Gout is a disorder due to an inborn error of metabolism. The result is an overproduction of uric acid. This overproduction process leads to an accumulation of monosodium crystals in multiple organ systems with the most common manifestations occurring in the joints and kidneys.

Gout is more common in men than women. However, postmenopausal women are at risk, particularly if they take thiazide diuretics.

Attacks of gouty arthritis are extremely painful and can, over time, lead to deformity and possibly crippling.

Persistent deposits of monosodium urate in the kidneys can lead to loss of kidney function.

Another important issue is the fact that gout is often accompanied by co-morbid conditions -other diseases that are common in gout patients- that can complicate the management of gout.

These co-morbid conditions include: obesity, diabetes, high blood pressure, chronic kidney disease, cardiovascular disease, heart failure, and elevated blood lipids.

The comprehensive treatment of the gout patient will then depend not only on controlling gouty arthritis but also should include careful attention to these other medical problems.

Some drugs may interfere with gout treatment. For instance, thiazide diuretics and low dose aspirin elevate uric acid levels. Allopurinol, a drug often used to treat gout, has potentially lethal interactions with ampicillin and azathioprine.

Treatment of gout is hampered by the lack of clear-cut guidelines as well as by the limited number of medications available.

The major indications for treating gout are:

• Frequent or disabling gout flares
• Tophaceous gout (gout accompanied by large soft tissue deposits of monosodium urate
• Gout with chronic kidney disease or kidney stones
• Radiation or chemotherapy for lymphoma or leukemia which will lead to massive overproduction of uric acid

Aims of therapy should be the following:

• Stop the acute painful attack
• Protect against future attacks
• Maintain normal urate levels by lowering serum urate

There are a number of errors that inexperienced physicians commit when treating gout. Much of this is due to gaps in knowledge. They include:

• Inadequate dosing... not getting the serum urate level low enough
• Not using non-steroidal anti-inflammatory drugs (NSAIDS) or low dose colchicines when instituting uric acid lowering therapy
• Not monitoring laboratory results frequently enough when treating patients with uric acid lowering therapies

Pitfalls surrounding current treatment strategies include:

• Increased frequency of acute attacks that may occur when urate lowering therapy is started
• A limited number of drugs capable of lowering serum urate levels

In a future article I will discuss specific treatment strategies.