Gout

:"Podagra" redirects here. For the moth genus, see Podagra (moth). Gout (also known as podagra when it involves the big toe) The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 μmol/L (7 and 8.9 mg/dL), the risk is 0.5% per year, while in those with a level greater than 535 μmol/L (9 mg/dL), the risk is 4.5% per year. Other triggers include physical trauma and surgery. This is believed to be partly due to their effect in reducing insulin resistance. A body mass index greater than or equal to 35 increases a male's risk of gout threefold. Lesch-Nyhan syndrome is often associated with gouty arthritis.

Medication

Diuretics have been associated with attacks of gout. However, a low dose of hydrochlorothiazide does not seem to increase the risk. as are the immunosuppressive drugs ciclosporin and tacrolimus. Other factors believed to be important in triggering an acute episode of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis, articular hydration, and extracellular matrix proteins, such as proteoglycans, collagens, and chondroitin sulfate. All synovial fluid samples obtained from undiagnosed inflamed joints should be examined for these crystals. The fluid must also be examined relatively quickly after aspiration, as temperature and pH affect their solubility. Thus, the diagnostic utility of measuring uric acid level is limited. Other blood tests commonly performed are white blood cell count, electrolytes, renal function, and erythrocyte sedimentation rate (ESR). However, both the white blood cells and ESR may be elevated due to gout in the absence of infection. A white blood cell count as high as 4.0×10⁹/L (40,000/mm³) has been documented. or other neoplasms.

Prevention

Both lifestyle changes and medications can decrease uric acid levels. Dietary and lifestyle choices that are effective include reducing intake of food such as meat and seafood, consuming adequate vitamin C, limiting alcohol and fructose consumption, and avoiding obesity. Coffee, but not tea, consumption is associated with a lower risk of gout. Gout may be secondary to sleep apnea via the release of purines from oxygen-starved cells. Treatment of apnea can lessen the occurrence of attacks.

Treatment

The initial aim of treatment is to settle the symptoms of an acute attack. Repeated attacks can be prevented by different drugs used to reduce the serum uric acid levels. Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine and steroids, For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given.

Colchicine

Colchicine is an alternative for those unable to tolerate NSAIDs. Gastrointestinal upset, however, depends on the dose, and the risk can be decreased by using smaller yet still effective doses.

Steroids

Glucocorticoids have been found to be as effective as NSAIDs and may be used if contraindications exist for NSAIDs. It will be an option for the 3% of people who are not adequately treated with other medications due to their association with severe allergic reactions.

Prophylaxis

A number of medications are useful for preventing further episodes of gout, including xanthine oxidase inhibitor (including allopurinol and febuxostat) and uricosurics (including probenecid and sulfinpyrazone). They are not usually commenced until one to two weeks after an acute attack has resolved, due to theoretical concerns of worsening the attack, as it is not until this point that medications have been found to be cost effective. They are, however, contraindicated if the person has a history of renal stones.

Prognosis

Without treatment, an acute attack of gout will usually resolve in 5 to 7 days. However, 60% of people will have a second attack within one year. This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.

Epidemiology

Gout affects around 1–2% of the Western population at some point in their lifetimes, and is becoming more common. Rates of gout have approximately doubled between 1990 and 2010. This rise is believed to be due to increasing life expectancy, changes in diet, and an increase in diseases associated with gout, such as metabolic syndrome and high blood pressure. A number of factors have been found to influence rates of gout, including age, race, and the season of the year. In men over the age of 30 and women over the age of 50, prevalence is 2%.

In the United States, gout is twice as likely in African American males as it is in European Americans. Rates are high among the peoples of the Pacific Islands and the Māori of New Zealand, but rare in Australian aborigines, despite a higher mean concentration of serum uric acid in the latter group. It has become common in China, Polynesia, and urban sub-Saharan Africa.

History

described the microscopic appearance of uric acid crystals in 1679. or "rich man's disease". The first documentation of the disease is from Egypt in 2,600 BC in a description of arthritis of the big toe. The Greek physician Hippocrates around 400 BC commented on it in his Aphorisms, noting its absence in eunuchs and premenopausal women. Aulus Cornelius Celsus (30 AD) described the linkage with alcohol, later onset in women, and associated kidney problems:

Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera... Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed... some have obtained lifelong security by refraining from wine, mead and venery.

While in 1683, Thomas Sydenham, an English physician, described its occurrence in the early hours of the morning, and its predilection for older males:

Gouty patients are, generally, either old men, or men who have so worn themselves out in youth as to have brought on a premature old age - of such dissolute habits none being more common than the premature and excessive indulgence in venery, and the like exhausting passions. The victim goes to bed and sleeps in good health. About two o'clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle or instep. The pain is like that of a dislocation, and yet parts feel as if cold water were poured over them. Then follows chills and shivers, and a little fever... The night is passed in torture, sleeplessness, turning the part affected, and perpetual change of posture; the tossing about of body being as incessant as the pain of the tortured joint, and being worse as the fit comes on.

The Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679.

In other animals

Gout is rare in most other animals due to their ability to produce uricase, which breaks down uric acid. Humans and other great apes have lost this ability, and thus gout is common.

Research

A number of new medications are under study for treating gout, including anakinra, canakinumab, and rilonacept. A recombinant uricase enzyme (rasburicase) is available; its use, however, is limited, as it triggers an autoimmune response. Less antigenic versions are in development.

References

External links

My Literary Malady - New York Times Book Review essay by novelist Geoff Nicholson

Category:Uric acid Category:Arthritis Category:Rheumatology Category:Skin conditions resulting from errors in metabolism Category:Inflammatory polyarthropathies