Gout is an extremely painful form of arthritis due to the accumulation of uric acid crystals inside joints. These crystals can cause acute inflammation characterized by joint pain, swelling, redness, and heat.
The attacks often occur without any warning and can be debilitating. Attacks, without treatment, can last for days to weeks.
Without adequate treatment gout attacks become more frequent, more severe, and can begin to affect multiple joints. This isn't the only danger.
Untreated gout can cause severe damage to the kidneys. In addition, it is often associated with other conditions including hypertension, obesity, elevated blood lipids, and diabetes.
Uric acid is derived from substances called purines. Purines are a natural byproduct of the body’s normal metabolism. Purines also come from diet. People who get gout either overproduce purines or are unable to get rid of them fast enough through the bowel or kidneys.
When that occurs, the uric acid that is derived from purines builds up in the body. Since roughly a third of uric acid comes from dietary purines, the notion of controlling gout through diet alone may not be enough. However it is a start. Foods that are high in purines include red meat, alcohol-based beverages such as beer, wine, and hard liquor, shellfish, and soda pop.
By restricting dietary intake of purines, blood uric acid can be lowered by 1 mg/dl. However, the goal is to get it below 6 mg/dl, which is often difficult to do through diet alone.
It’s important to establish the diagnosis of gout first. While the history and exam can be helpful, they are not always diagnostic. The only 100% certain way to make the diagnosis is to examine fluid from an inflamed joint. This requires the insertion of a needle using ultrasound guidance into the affected joint and aspirating the fluid and then examining the fluid using a polarized microscope. If uric acid crystals are identified, the diagnosis is absolute.
This is important because there are other types of arthritis that can look like gout. Examples include pseudogout, septic (infected) joint, Reiter’s disease, psoriatic arthritis, and so on.
There are two modes of attack for treating gout. The first task is to treat the acute attack using drugs such as non-steroidal- anti-inflammatory drugs, colchicine (Colchrys), or glucocorticoids (steroids). While these methods are often successful, some patients may require injections of steroid into an acutely inflamed joint. The steroids can be injected at the same time as fluid is obtained for examination with the polarizing microscope.
Once the acute attack is managed, attention can be turned to the long term management. That involves the use of uric acid lowering drugs.
Institution of uric acid lowering drugs should not be undertaken during the acute attack since it will prolong the resolution of the acute attack and even make it worse.
If a patient has normal kidney function and does not excrete too much uric acid into the urine, then a drug called a uricosuric (makes the patient urinate uric acid) may be the solution. An example is a drug called probenecid. If a patient already puts out a lot of uric acid in the urine, then a uricosuric is not recommended because this can lead to the formation of uric acid kidney stones.
For many patients with gout, a drug that lowers the metabolism of purines to uric acid is used. Drugs that fall into this category are allopurinol or febuxostat (Uloric). By lowering blood uric acid, over time, the total body uric acid burden is reduced and gout will be controlled.
All of these medications mentioned have potential side effects. It’s important to discuss them with the prescribing physician.
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