Gout is a form of arthritis characterized by inflammation in a joint. The touch of a bedsheet or the sensation of a passing breeze on an affected joint can provoke excruciating pain for people suffering with gout.
The most common site of an acute gout attack is the big toe. However, other joints can also be affected, including:
Unlike other arthritic diseases, gout is a result of body metabolism rather than the immune system.
What Causes Gout?
Gout is often related to an inherited abnormality in the body to process uric acid. Uric acid levels can become elevated by eating a lot of purine-rich foods such as meats, by the overproduction of uric acid by the body, or if the kidneys do not eliminate excess uric acid. When uric acid reaches a certain level in the blood it precipitates out in the form of monosodium urate crystals. In gout, the crystals are deposited in connective tissue and joint spaces evoking intense inflammation.
People with high levels of uric acid in the blood (hyperuricemia) do not always develop gout. Actually most people with hyperuricemia do not develop gout. Therefore, it is not necessarily the high level of uric acid causing gout but perhaps a rapid change in its level. Gout attacks can be precipitated by dehydration, injury, fever, heavy eating, heavy drinking of alcohol, and recent surgery. Other contributory factors include obesity, weight gain, high blood pressure, abnormal kidney function, and certain medications.
What Are Gout Attacks?
Gout usually attacks a single joint suddenly and intensely. Gouty joints show the most visibly red signs of inflammation of any type of arthritis. An initial attack of gout may last several days and disappear even if untreated. Subsequent attacks may not occur for weeks, months, years, or not at all. In severe cases, repeated attacks occurring over a long period may cause damage to the joints and loss of mobility.
A definitive diagnosis of gout can be made by examination of aspirated joint fluid with a polarizing light microscope for evidence of crystals. Approximately one million people in the United States suffer from gout. It is nine times more common in men than women, predominantly after puberty with a peak age of 75. Gout attacks in women usually occur after menopause.
Prevention of acute gout involves:
- maintaining adequate fluid intake
- weight reduction
- dietary changes
- reduction in alcohol consumption
- medications to reduce hyperuricemia
Medication treatment of gout includes:
- Acetaminophen ( brand name - Tylenol) or other analgesic painkillers - for pain.
- NSAIDs (nonsteroidal anti-inflammatory drugs), more specifically indomethacin (brand name - Indocin) - for inflammation.
- Colchicine - prevents or relieves gout attacks by reducing inflammation.
- Corticosteroids - for anti-inflammatory response.
- Probenecid (brand names - Benemid, Probalan) - to decrease uric acid blood levels by increasing the excretion of uric acid into the urine.
- ColBenemid (other brand names are Col-Probenecid and Proben-C) - contains Probenecid, a uricosuric agent, and Colchicine, has anti-gout properties.
- Allopurinol (brand name - Zyloprim) - to lower blood uric acid by preventing uric acid production. Allopurinol blocks the conversion of purine in foods to uric acid.
- Febuxostat (brand name - Uloric) - lowers serum uric acid levels by blocking xanthine oxidase.
- Losartan (brand names - Cozaar and Hyzaar) - not specifically a gout medication but is an angiotensin II receptor antagonist, antihypertensive drug that may help control uric acid levels.
- Fenofibrate (brand name - Tricor) - not a specific gout medication but it a lipid-lowering drug that may help uric acid levels.
- Krystexxa (generic name pegloticase) - biologic drug works by breaking down uric acid.
Duke University Medical Center Book of Arthritis. David S. Pisetsky. 1995.