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Gout is an inflammatory arthritis related to a hyperuricemia (serum uric acid [SUA] level >6.8 mg/dL) (1).
Acute gouty arthritis can affect ≥1 joints; the first metatarsophalangeal joint is most commonly involved at presentation (podagra).
Although hyperuricemia is necessary for the development of gout, it is not the only determining factor.
Characterized by deposition of monosodium urate (MSU) crystals that accumulate in joints and soft tissues, resulting in acute and chronic arthritis, soft-tissue masses called tophi, urate nephropathy, and uric acid nephrolithiasis
After an initial flare, a second flare occurs in ∼60% of patients within 1 year and 78% within 2 years of the initial attack (2).
Management involves treating acute attacks and preventing recurrent disease by long-term reduction of SUA levels through pharmacology and lifestyle adjustments
Uric acid 7 to 8.9 mg/dL is 0.5%.
Uric acid >9 mg/dL is 4.5%.
Increasing prevalence over the past decades (3)
2007 to 2008 prevalence of gout in the United States (3)
Men 5.8% (6.1 million)
Women 2.0% (2.2 million)
2008 prevalence of hyperuricemia in the United States (3)
Men 21.2% (SUA >7.0 mg/dL)
Women 21.6% (SUA >5.7 mg/dL)
Hyperuricemia results from urate overproduction, underexcretion, or often a combination of the two.
Gout occurs when MSU, a product of purine metabolism, precipitates out of solution and accumulates in joints and soft tissues.
Transient changes in urate solubility caused by local temperature decrease, trauma, or acidosis may lead to an acute gouty attack.
Urate crystals that precipitate trigger an immune response.
Left untreated, this crystal deposition leads to permanent joint damage and tophus formation.
Phosphoribosyl pyrophosphate (PRPP) deficiency and hypoxanthine-guanine-phosphoribosyltransferase (HGPRT) deficiency (Lesch-Nyhan syndrome) are inherited enzyme defects associated with overproduction of uric acid.
Polymorphisms in the URAT1 and SLC 2A9 (GLUT9) renal transporters are hereditary enzyme defects resulting in primary underexcretion of uric acid.
Age >40 years
Increased purine uptake (meats and seafood)
Alcohol intake (especially beer)
High fructose intake
Congestive heart failure
Coronary artery disease
Thiazide diuretics: ethambutol
Loop diuretics (less of a risk vs. thiazides)
Calcineurin inhibitors (cyclosporine and tacrolimus)
Acetylsalicylic acid (not recommended in high doses)
Maintain optimal weight.
Diet modification (purine-rich foods)
Reduce alcohol consumption (beer and liquor).
Maintain fluid intake and avoid dehydration.
Nontraumatic joint disorders
Urinary tract disease
Classic presentation of acute gouty arthritis:
Intense pain and tenderness in the first metatarsophalangeal joint (podagra)
Can occur in the midtarsal, ankle, or knee joints
Joint may be swollen, warm, and red
Often awakes patients from sleep due to an intolerance to contact with clothing or bed sheets
There is a rapid onset of intense pain, often beginning in the early morning and progressing rapidly over 12 to 24 hours.
In the absence of treatment, flares can last up to 10 days.
Fever can be seen.
SC or intraosseous nodules, referred to as tophi
Pain with urination secondary to uric acid renal stones
Examine suspected joint(s) for tenderness, swelling, and range of motion (ROM).
Assess for presence of firm nodules known as tophi.
In patients with chronic gout, tophi can frequently be found in the helix of the ear, over the olacrenon process, or on the Achilles tendon.
Patients with untreated chronic gout can have evidence of joint inflammation and deformity.
SUA (may be normal during an acute flare)
CBC (can see elevation of WBC during an acute gout flare)
Synovial fluid analysis: urate crystals (negatively birefringent under polarizing microscopy), cell count (WBC usually 2,000 to 5,000 cells/mm3); culture to rule out infection. Some guidelines suggest that gout can be diagnosed clinically without synovial fluid analysis.
Screen for uric acid overproduction 24-hour urinary uric acid in those patients with gout onset before the age of 25 years or had a history of urolithiasis (1)[C].
Radiograph is normal early in disease but can reveal
Swelling in acute gout
Periarticular erosions with periosteum overgrowth in chronic gout
Urate kidney stones are radiolucent and thus invisible on radiograph.
Acute gouty arthritis attacks should be treated with pharmacologic therapy (4)[C].
Pharmacologic treatment should be initiated within 24 hours of acute gout attack onset (4)[C].
Ongoing pharmacologic urate-lowering therapy should not be interrupted during an acute gout attack (4)[C].
Choice of agent is based on severity of pain and the number of joints involved (4).
Mild/moderate gout severity (≤6 of 10 on visual analog pain scale, particularly for an attack involving only one or a few small joints or one to two large joints)
Naproxen (Naprosyn, Anaprox, Aleve): 750 mg followed by 250 mg q8h for 5–8 days (4)[A]
Indomethacin (Indocin): 50–150 mg/day for 2–7 days (4)[A]
Sulindac (Clinoril): 200 mg BID for 7–10 days (4)[A]
Not FDA approved but can be considered in selected patients with contraindications or intolerance to NSAIDs (4)[B].
Those with an acute flare involving one to two large joints can consider intra-articular corticosteroids; can consider using PO corticosteroids in combination.
