Gout is a painful arthritis caused when uric acid crystallizes and lodges in joints and tissues causing an  exquisitely painful inflammation.
Treatment is aimed at reducing the inflammation and when resolved, preventing further attacks.
This article deals with how to prevent further attacks and does not discuss treatment used in acute attacks.
Standard pharmacological therapy works in 2 ways:

• reducing uric acid production OR
• increasing uric acid excretion

Urate develops as a byproduct of purine metabolism and in fact, urate is thought to be beneficial due to its antioxidant properties that rival the benefits of Vitamin C.
However, too much urate leads to hyperuricemia, a condition defined as high serum uric acid levels that exceed 7 mg/dL.
At this level, the urate crystals become supersaturated in plasma.
Not all people who have hyperuricemia develop gout but in those that do, the crystals become lodged in the tissue and joints causing pain and inflammation.
Whether urate levels become problematic depends on striking a balance in three areas:

• the body's rate of uric acid production
• the body's rate of uric acid excretion and
• intake from dietary sources

Treatment is therefore aimed at these three areas with medication working to either reduce the formation of uric acid or increase the body's ability to excrete the crystals.
Uricosuric Agents Uricosuric agents work by enhancing excretion of uric acid by the kidneys.
People who suffer from kidney stones are generally not candidates for these medications because of the increased risk of stone formation.
These agents are generally reserved for people for whom it has been shown actually under-excrete uric acid.
There are several uricosuric agents on the market in the U.
S.
: probenecid and benzobromarone of which the former is the most widely known and used.
  Starting doses are low and are gradually increased over a period of several weeks.
The major side effects of uricosuric agents are:

• rash
• GI disturbances
• recurrence of acute gouty attack
• kidney stones

The reasons for recurrence of acute gouty attacks are not well understood but are felt to occur because of changes in the surface coating of crystal deposits that interact with local cells causing an inflammatory response.
Other medications felt to have a uricosuric effect include:

• Losartan (an antihypertensive agent)
• Fenofibrate (used in the treatment of high cholesterol and
• Vitamin C

Xanthine Oxidase Inhibitors These agents work by decreasing the synthesis of urate.
Allopurinal is currently the only drug available in this category in the U.
S.
The major side effects of allopurinal include:

• can cause an acute gouty attack
• GI disturbances
• rash
• leukopenia (decrease in white blood cells)
• thrombocytopenia (decrease in platelets)

The drug is titrated according to overall urate levels which begin to fall within several weeks of starting treatment.
Once treatment is begun, it continues for an indefinite period of time.
How Long Should Treatment Continue? Studies have shown that once treatment is begun, discontinuation generally will cause an attack in the majority of patients.
Not all patients are candidates for long-term treatment.
Be sure to talk with your health care provider about the best treatment for you.