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Gout and Pseudogout

Gout and pseudogout are painful inflammatory disorders caused by the deposition of crystals in the joints. They are the two most common crystal-induced arthropathies. Gout results from high blood levels of uric acid which leads to a buildup of monosodium urate monohydrate crystals in joint tissue. Gout actually encompasses a variety of clinical presentations including hyperuricemia (elevated levels of uric acid in the blood), acute gouty arthritis (attacks of acute inflammatory arthritis due to the collection of monosodium urate monohydrate crystals in joint fluid), tophi (accumulations of monosodium urate monohydrate crystals within and around a joint and its surrounding soft tissues), gouty nephropathy (impairment of the kidneys due to crystal deposition), and uric acid urolithiasis (also known as urinary tract stones). Pseudogout is caused by the accumulation of calcium pyrophosphate crystals in the cartilage and joint fluid.

Epidemiology

Gout has become more prevalent over the last 30 years, not only in the United States, but also abroad. British and American studies have estimated gout to affect 2.6 to 8.4 per 1,000 adults. More than 2 million people in the United States live with this disease. Gout is nine times more common in men than in women. The 1995 National Health Interview Survey (American study) reported 8.5 per 1,000 adults have gout, and 5 percent of all arthritis cases are gouty arthritis. The onset of gout is most common in the fifth decade of life (ages 40–49). The disease is most prevalent in the elderly population; this is supported by a rate of 24 per 1,000 men and 16 per 1,000 women aged 65–74 years. These rates are increased from those published in 1986: 13.6 per 1,000 men and 6.4 per 1,000 women. It is the most common cause of inflammatory arthritis in men over 30 years of age. This condition is rarely seen in male children and teenagers as well as premenopausal women. Increased systemic estrogen during the reproductive years is likely to be the reason for lower rates of gout in women. Estrogen acts to increase elimination of uric acid from the body via the kidneys. There is also a racial predilection for gout: it is more common among Pacific Islanders. In the United States, it is twice as prevalent in African-American males than it is in Caucasian males.

Gout is twice as prevalent as pseudogout. The conditions are similar in that incidence increases with age: calcium pyrophosphate crystals are found in approximately 3 percent of adults in their 60s; however radiologic surveys show evidence of chondrocalcinosis (calcium deposits in the joints) in 50 percent of people in their 90s. Studies have differed on whether the disease is predominant in men versus women.

Pathogenesis

Gout is due to hyperuricemia, or high levels of uric acid in the bloodstream. Uric acid is produced when purines are metabolized by liver enzymes (such as uricase). Purines are a part of all normal tissue. They may be endogenously produced as a by-product of normal cell turnover or they may come from the diet (seafood, liver, beans, gravy, sweet breads, anchovies, beer, wine). Typically, the body is able to regulate the amount of uric acid by balancing production with excretion. If the body produces too much uric acid or if an insufficient amount is excreted from the body, uric acid builds up in the blood and precipitates as monosodium urate crystals. Most people with gout tend to be underexcretors of uric acid. This may be due to kidney or digestive system malfunction.

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