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U N I T 1 2
Musculoskeletal Function
Clinical Manifestations.
The typical acute attack of
gout is monoarticular and usually affects the first meta-
tarsophalangeal joint.
65,66
The tarsal joints, insteps,
ankles, heels, knees, wrists, fingers, and elbows also
may be initial sites of involvement. Acute gout often
begins at night and may be precipitated by excessive
exercise, certain medications or foods, alcohol, or diet-
ing. The onset of pain typically is abrupt, and redness
and swelling are observed. The attack may last for
days or weeks. Pain may be severe enough to be aggra-
vated even by the weight of a bed sheet covering the
affected area.
In the early stages of gout after the initial attack has
subsided, the person is asymptomatic, and joint abnor-
malities are not evident. This is referred to as
inter-
critical gout.
After the first attack, it may be months
or years before another attack. As attacks recur with
increased frequency, joint changes occur and become
permanent.
Diagnosis and Treatment.
Although hyperuricemia is
the biochemical hallmark of gout, the presence of hyper-
uricemia cannot be equated with gout because many per-
sons with this condition never develop gout. A definitive
diagnosis of gout can be made only when monosodium
urate crystals are present in the synovial fluid or in tissue
sections of tophaceous deposits. Synovial fluid analysis
is useful in excluding other conditions, such as septic
arthritis, pseudogout, and RA.
65–68
Diagnostic methods
also include measures to determine if the disorder is
related to overproduction or to underexcretion of uric
acid. This is done through measurement of serum uric
acid levels and collection of a 24-hour urine sample for
determination of urate excretion in the urine.
The objectives for treatment of gout include the ter-
mination and prevention of the acute attacks of gouty
arthritis and the correction of hyperuricemia, with con-
sequent inhibition of further precipitation of sodium
urate and absorption of urate crystal deposits already
in the tissues.
Pharmacologic management of acute gout is directed
toward reducing joint inflammation.
65–68
Hyperuricemia
and related problems of tophi, joint destruction, and
renal problems are treated after the acute inflammatory
process has subsided. Nonsteroidal anti-inflammatory
drugs, particularly indomethacin and ibuprofen, are used
for treating acute gouty arthritis.
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Alternative therapies
include colchicine and intra-articular deposition of cor-
ticosteroids. Colchicine produces its anti-inflammatory
effects by inhibition of leukocyte migration and phago-
cytosis. Although the drug usually is given orally, a more
rapid response is obtained when colchicine is given intra-
venously. The acute symptoms of gout usually subside
within 48 hours after treatment with oral colchicine has
been instituted and within 12 hours after intravenous
administration of the drug. The corticosteroid drugs have
not been systemically studied, but can be useful in the
treatment of acute gout limited to a single joint or bursa.
Between acute attacks nonpharmacologic and phar-
macologic measures are used to normalize uric acid lev-
els as a means of reducing or preventing the frequency
and severity of recurrence.
65–68
Nonpharmacologic meth-
ods include maintenance of ideal weight, moderation
in alcohol consumption, and avoidance of purine-rich
foods (e.g., liver, kidney, sardines, anchovies, and sweet-
breads). Avoidance of medications that inhibit renal
excretion of uric acid (e.g., loop and thiazide diuretics,
low-dose aspirin, and niacin) is also needed.
Three classes of drugs may be used to lower the serum
uric acid–xanthine oxidase inhibitors, uricosuric agents,
and uricase agents. Xanthine oxidase inhibitors block
the synthesis of uric acid. In this classification, the most
commonly prescribed drug to lower urate levels is allo-
purinol. Another xanthine oxidase inhibitor, febuxostat,
is used for treatment in persons with a hypersensitiv-
ity to allopurinol. The uricosuric agents (e.g., proben-
ecid, sulfinpyrozone, and benzobromarone) prevent the
tubular reabsorption of urate and increase its excretion
in the urine. The serum urate concentrations are moni-
tored to determine efficacy and dosage. Uricase agents
convert insoluble uric acid to a soluble product that
A
B
FIGURE 44-13.
(A)
Gouty tophi of the hands appear as
multiple rubbery nodules, one of which is ulcerated.
(B)
A cross-section of a digit demonstrates the trophaceous
collection of toothpaste-like urate crystals. (From: Garcia RA,
Klein MJ, Schiller AL. Bones and joints. In: Rubin R, Strayer
DS, eds. Rubin’s Pathology: Clinicopathologic Foundations of
Medicine. 6th ed. Philadelphia, PA: Wolters Kluwer Health |
Lippincott Williams &Wilkins; 2012:1282.)
