COPYRIGHT © by Michaelidou Maria
Dr. Maria Michailidou
Essentials of Diagnosis
Caused by deposition of uric acid crystals and usually associated with hyperuricemia.
Usually begins as an intermittent, acute monoarthritis, especially of the first metatarsophalangeal
joint. Over time, attacks become more frequent, less intense, and involve more joints.
Diagnosed by demonstrating uric acid crystals in joint fluid. Extra-
The underlying basis for gout is an increased total body urate pool. This is generally manifested as hyperuricemia, which is defined as a serum urate concentration more than 7.0 mg/dL. The concentration of 7.0 mg/dL is important because fluids with urate content greater than that are supersaturated with urate, a condition that favors urate crystal precipitation.
At least 5% of asymptomatic Americans manifest hyperuricemia on at least one occasion during adulthood. Hyperuricemia may be even more common in Europe and in countries in the Far East.
The likelihood of developing symptomatic gout and the age at which that occurs correlates
with the duration and magnitude of hyperuricemia. In one study, persons with urate
levels between 7.0 and 8.0 mL/dL had a cumulative incidence of gouty arthritis of
3% while those with urate levels greater than 9.0 mL/dL had a 5-
Gout presents predominantly in men with a peak age of onset in the fifth decade.
The incidence of gout in women approaches that of men only after they have reached
age 60 years. The onset of disease in men prior to adulthood or in women before menopause
is quite rare and is almost always due to an inborn error of metabolism or congenital
condition. The prevalence of self-
Hyperuricemia can result from increased urate production, decreased uric acid excretion
by the kidneys, or a combination of the two mechanisms. Fewer than 5% of patients
with gout are hyperuricemic because of urate overproduction. These persons can be
recognized because they excrete more than 800 mg of uric acid in their urine during
Symptoms and Signs
The natural history of gout can be divided into three distinct stages
1. Asymptomatic hyperuricemia.
2. Acute and intermittent (or intercritical) gout.
3. Chronic tophaceous gout.
Although most untreated patients with gout will progress to chronic tophaceous gout, the course varies considerably from one patient to another. Some patients experience only one or two attacks of acute gouty arthritis during their lifetime. It is quite unusual for tophi to develop in a patient with no history of acute gouty arthritis.
The initial episode of acute gouty arthritis usually follows 10 to 30 years of asymptomatic
hyperuricemia, and there is no evidence that damage occurs to any organ system during
that time. Just why and when the first attack of gout occurs in susceptible persons
remains a mystery. Although some patients experience prodromal episodes of mild discomfort,
the onset of a gouty attack is usually heralded by the rapid onset of exquisite pain
associated with warmth, swelling, and erythema of the affected joint (. The pain
escalates from the faintest twinges to its most intense level over an 8-
Symptoms resolve quickly with appropriate treatment, but even untreated, an acute attack resolves spontaneously over 1 to 2 weeks. With resolution of the attack, patients enter an interval termed the "intercritical period" when they are again completely asymptomatic. The rare patient will not experience a second attack of gout but most will. Early in the intermittent stage, episodes of arthritis are infrequent and the intervals between the attacks vary from months to years. Over time, the attacks become more frequent, less acute in onset, longer in duration, and tend to involve more joints.
During the intercritical periods of acute intermittent gout, the previously involved joints are virtually free of symptoms. Despite this, monosodium urate crystal deposition continues. Urate crystals often can be identified in the synovial fluid despite the absence of symptoms and erosive changes indicative of bony tophi begin to appear on radiographs.
Although the reasons why acute gout develops when it does are not clear, attacks
tend to be associated with rapid increases, and more often, decreases in the concentration
of urate in synovial fluid. These concentrations mirror the fluctuations seen in
the serum. Accordingly, a person may experience a sudden drop in the serum urate
level, leading to an acute attack and, therefore, is found to be normouricemic when
blood is tested at that time. Trauma, alcohol ingestion, and the use of certain drugs
are known to trigger gout attacks as well. Gouty attacks not infrequently occur as
a person is recovering from an alcoholic binge. Drugs known to precipitate attacks
do so by rapidly raising or lowering serum urate levels. Candidate agents include
, , and the urate-
As gout continues to progress, the patient gradually enters the stage of chronic
gouty arthritis. This usually develops after 10 or more years of acute intermittent
gout. The transition to chronic gout is complete when the intercritical periods are
no longer pain free. The involved joints are now persistently uncomfortable and may
be swollen. Patients report stiffness or gelling sensations as well. Visible or palpable
tophi may be detected on physical examination during this stage of gout, even though
they may have been recognized by radiographs prior to entry into this stage ). The
development of tophaceous deposits in individual patients varies; in general, they
are a function of the duration and severity of the hyperuricemia, with a mean occurrence
approximately 12 years after the onset of the first attack of gout in those not treated
Hyperuricemia remains the cardinal feature of gout. The usefulness of this laboratory
finding in establishing the diagnosis of gout is limited. Whereas most patients with
gout will have an elevated serum urate (greater than 7.0 mg/dL), levels may fall
within the normal range on occasion; in fact, levels in the normal range are not
uncommon during acute attacks, as described above. In addition, during the acute
attack, the complete blood cell count may show a leukocytosis with increased polymorphonuclear
leukocytes on the differential and elevations of the erythrocyte sedimentation rate
During an acute attack, the synovial fluid findings are consistent with moderate to severe inflammation . The leukocyte count usually ranges between 5 and 80,000 cells/L with an average between 15,000 and 20,000 cells/L. The cells are predominately polymorphonuclear leukocytes.
The definitive diagnosis of gout is made by examination of synovial fluid or tophaceous
material with compensated polarized light microscopy and identifying the characteristic
monosodium urate crystals. These crystals appear as bright yellow needle-
No radiographic abnormalities are present early in the disease course. In acute gouty arthritis, the only finding may be soft tissue swelling in the involved joint. Bony abnormalities indicative of deposition of urate crystals (microtophi) develop only after years of disease. These abnormalities are most frequently asymmetric and confined to previously symptomatic joints. The advanced bony erosions of advanced gout are often radiographically distinct. Typically, they are slightly removed from the joint space, have a rounded or oval shape, and are characterized by a hypertrophic calcified "overhanging edge." The joint space may be preserved or show osteoarthritic type narrowing.
Patients with gout often suffer from hyperlipidemia, intolerance, hypertension, coronary artery disease, and obesity. Accordingly, it is appropriate to measure serum lipids and fasting blood sugars in patients with gout. Because renal dysfunction develops in many patients with hypertension and gout, it is appropriate to monitor serum creatinine levels as well.