NSAIDs are the most common treatment for gout. No specific type of NSAID is significantly more or less effective than any other. Improvement may be seen within 4 hours. Treatment is recommended for 1–2 weeks. NSAIDs are not recommended for people with certain other health problems such as bleeding from the stomach, esophagus or intestines, renal failure, or heart failure. While indomethacin has historically been the most commonly used NSAID, ibuprofen may be preferred due to its lack of side effects. A proton pump inhibitor may be given to people at risk of experiencing gastric side effects.
Colchicine is an alternative treatment for people that are unable to tolerate NSAIDs. Its side effects, primarily gastrointestinal upset limit its use. The occurrence of gastrointestinal upset depends on the dose. The risk of experiencing this side effect can be reduced by using smaller, yet still effective doses. Colchicine may interact with other commonly prescribed drugs such as atorvastatin and erythromycin.
Glucocorticoids (otherwise known as steroids) have been found to be as effective as NSAIDs for treating gout. Glucocorticoids may be used if it is not possible to use NSAIDs. Using glucocorticoids also lead to improvement when it is injected into the joint. A joint infection must be excluded if the condition worsens.
Pegloticase (Krystexxa) was approved in the USA to treat gout in 2010. It will be a treatment option for the 3% of people who are intolerant to other medications. Pegloticase is administered as an intravenous infusion every two weeks and has been found to reduce uric acid levels in this population.
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 given until one to two weeks after an acute attack has resolved due to concerns that it may worsen attack symptoms. These medications are often used in combination with either an NSAID or colchicine for the first 3–6 months. This treatment is not recommended until a person has suffered two gout attacks, unless destructive joint changes, tophi, or urate nephropathy exist. This type of treatment is delayed until this point because is not cost effective to offer this treatment sooner. Urate-lowering measures should be increased until serum uric acid levels are below 300–360 µmol/L (5.0-6.0 mg/dL). This treatment should be continued forever. These medications should be continued even if the person experiences a gout attack while on the medication.
Uricosuric drugs are preferred for treating gout if there is not enough uric acid in the urine defined by a 24-hour collection of urine with less than 800 mg of uric acid. Uricosuric drugs are not recommended if the person has a history of renal stones. A 24-hour urine excretion of more than 800 mg indicates overproduction and xanthine oxidase inhibitors are the preferred drugs for providing treatment. Note that probenecid appears to be less effective than allopurinol.
Xanthine oxidase inhibitors (including allopurinol and febuxostat) block uric acid production. Long term therapy is safe and well tolerated, and can be used in people with reduced renal function or urate stones. Allopurinol has caused hypersensitivity in a small number of individuals. In such cases, the alternative drug febuxostat has been recommended.
Without treatment, an acute attack of gout will usually resolve in 5 to 7 days. 60% of people will have a second attack within one year. Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and renal and cardiovascular disease and at increased risk of death. This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be simply due to having gout.
Without treatment, acute gout attacks may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi. These tophi occur in 30% of those who are untreated for five years, often in the outer part of the ear, over the outer part of the elbow, or on the Achilles tendons. With aggressive treatment, they may dissolve. Kidney stones also frequently complicate gout, affecting between 10 and 40% of people. Kidney stones occur due to low urine pH promoting the crystallization of uric acid. Other forms of chronic renal dysfunction may occur.
Gout affects around 1–2% of the Western population at some point in their lives and it 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 to occur 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 average concentration of serum uric acid in the aboriginal group. Gout has become common in China, Polynesia, and urban sub-Saharan Africa. Some studies have found that gout attacks occur more frequently in the spring. This has been attributed to seasonal changes in diet, alcohol consumption, physical activity, and temperature.
The word "gout" was initially used by Randolphus of Bocking, around 1200 a.d. It is derived from the Latin word "gutta", meaning "a drop" (of liquid). According to the Oxford English Dictionary, this is derived from humorism and "the notion of the 'dropping' of a morbid material from the blood in and around the joints".
People have been aware of gout since ancient times. Historically, it has been referred to as "the king of diseases and the disease of kings" or "the disease of rich men". The first documentation of the disease is from Egypt in 2,600 b.c. in a description of arthritis of the largest toe. The Greek physician Hippocrates around 400 b.c. commented on it in his "Aphorisms" and noted its absence in eunuchs (men who have had there testicles removed at a young age) and women before menopause. Aulus Cornelius Celsus (30 a.d.) 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.
In 1683, Thomas Sydenham, an English physician, described its occurrence in the early hours of the morning, and its more frequent occurrence in 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.