Drugs Used in Gout
Gout is characterized biochemically as a disorder of uric acid metabolism and clinically by hyperuricemia and recurrent
attacks of acute arthritis. Gouty arthritis is most frequently seen as an acute
inflammation pri-marily in the large toe, instep, ankle, or heel. Less often
the initial symptoms appear in the knee or elbow; occasionally they are seen in
the wrist. If the condition remains untreated over years, sodium urate crystals
may form in the subcutaneous tissue, joints, renal parenchyma, and renal
pelvis. Uric acid stones may form in the lumen of the urinary tract, and
progressive renal failure often occurs in the later stages of untreated gout.
Also, microcrystalline deposits of sodium urate frequently result in
inflammatory bulges or bumps, termed tophi,
appearing in the subcutaneous tissue of the earlobes, elbows, and hands and at
the base of the large toe.
The elevated blood uric acid
concentration in gout is an easily identified and readily treated abnormality.
However, it is essential to identify the condition and in-stitute therapy early
to avoid the complications that re-sult from a prolonged elevated uricemia.
Complications include arthritis, tophi, urinary calculi, and gouty nephropathy.
Although all forms of gout
have the common trait of hyperuricemia, their causes can be manifold. Primary, or genetic, gout results from either increased synthesis of uric acid
or decreased renal excretion of the substance. Some gout patients have an
unusual shunt mechanism that converts glycine directly to uric acid rather than
to its normal metabolic products. Secondary
gout may re-sult from either overproduction or impaired elimination of uric
acid. Overproduction is usually secondary to some other disorder, most frequently of hematological origin. For
instance, in leukemia, myeloid metaplasia, lymphoma, polycythemia vera, and
rapid weight loss (dieting), breakdown of cellular nucleoprotein is in-creased,
which can lead to excess formation of uric acid.
In secondary gout, diminished elimination of
uric acid can be due to lead nephropathy, glycogen storage disease, or sickle
cell anemia. In addition, several drugs, including salicylates, pyrazinamide,
alcohol, ethambu-tol, nicotinic acid, cyclosporine, fructose, cytotoxic agents,
and certain diuretics (e.g., thiazides, furosemide, bumetanide) will impair the
renal elimination of uric acid. These drugs competitively inhibit the active
secre-tion of uric acid into the urine,
with resulting hyperuricemia
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