Section IV. ANTIGOUT AGENTS
4-7. BACKGROUND
a. Gout is a metabolic disease characterized by attacks of acute pain,
tenderness, and swelling of such joints as the instep, ankle, great toe, and elbow. Gout
is caused by the deposition of sodium urate micro crystals. This condition is seen
primarily in males. It is thought that heredity plays a major factor in gout, because gout
occurs more often in relatives of those who have gout than in the population in general.
b. Gout is caused by defective purine metabolism. Humans lack the enzyme
uricase, an enzyme that converts uric acid to allantoin. Uric acid is a major end product
of the metabolism of purine (indirectly of amino acid metabolism). The level of uric acid
in the plasma and urine is normally high (saturated). Sometimes a moderate increase
in uric acid production can lead to the deposition of sodium urate microcrystals as
described above.
c. The treatment of gout is usually designed to (1) relieve pain and (2) increase
the elimination of uric acid from the body. Drugs administered to increase the
elimination of uric acid from the body are referred to as uricosuric agents.
4-8. DRUGS USED TO TREAT GOUT
a. Colchicine. While the exact mechanism of action of colchicine is unknown,
the administration of the drug causes a decrease in the amount of urate crystals
deposited in the various parts of the body--the result is a decrease in the inflammatory
process. This drug is the oldest and most effective agent used in the treatment of acute
attacks of gout. The usual dose of an acute gout attack is 1.2 milligrams immediately,
then 0.6 milligram every 30 minutes to one hour until nausea and vomiting or diarrhea
starts or pain is relieved. Each patient must initially titrate his own dosage. If seven
tablets caused adverse effects the first administration, the patient should reduce the
dosage to six tablets on the next acute attack. The usual side effect associated with the
administration of colchicine is gastrointestinal irritation. Occasionally antidiarreheals are
prescribed to offset this adverse effect. The patient should be informed to allow an
interval of at least three days between treatments--otherwise, toxic effects may occur
from accumulation.
b. Sulfinpyrazone (Anturane). Sulfinpyrazone potentiates the urinary
excretion of uric acid. This anti-gout agent has the primary side effect of gastrointestinal
upset. The patient taking this medication should be told to take this medication with
food or milk. This medication should not be taken with salicylates.
c. Allopurinol (Zyloprim). Allopurinol acts by decreasing the production of
uric acid. This drug is not effective in the treatment of acute gout attacks, because it
has no anti-inflammatory action. In fact, allopurinol may actually intensify the
inflammation seen during an acute gout attack. Although the drug cannot be used to
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