (eg, of NSAIDs) are limited by toxicity, colchicine can be combined with NSAIDs or corticosteroids.

In addition to NSAIDs or corticosteroids, supplementary analgesics, rest, ice application, and splinting of the inflamed joint may be helpful. If patients are taking urate-lowering drugs when an acute flare begins, the drugs should be continued at the same dose; dose adjustments are deferred until the flare has subsided. There is no contraindication to lowering serum urate levels during an acute flare if appropriate antiinflammatory therapy is being provided.

If corticosteroids, colchicine, and NSAIDs are contraindicated or ineffective, an IL-1 antagonist, such as anakinra, can be used. Anakinra may hasten resolution of a flare and shorten the hospital stay of a patient with multiple comorbidities that limit the use of the other drugs. Anakinra is typically given as 100 mg subcutaneously once/day until symptoms resolve.

Prevention of recurrent flares

The frequency of acute flares is reduced by taking one to two 0.6-mg tablets of colchicine daily (depending on tolerance and severity). An extra two 0.6-mg tablets of colchicine taken at the first suggestion of a flare may abort flares. If the patient is taking prophylactic doses of colchicine and has had higher doses of colchicine to treat an acute flare within the past 2 weeks, an NSAID should be used instead to try to abort the flare.

A (reversible) neuropathy and/or myopathy can develop during chronic colchicine ingestion. This condition is more likely to occur in patients with renal insufficiency, and in patients also receiving certain statins or macrolides, but can occur in patients with none of these risk factors.

Flare frequency can also be decreased with daily low-dose NSAIDs.

Lowering the serum urate level

Colchicine, NSAIDs, and corticosteroids do not retard the progressive joint damage caused by tophi, because they do not lower the serum urate level. Joint damage can be prevented and, if present, reversed with urate-lowering drugs. Tophaceous deposits are resorbed by lowering serum urate. Maintaining a serum urate level below the saturation point (target is usually < 6 mg/dL [0.4 mmol/L]) will ultimately decrease the frequency of acute arthritic flares as the deposits are dissolved. This decrease is accomplished by

  • Blocking urate production with xanthine oxidase inhibitors (XOI) (allopurinol or febuxostat)

  • Increasing urate excretion with a uricosuric drug (probenecid or losartan)

  • Using both types of drugs together in severe tophaceous gout or in patients intolerant of higher doses of a XOI

Urate-lowering therapy is indicated for patients with

  • Tophaceous deposits

  • Frequent or disabling flares (eg, > 2 flares/year) of gouty arthritis

  • Urolithiasis

  • Patients with infrequent flares but whose serum uric acid level is > 9.0 mg/dL (> 0.5 mmol/L) or for whom having any flares poses particular hardship

  • Multiple comorbidities (eg, peptic ulcer disease, chronic kidney disease) that are relative contraindications to the drugs used to treat acute flares (NSAIDs or corticosteroids)

Hyperuricemia is not usually treated in the absence of gout flares.

The goal of urate-lowering therapy is to lower the serum urate level. If tophi are not present, a reasonable target level is < 6 mg/dL (0.4 mmol/L), which is below the level of saturation (> 6.8 mg/dL [0.40 mmol/L] at normal core body temperature and pH). If palpable tophi are present or if there is marked disability from tophaceous deposits the goal is to dissolve them more rapidly, and this requires a lower target level. A reasonable target level is 5 mg/dL (0.30 mmol/L), and the lower the urate level, the faster tophi resolve. These target levels should be maintained indefinitely.

Drugs are effective in lowering serum urate; dietary restriction of purines is less effective, but high intake of high-purine food, alcohol (beer in particular), and nonalcoholic beer should be avoided. Carbohydrate restriction and weight loss can lower serum urate in patients with insulin resistance because high insulin levels suppress urate excretion. Intake of low-fat dairy products should be encouraged. Because acute flares tend to develop during the first months of urate-lowering therapy, such therapy should be started in conjunction with once or twice daily colchicine or NSAIDs and during a symptom-free period.

