Doctors decide a patient has gout if they find crystals in the joint fluid. Treatment with anti-inflammatory drugs, steroids, or colchicine improves symptoms. Once an attack goes away, the patient can change his or her lifestyle to reduce levels of uric acid. People who have gout attacks often may take allopurinol or probenecid to prevent symptoms later.
Gout has become more common. It affects approximately one to two percent of people in the West during their lifetimes. Risk factors have been increasing and may be causing the increase in gout. Metabolic syndrome, longer life expectancy, and changes in diet are the most common risk factors. Gout was historically known as “the disease of kings” or “the disease of rich men".
Gout can present in a number of ways, although the most common is a recurrent attack of intense inflammatory arthritis (a red, tender, hot, swollen joint). Joint pain usually begins over 2–4 hours and during the night. Symptoms occur at night because of the lower body temperature at this time.
High levels of uric acid in the blood over a long period of time (hyperuricemia) may cause other symptoms such as hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion. High levels of uric acid in the blood may also cause crystals to form in the kidneys. This causes stone formation followed by urate nephropathy.
A very high, abnormal level of uric acid in the blood (hyperuricemia) is the basic cause of gout. Diet and a person's genes are two of several possible causes of the high levels. Levels can also become high if the body cannot excrete enough urate, the salts of uric acid.
The kinds and amounts of foods people eat cause about 12% of gout. Drinking alcohol or fructose-sweetened drinks, and eating meat and seafood can cause this disease. Injuries and surgery may also start an attack of gout. Recent studies showed that some beliefs about connections between diet and gout were not true. Eating purine-rich vegetables (e.g., beans, peas, lentils, and spinach) large amounts of protein do not contribute to developing gout. Coffee, vitamin C, and dairy products, as well as physical fitness appear to decrease the risk. These things reduce insulin resistance and may reduce cases of gout.
Inherited factors are about 60% responsible for the variability in uric acid level. Two genes called SLC2A9 and ABCG2 are commonly associated with gout. Variations in these genes can almost double the risk of developing this disease.
Gout often happens with other medical problems. Metabolic syndrome happens along with nearly 75% of all cases of gout. Gout often makes these other problems worse or harder to treat: polycythemia, lead poisoning, renal failure, hemolytic anemia, psoriasis, and solid organ transplants. Males have three times the chance of getting gout when the body mass index is greater than or equal to 35. Frequent lead exposure and lead-contaminated alcohol are risk factors for gout because lead harms the kidney function.
Gout is a disorder of purine metabolism, and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate. The blood deposits the crystals in joints, on tendons, and in the surrounding tissues. These crystals then trigger a localimmune system inflammatory reaction. Uricase is required to breakdown uric acid. An evolutionary loss of uricase in humans and higher primates has made this condition so common.
The triggers that cause uric acid to build up in the blood are not well understood. While it may crystallize at normal levels, it is more likely to do so as uric acid levels increase. 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 matrixproteins, such as proteoglycans, collagens, and chondroitin sulfate. The increased critilization at low temperatures partly explains why the joints in the feet are most commonly affected. Rapid changes in uric acid may occur due to a number of factors, including trauma, surgery, chemotherapy, diuretics, and stopping or starting the medication allopurinol.
Gout may be diagnosed and treated without further investigations in someone with hyperuricemia and the classic podagra. If there is any doubt about the diagnosis, synovial fluid analysis should be done. X-rays are useful for identifying chronic gout only. X-rays are not useful for treating acute gout attacks.
A definitive diagnosis of gout is based upon the identification of monosodium urate (MSU) crystals in joint fluid or a tophus. All synovial fluid samples obtained from undiagnosed, inflamed joints should be examined for these crystals. Under polarized light microscopy, the crystals have a needle-like shape and strong negative birefringence. This test is difficult to perform, and often requires a trained technician. The fluid must also be examined relatively quickly after aspiration, as temperature and pH affect their solubility.
Hyperuricemia is a classic feature of gout. Gout occurs nearly half of the time without hyperuricemia and most people with raised uric acid levels never develop gout. The usefulness of measuring uric acid levels is limited. Hyperuricemia is defined as a plasma urate level greater than 420 "μ"mol/L (7.0 mg/dL) in males and 360 "μ"mol/L (6.0 mg/dL) in females. Other blood tests commonly performed are white blood cell count, electrolytes, renal function, and erythrocyte sedimentation rate(ESR). 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 40.0×10/L (40,000/mm) has been documented in people with gout.
The most important diagnosis to rule out in gout is septic arthritis (an infection in the joint). This should be considered in those with signs of infection or those who do not improve with treatment. A joint fluid Gram stainand culture may be performed to support the diagnosis. Other conditions which present similarly include pseudogout and rheumatoid arthritis. Gouty tophi, especially when not in a joint, can be mistaken for basal cell carcinoma, or other cancers.
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, eating adequate vitamin C, limiting alcohol and fructose consumption, and avoiding obesity. A low-calorie diet in obese men decreased uric acid levels by 100 µmol/L (1.7 mg/dL) on average. Vitamin C intake of 1,500 mg per day decreases the risk of gout by 45%. Coffee, but not tea, consumption is associated with a lower risk of gout. Gout may be secondary to sleep apnea through the release of purines from oxygen-starved cells. Treatment of sleep apnea can lessen the occurrence of gout attacks.
The first goal of treating gout is to reduce the symptoms of an acute attack. Repeated attacks can be prevented by using different drugs that reduce the uric acid levels in the blood. Ice applied for 20 to 30 minutes several times a day decreases pain. Options for immediate treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine and steroids. Options for prevention include allopurinol, febuxostat and probenecid. Lowering uric acid levels can cure the disease. Treatment of comorbidities is also important.