Gouty arthritis: How to make the diagnosis
In gout, urate crystals (purple) form around the joint, causing arthritic swelling and pain.
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At a glance
- The great toe is typically affected, but gout may also occur
in the knee, shoulder, or hand, or other areas of the foot.
- Joint arthrocentesis is the definitive diagnostic study for gouty arthritis.
- Whereas gouty arthritis waxes and wanes, rheumatoid arthritis is a slowly progressing disease.
- The most effective long-term treatment is lifestyle modification and prevention of such comorbidities as diabetes.
The most common form of inflammatory arthritis in men is gouty arthritis, occurring in about 1.3% of the population in the fourth decade and later.1 Approximately 90% of men with primary gout are older than age 30 years.2 An estimated 2.13% of the U.S. population was diagnosed with gout in 2009.3 In adults older than age 20 years, more than 6 million have had gout.4 For women, the incidence is half that of men, but this risk increases after menopause.3 Age raises the risk for developing this disease, as does ethnicity, with a higher prevalence in Pacific Islanders, Polynesians, and people of African descent.1,2
Gout is a disorder that involves abnormal metabolism of uric acid resulting in increased urate levels in the blood. This hyperuricemia can be caused by increased production of uric acid, decreased excretion of uric acid, or a combination of the two.5 At a high enough concentration in the blood, urate starts to precipitate into crystals that collect in tissue and joint spaces, resulting in inflammation and pain. Gout can be categorized as either primary or secondary. Primary gout is a result of increased production of purine and decreased renal clearance of uric acid.2 Secondary gout is an acquired disorder resulting from such causes as medication side effects, multiple myeloma, myeloproliferative disorders, renal disease, hypothyroidism, psoriasis, sarcoidosis, and lead poisoning.2
Gouty arthritis is excruciatingly painful and greatly affects activities of daily living during flares. The disease is episodic in nature, with waxing and waning episodes of affected joints. Periods between flares become shorter as the disease progresses, and chronic joint swelling may occur.6 Individuals with gout also may develop such comorbidities as hypertension, renal disease, nephrolithiasis, diabetes mellitus, atherosclerosis, and hypertriglyceridemia.2 Appropriate diagnosis, treatment, and lifestyle modification of gout during its initial episode is imperative for improving patients' well-being and preventing long-term effects.
While the presentation of acute gouty arthritis has classic findings (sudden onset of intense pain, induration, erythema, and warmth to the touch in a single joint), these findings are not always present, and other diagnoses may present similarly. Additional signs and symptoms of the disease include painful range of motion, fever, and superficial desquamation of skin over the affected joint later in the course of the attack.2 Typically, the first metatarsophalangeal (MTP) joint is affected, but gouty arthritis may occur in the knee, shoulder, or hand, or other areas of the foot. These joints are affected in 30%-50% of patients.1
According to several studies, the joint most commonly affected is the great toe. In a study of 57 men with gout, 57% had the attack at this site.7 The great toe was the symptomatic joint in 92% of men with multiple attacks.7 In one study performed on postsurgical gout patients, the lower-extremity joints were affected 97% of the time, with involvement of the great toe 62.7% of the time.8
The great toe is affected more often as a result of the nature of urate crystallization. Urate has a higher tendency to crystallize at lower temperatures, and the MTP joint is the coolest part of the body.1 A high index of suspicion toward gouty arthritis is reasonable if a patient presents with sudden onset of pain and swelling of the great toe with no history of recent trauma. However, multiple joints may be affected simultaneously in 10%-15% of patients in the initial attack.9
On physical examination, other associated findings may include tophi, which are precipitant urate deposits in tissues.5 Tophi are nodular and appear yellowish in color. They usually develop after the initial episode and are found on such extremities as hands, feet, olecranon bursae, prepatellar bursae, and ears.2
A thorough history may also aid in narrowing the differential. Typically, the attack is abrupt in onset and occurs after such a precipitating event as alcohol excess, changes in medications that affect urate metabolism, and postoperative hospitalization.2 Drugs that may cause an attack of gouty arthritis include thiazide diuretics and cyclosporine.10,11 Drugs that may induce hyperuricemia include loop diuretics, pyrazinamide, ethambutol, nicotinic acid, vitamin B12, chemotherapy, low-dose salicylates, and levodopa.10,11 Patients may also have a recent history of high seafood or meat intake, which increases the risk for developing the disorder.12 Obtain a detailed history that includes the usage of the above medications or recent hospitalization.
Other important components of the medical history may include renal stones, obesity, diabetes mellitus, hyperlipidemia, and atherosclerotic cardiovascular disease.9,13,14 A positive family history may also be notable. Genetic analysis has uncovered several mutations that may predispose a patient to developing gout. These mutations may be familial or nonfamilial. The familial genetic mutations are very uncommon, and the onset of gout occurs in childhood or early adulthood. The ABCG2 allele is an example of a nonfamilial genetic variation that has been identified. Nonfamilial variations in the ABCG2 allele result in decreased renal secretion of uric acid, thereby causing hyperuricemia and increased risk for gout.15 Approximately 10% of whites with gout have a mutation in this allele.16 Other genetic risk factors have been found to increase the risk for gout and are still being studied.
Joint arthrocentesis is the definitive diagnostic study for gouty arthritis. Since urate crystals precipitate within the affected joint, their presence is viewable under polarized light microscopy of synovial fluid.17 If observed, this is diagnostic for gouty arthritis. However, arthrocentesis of the affected joint is not often performed, especially when given the classic presentation. Joint aspiration is performed on an estimated 11% of patients during the initial presentation.17
Additional lab studies that are useful when diagnosing an initial attack include a serum uric acid (sUA) level, erythrocyte sedimentation rate (ESR), complete blood count (CBC) with differential, and 24-hour urine uric acid measurement. However, these are not necessary for establishing a diagnosis. Serum uric acid is elevated in 95% of patients during a flare.2 This is suggestive of a gouty attack but not definitive. According to the Arthritis Foundation, sUA levels do not assist in the diagnosis of gout, as people with high levels may never develop gouty arthritis.6 ESR and WBC may also be elevated.2 A 24-hour urine specimen may help in identifying a cause and selecting a treatment plan by determining if the patient is over- or under-excreting urate.6,9
There are several clinical criteria guidelines that can be used to help diagnose gout. These include the American College of Rheumatology (ACR) criteria, Rome criteria and New York criteria (Table 1).18