Resolution of tophi may take many months even with maintenance of serum urate at low levels. Serum urate should be measured periodically, usually monthly while determining required drug dosage and then yearly to confirm the effectiveness of therapy or more often if there are drug changes or weight gain. Urate-lowering therapy should not be stopped if a patient has a flare.

Allopurinol, which inhibits urate synthesis, is the most commonly prescribed and preferred initial urate-lowering therapy. Uric acid stones or gravel may dissolve during allopurinol treatment. Treatment usually begins with 50 to100 mg orally once/day and can be slowly dose escalated up to 800 mg orally once/day. The dose can be split if single daily dosing causes gastrointestinal distress. Some clinicians recommend decreasing the starting dose in patients with renal insufficiency (eg, 50 mg orally once/day if creatinine clearance is < about 60 mL/min/1.73 m2) to decrease the incidence of rare but severe systemic hypersensitivity reactions; however, data that confirm the effectiveness of this intervention are limited. The final dose of allopurinol should be determined by the target serum urate level. The most commonly used daily dose is 300 mg, but this dose is effective in lowering serum uric acid levels to < 6.0 mg/dL (< 0.4 mmol/L) in fewer than 40% of patients with gout. Absorption of allopurinol may decrease at doses higher than 300 mg, so at these higher doses, split dosing (eg, twice daily dosing) is often used.

Adverse effects of allopurinol include mild gastrointestinal distress and rash, which can be a harbinger of Stevens-Johnson syndrome, life-threatening hepatitis, vasculitis, or leukopenia. Adverse effects are more common among patients with renal dysfunction. Some ethnic groups (eg, Koreans with renal disease, Thai, Han Chinese, and black Americans) are at high risk of allopurinol reactions; HLA B*5801 is a commercially available genetic marker for that risk in these ethnic groups (1). The 2020 American College of Rheumatology Guideline for the Management of Gout recommends testing of Asians and black Americans for HLA B*5801 and using an alternative drug if that genetic marker is present. Allopurinol is contraindicated in patients taking azathioprine or mercaptopurine because it can decrease metabolism of and thus potentiate the immunosuppressive and cytolytic effects of these drugs.

Febuxostat is a far more costly (in the US) but potent inhibitor of urate synthesis. It is especially useful in patients who do not tolerate allopurinol, who have contraindications to allopurinol, or in whom allopurinol does not sufficiently decrease urate levels. It is begun at 40 mg orally once/day and increased to 80 mg orally once/day if urate does not decrease to < 6 mg/dL. Febuxostat (like allopurinol) is contraindicated in patients taking azathioprine or mercaptopurine because it can decrease metabolism of these drugs. Febuxostat increased the risk of mortality in one study of patients with known cardiovascular disease and should be used with caution in patients with known heart disease (2). Additional studies have not confirmed this observation. Transaminase levels can become elevated and should be measured periodically.

Pegloticase is a pegylated form of recombinant uricase. Uricase is an enzyme that converts urate to allantoin, which is more soluble. Pegloticase is very expensive and is used primarily in patients with gout in whom other treatments have been unsuccessful in lowering the serum urate level. It is given IV every 2 to 3 weeks for many months (typically 6 to 9 months) to totally deplete the excess urate deposits; it often lowers the serum urate level to < 1 mg/dL (< 0.1 mmol/L). Pegloticase is contraindicated in patients with G6PD deficiency because it can cause hemolysis and methemoglobinemia. Failure of urate levels to decrease to < 6 mg/dL after a pegloticase infusion indicates the likely presence of pegloticase antibodies and an increased risk of future allergic reactions; regular infusions are then stopped. To prevent other urate-lowering drugs from masking the ineffectiveness of pegloticase, other urate-lowering drugs should not be used with pegloticase.

