PRINCIPLES OF GOUT MANAGEMENT
Initial treatment of gout and its associated hyper-uricemia must involve therapy directed toward termi-nating the painful inflammatory process that is a promi-nent feature of acute gouty arthritis. A variety of nonsteroidal antiinflammatory compounds (e.g., in- domethacin, oxyphenbutazone, ibuprofen, naproxen, sulindac) can be administered either alone or in combi-nation with colchicine, a relatively specific agent for use in acute gouty attacks. Glucocorticosteroids, such as prednisone, can be given as a tapered dose over 10 days to replace colchicine. These steroids cause fewer side ef-fects than does colchicine. If the diagnosis is uncertain, colchicine should be used, since a response to this drug is generally taken as establishing the diagnosis of acute gouty arthritis.
Although the treatment of the hyperuricemia of gout depends upon lowering blood uric acid levels, most physicians caution against employing drugs such as al-lopurinol, probenecid, or sulfinpyrazone during an acute attack, since the therapy itself, at least during the initial stages, may exacerbate the condition. Once the acute symptoms are under control and the patient is asymptomatic, appropriate treatment should include not only drug therapy but also management of body weight and control of dietary purine intake. Long-term treatment is directed toward decreasing uric acid produc-tion from nucleoprotein, increasing excretion, or both.
Uric acid production is more easily controlled by drug therapy than by dietary restriction, because only a small portion of blood uric acid is derived from the di-etary intake of purines. Excretion of uric acid may be in-creased by increasing the rate of urine flow or by using uricosuric agents. Since uric acid is filtered at the glomerulus and both actively secreted and reabsorbed by the proximal tubule cells, both approaches are effective.
Since overproducers are already excreting large quantities of uric acid in their urine, drugs that further increase the rate of excretion (i.e., uricosuric com-pounds) increase the likelihood of renal stone forma-tion. In these patients, the use of a compound that in-hibits uric acid synthesis is preferable. Although at first glance the use of a combination of drugs—a drug that reduces production along with one that is uricosuric— would seem to be a rational therapeutic approach, in practice this has not worked well. Apparently the effec-tiveness of a drug that inhibits uric acid synthesis can be diminished by uricosuric agents, and therefore the com-bination has less value than each drug used separately. Furthermore, side effects appear to occur more fre-quently during combination drug therapy.
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