Gout is defined as a hereditary metabolic disease caused by hyperuricemia that is a form of acute arthritis and is marked by joint inflammation (Thomas, 1997). In gout, monosodium urate crystals form in the joints and/or organs of the body when uric acid levels in the blood are high (hyperuricemia).
Gouty attacks can occur at any time without warning and are often painful. They can be initiated by injury or stress, as these cause increased uric acid production in the blood. With a gouty attack, the joint swells and the skin over the area becomes red, swollen, warm, and tight. The joint can be sensitive to palpation. The patient may also have a fever, chills, or other constitutional symptoms. There are some risk factors that predispose individuals to gout such as obesity, hypertension, cardiovascular disease, and diabetes (Wikipedia, 2008).
Urate crystals often form in the distal extremities because the extremities are cooler than the core part of the body and urate tends to crystallize at these cooler temperatures. These crystals, when they build up, can cause a tophus, which are hard lumps of urate crystals. Gout often affects the joints of the big toe, but these crystals can also build up in the ears, elbows, or even in other organs such as the kidneys. Most tophi can decrease in size slowly when blood uric acid levels decrease, but large tophi may have to be surgically removed (Berkow, et al., 1997). Deposits often increase in size and burst through the skin to form a sinus that discharges a chalky white material (Wikipedia, 2008). These crystals build up and can cause visible peripheral deformity (as in the ears) as well as causing deformity in the joints as they inhibit joint movement and cause damage to the joint itself (Berkow, et al., 1997).
Uric acid is the byproduct of cell/tissue breakdown during normal cell turnover and is able to be detected in the blood by a simple blood sample (eMedicineHealth, 2008). It is also produced when purine metabolism takes place, which happens after purine is consumed by the patient and processed by the body (Wikipedia, 2008). It is eliminated from the body by the kidneys and in the intestine (Wikipedia, 2008). If either too much uric acid is being created or if not enough is being eliminated, hyperuricemia will develop (Berkow, et al., 1997). Hyperuricemia is defined as a plasma urate (uric acid) level greater than 420 ¼mol/L (7.0 mg/dL) in males (or 380 ¼mol/L in females (Wikipedia, 2008).
Some patients with gout (10%) generate too much uric acid through diet intake or increased cell breakdown, while the others (90%) do not effectively eliminate enough uric acid into the urine (eMedicineHealth, 2008). A sudden increase in uric acid levels can be caused by many different things such as:
1. Excess intake of alcohol or red meat. Protein is a crude proxy for purines; a more precise proxy is muscle. Purine metabolism gives rise to uric acid, which is normally excreted in the urine. The main source of dietary purines is DNA and RNA, via their bases adenine and guanine. A diet low in purines reduces the serum level of uric acid. Notable sources of dietary purines include beer (which is high in guanosine; coffee, tea, and other caffeinated beverages; and chocolate (for its theobromine content) (Wikipedia, 2008).
2. Trauma or illness. During infection or trauma, the immune system is rapidly breaking down cells for repair, which releases excess uric acid into the blood.
3. Starvation/dehydration. During dehydration, urate concentrations are increased and their elimination is decreased through the kidneys.
4. IV contrast dyes can affect the kidneys and decrease their ability to eliminate urates from the blood.
5. Chemotherapy. Some medicines are purine-based. Chemotherapy agents are notable for this (the purine-analog antimetabolite drugs [Wikipedia, 2008]) and for the action they take on cell breakdown (such as in the treatment of cancer).
6. Other Medications
- Diuretics (increases dehydration)
- Aspirin (aspirin in low doses can impair the excretion of uric acid from the kidneys (Shiel, 2006).
- Nicotinic acid. For example, the body's ability to remove uric acid can be negatively affected by taking nicotinic acid (FootPhysicians.com, 2005).
8. Kidney disease or certain medications can prevent the kidneys from being able to adequately eliminate uric acid as well (Berkow, et al., 1997).
A definitive diagnosis of gout is made using light microscopy of fluid aspirated from the joint. This fluid is examined to see if it demonstrates intracellular monosodium urate crystals in the synovial fluid (Wikipedia, 2008).
Treatment
Treatment for patients with gout consists of controlling pain/inflammation first and then preventing recurrent attacks. Once the diagnosis has been confirmed, the drugs of choice for pain control are indomethacin and other nonsteroidal anti-inflammatory drugs (NSAIDs), oral glucocorticoids, or intra-articular glucocorticoids administered via a joint injection (Wikipedia, 2008).
Some medications used to reduce uric acid in the blood include:
1. Colchicine. Interferes with white blood cells in initiating the perpetuating the inflammatory response to monosodium urate crystals (Deglin and Vallerand, 2001).
2. Allopurinol (inhibits production of uric acid).
3. Sulfinpyrazone (increases the excretion of uric acid in the urine).
4. Probenecid, a drug that promotes the excretion of uric acid in urine, is commonly prescribed often in conjunction with colchicine.
5. Sodium bicarbonate (baking soda) is an old remedy, thought to work by raising blood pH (lowering blood acidity).
However, the added sodium may be inappropriate for some people (Wikipedia, 2008).
Prevention
Reduce intake of purines through the diet by avoiding purine-rich foods like those listed above. Other indirect methods to reduce gout include reducing risk factors such as obesity, hypertension, cardiovascular disease, and diabetes (Wikipedia, 2008).
Avoid dehydration by drinking plenty of liquids, especially water, to help excrete urates from the blood. Also avoiding diuretic foods or medicines (caffeinated beverages, aspirin, alcohol, etc.) (Wikipedia, 2008).
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