Uricosuric therapy is useful in patients who underexcrete uric acid (the majority of patients with hyperuricemia), have normal renal function, and have not had renal stones. Probenecid is the only uricosuric drug approved by the U.S. Food and Drug Administration (FDA).

Probenecid can be used as monotherapy if both allopurinol and febuxostat are contraindicated or not tolerated. Probenecid loses efficacy with declining renal function and is generally not useful with a glomerular filtration rate < 50 mL/min/1.73 m2. Probenecid treatment begins with 250 mg orally 2 times a day, with doses increased as needed, to a maximum of 1 g orally 3 times a day. It is also effective when added to an XOI.

The antihypertensive drug losartan and the triglyceride-lowering drug fenofibrate both have uricosuric effects and can be used to decrease uric acid in patients who have other reasons for taking these drugs. Low doses of salicylates may worsen hyperuricemia, but only trivially, and should not be avoided if otherwise indicated as in secondary prevention of cardiovascular disease.

Other treatments

Fluid intake 3 L/day is desirable for all patients, especially those who chronically pass urate gravel or stones.

Alkalinization of urine (with potassium citrate 20 to 40 mEq orally 2 times a day or acetazolamide 500 mg orally at bedtime) is also occasionally effective for patients with persistent uric acid urolithiasis despite hypouricemic therapy and adequate hydration. However, excessive urine alkalinization may cause deposition of calcium phosphate and oxalate crystals.

Extracorporeal shock wave lithotripsy may be needed to disintegrate renal stones.

Large tophi in areas with healthy skin may be removed surgically; all others should slowly resolve under adequate hypouricemic therapy.

Treatment references

  • 1. Jutkowitz E, Dubreuil M, Lu N, et al: The cost-effectiveness of HLA-B*5801 screening to guide initial urate-lowering therapy for gout in the United States. Semin Arth Rheum 46:594-600, 2017. doi: 10.1016/j.semarthrit.2016.10.009

  • 2. White WR, Saag KG, Becker MA, et al: Cardiovascular safety of febuxostat or allopurinol in patients with gout. N Engl J Med 378:1200-1210, 2018. doi: 10.1056/NEJMoa1710895

Key Points

  • Although increased purine intake and increased production can contribute to hyperuricemia, the most common cause of gout is decreased urate excretion secondary to kidney disorders or hereditary variations.

  • Suspect gout in patients with sudden, unexplained acute monoarticular or oligoarticular arthritis, particularly if the great toe or midfoot is affected or there is a prior history of sudden, unexplained acute arthritis with spontaneous remission.

  • Confirm the diagnosis by finding needle-shaped, strongly negatively birefringent urate crystals in joint fluid; or by dual-energy CT scans or ultrasound imaging. Documentation of hyperuricemia is insufficient to confirm the diagnosis of gouty arthritis.

  • Treat acute flares of gout with oral colchicine, an NSAID, a corticosteroid, or a combination of colchicine with an NSAID or a corticosteroid.

  • Decrease the risk of future flares by prescribing colchicine, an NSAID, and drugs to decrease the serum urate level.

  • Give drugs that decrease serum urate if patients have tophi, > 2 flares of gout per year, urolithiasis, or multiple comorbidities that contraindicate the drugs used to relieve acute flares; individualize the use of urate-lowering therapy in other patients.

  • Decrease urate levels usually by prescribing allopurinol or febuxostat alone or in combination with a uricosuric drug.

Asymptomatic Hyperuricemia

Asymptomatic hyperuricemia is elevation of serum urate > 7 mg/dL (> 0.4 mmol/L) in the absence of clinical gout.

Generally, treatment of asymptomatic hyperuricemia is not required. However, patients with overexcretion of urate who are at risk of urolithiasis may receive allopurinol.

Accumulating data suggest that hyperuricemia may contribute to the progression of chronic kidney disease, cardiovascular disease, and, in adolescents, primary hypertension.

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