CLINICAL PHARMACOLOGY
The exact mechanism of action of colchicine in gout is
not completely known, but it involves (1) a reduction
in lactic acid production by leukocytes, which results
in a decrease in uric acid deposition, and (2) a reduction
in phagocytosis, with abatement of the inflammatory response.
Colchicine is not an analgesic, though it relieves pain
in acute attacks of gout. It is not a uricosuric agent
and will not prevent progression of gout to chronic gouty
arthritis. It does have a prophylactic, suppressive effect
that helps to reduce the incidence of acute attacks and
to relieve the residual pain and mild discomfort that
patients with gout occasionally feel.
In man and certain other animals, colchicine can produce
a temporary leukopenia that is followed by leukocytosis.
Colchicine has other pharmacologic actions in animals:
it alters neuromuscular function, intensifies gastrointestinal
activity by neurogenic stimulation, increases sensitivity
to central depressants, heightens response to sympathomimetic
compounds, depresses the respiratory center, constricts
blood vessels, causes hypertension by central vasomotor
stimulation, and lowers body temperature.
Colchicine is rapidly absorbed after oral administration.
Large amounts of the drug and metabolites enter the intestinal
tract in bile and intestinal secretions. High concentrations
of colchicine are found in the kidney, liver, and spleen,
as well. Colchicine does not appear to be tightly bound
to serum protein, hence the drug rapidly leaves the blood
stream. Excretion occurs primarily by biliary and renal
routes.
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