For other acute flares, use PO corticosteroids:
Methylprednisolone (Medrol) dose pack (4)[C]
Triamcinolone acetonide (Trivaris): 60 mg IM single dose followed by oral corticosteroids (4)[C]
Used for gout attacks where the onset was <36 hours prior to treatment initiation (4)[A]
Begin a loading dose of 1.2 mg followed by 0.6 mg 1 hour later, followed by 0.6 mg once or twice daily 12 hours later, until the gout attack resolves (4)[C].
Dose reduction recommended in moderate to severe kidney disease and in those on inhibitors of cytochrome P450 3A4 and P-glycoprotein (clarithromycin, erythromycin, cyclosporine, and disulfiram) (4).
Severe gout (≥7 of 10 on visual analog pain scale, involving ≥4 joints with arthritis involving >1 region, or involving 3 separate large joints)
Initial combination therapy is an option and includes the use of full doses of the following (4)[C]:
Colchicine and NSAIDs
PO corticosteroids and colchicine
Intra-articular steroids with all other modalities
For patients not responding to initial pharmacologic monotherapy, add a second agent (4)[C].
Indications for pharmacologic urate-lowering therapy include any patient with
Chronic kidney disease (CKD) stage 2 or worse (1)[C]
Past urolithiasis (1)[C]
Treat to the serum urate:
Urate-lowering agents can be prescribed during an acute attack provided that effective anti-inflammatory prophylaxis has been initiated prior to urate-lowering therapy (1)[C].
Anti-inflammatory prophylaxis required when initiating urate-lowering therapy include the following:
Low-dose colchicine: 0.6 mg once or twice daily (4)[A]
Low-dose NSAIDs with proton pump inhibitor if indicated: naproxen 250 mg PO BID (4)[C]
Second line: Use of colchicine and NSAIDs both are not tolerated, contraindicated, or ineffective:
Low-dose prednisone or prednisolone at ≤10 mg/day (4)[C]
Treatment duration for the greater of
At least 6 months (4)[A] or
3 months after achieving serum urate appropriate for the patient with no tophi on exam (4)[B], or for 6 months after achieving serum urate appropriate for the patient with ≥1 tophi on exam (4)[C]
Pharmacologic urate-lowering agents:
Acute treatment: adrenocorticotropic hormone (ACTH): 25 to 40 IU SC (4)[A]; especially in those NPO
Pegloticase in select severe instances (1)
SUA q2–5wk while titrating urate-lowering treatment to goal (1)[C]
Regularly monitor CBC, renal function, liver function test, and urinalysis.
General lack of evidence regarding specific recommendations, although the American College of Rheumatology has outlined the following (1)[C]:
Weight loss for obese patients
Healthy overall diet
Stay well hydrated
Organ meats high in purine content (sweetbreads, liver, kidney) (1)[A]
High-fructose corn syrup–sweetened sodas, other beverages, or foods
Alcohol overuse (>2 servings per day for men and >1 serving per day for women) (1)[A]
Any alcohol use in gout during periods of frequent gout attacks or advanced gout under poor control
Serving sizes of beef, lamb, pork, and seafood with high purine content such as sardines and shellfish (1)[B]
Servings of naturally sweetened fruit juices
Table sugar and sweetened beverages and desserts
Table salt, including in sauces and gravies
Alcohol (particularly beer) in all gout patients (1)[B]
Low-fat or nonfat dairy products
Dietary and lifestyle modifications (1)[B]
Patient instructions on initiating treatment on signs and symptoms of an acute gout attack without the need to consult health care provider for each attack (1)[B]
Discussion that gout is caused by excess uric acid and that effective urate-lowering therapy is essential treatment (1)[B]
Increased susceptibility to infection
M10.9 Gout, unspecified
M10.00 Idiopathic gout, unspecified site
M10.30 Gout due to renal impairment, unspecified site
M1A.30X0 Chronic gout due to renal impairment, unsp site, w/o tophus
M1A.9XX1 Chronic gout, unspecified, with tophus (tophi)
M10.09 Idiopathic gout, multiple sites
M10.39 Gout due to renal impairment, multiple sites
M10.079 Idiopathic gout, unspecified ankle and foot
M10.072 Idiopathic gout, left ankle and foot
M10.40 Other secondary gout, unspecified site
M10.49 Other secondary gout, multiple sites
M10.071 Idiopathic gout, right ankle and foot
M1A.9XX0 Chronic gout, unspecified, without tophus (tophi)
M10.379 Gout due to renal impairment, unspecified ankle and foot
M10.479 Other secondary gout, unspecified ankle and foot
M1A.30X1 Chronic gout due to renal impairment, unsp site, with tophus
274.9 Gout, unspecified
274.00 Gouty arthropathy, unspecified
274.10 Gouty nephropathy, unspecified
274.19 Other gouty nephropathy
274.89 Gout with other specified manifestations
274.11 Uric acid nephrolithiasis
274.03 Chronic gouty arthropathy with tophus (tophi)
274.02 Chronic gouty arthropathy without mention of tophus (tophi)
274.01 Acute gouty arthropathy
90560007 Gout (disorder)
190828008 gouty arthropathy (disorder)
239844009 Gout secondary to renal impairment (disorder)
190829000 chronic urate nephropathy (disorder)
24595009 Primary gout (disorder)
48440001 Articular gout (disorder)
402469004 Gouty tophus (disorder)
MSU crystals found in synovial fluid aspirate are pathognomonic for gout.
Acute gout and sepsis can coexist.
Asymptomatic hyperuricemia does not require treatment.
Losartan possesses uricosuric properties, therefore it may be an excellent agent if patient is hypertensive.