Gout Symptoms, Causes & Diet Recommendations Piedmont Eastside Rheumatology May 18, 2022
Gout Symptoms, Causes & Diet Recommendations

Gout is due to persistently elevated levels of uric acid in the blood This occurs from a combination of diet , other health problems , and genetic factors. At high levels, uric acid crystallizes and the crystals deposit in joints, tendons , and surrounding tissues , resulting in an attack of gout.
Gout occurs more commonly in those who regularly drink beer or sugar-sweetened beverages or who eat foods that are high in purines such as liver, shellfish, or anchovies, or are overweight. Diagnosis of gout may be confirmed by the presence of crystals in the joint fluid or in a deposit outside the joint. Blood uric acid levels may be normal during an attack .

Gout symptoms

Gout can present in several ways, although the most common is a recurrent attack of acute inflammatory arthritis (a red, tender, hot, swollen joint). The joint at the base of the big toe is affected most often, accounting for half of cases. Other joints, such as the heels, knees, wrists, and fingers, may also be affected.  Joint pain usually begins during the night and peaks within 24 hours of onset. This is mainly due to lower body temperature. Other symptoms may rarely occur along with the joint pain, including fatigue and a high fever.

Long-standing elevated uric acid levels ( hyperuricemia ) may result in other symptoms, including hard, painless deposits of uric acid crystals known as tophi . Extensive tophi may lead to chronic arthritis due to bone erosion. Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent uric acid pile up .

Cause

The crystallization of uric acid , often related to relatively high levels in the blood, is the underlying cause of gout. This can occur because of diet, genetic predisposition, or underexcretion of urate , the salts of uric acid .

Underexcretion of uric acid by the kidney is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. About 10% of people with hyperuricemia develop gout at some point in their lifetimes .

Long-standing elevated uric acid levels ( hyperuricemia ) may result in other symptoms, including hard, painless deposits of uric acid crystals known as tophi . Extensive tophi may lead to chronic arthritis due to bone erosion. Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent uric acid pile up .

Lifestyle

Dietary causes account for about 12% of gout ,  and include a strong association with the consumption of alcohol, sugar-sweetened beverages, meat, and seafood.  Among foods richest in purines yielding high amounts of uric acid are dried anchovies , shrimp, organ meat , dried mushrooms, seaweed and beer yeast . Chicken and potatoes also appear related. Other triggers include physical trauma and surgery .

Diagnosis

Gout may be diagnosed and treated without further investigations in someone with hyperuricemia and the classic acute arthritis of the base of the great toe (known as podagra). Synovial fluid analysis should be done if the diagnosis is in doubt. Plain X – rays are usually normal and are not useful for confirming a diagnosis of early gout. They may show signs of chronic gout such as bone erosion . A definitive diagnosis of gout is based upon the identification of crystals in synovial fluid or a tophus .

Prevention

Risk of gout attacks can be lowered by complete abstinence from drinking alcoholic beverages , reducing the intake of fructose (e.g. high fructose corn – syrup)  and purine – rich foods of animal origin, such as organ meats and seafood . Eating dairy products ,vitamin c – rich foods, coffee , and cherries may help prevent gout attacks, as does losing weight. 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 medications that reduce serum uric acid levels. Tentative evidence supports the application of ice for 20 to 30 minutes several times a day to decrease pain . Options for acute treatment include non steroidal anti inflammatory drugs (NSAIDs), colchine ,and Glucocorticoids.

While glucocorticoids and NSAIDs work equally well, glucocorticoids may be safer. Options for prevention include allopurinol  , febuxostat , and probenecid. Lowering uric acid levels can cure the disease. Treatment of associated health problems is also important. Lifestyle interventions have been poorly studied. It is unclear whether dietary supplements have an effect in people with gout.

NSAIDs

NSAIDs are the usual first-line treatment for gout. No specific agent is significantly more or less effective than any other . Improvement may be seen within four hours and treatment is recommended for one to two weeks. They are not recommended for those with certain other health problems, such as gastrointestinal bleeding , kidney or heart failure. While indometacin has historically been the most commonly used NSAID, an alternative, such as ibuprofen , may be preferred due to its better side effect profile in the absence of superior effectiveness.  For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given.

Colchicine

Colchine is an alternative for those unable to tolerate NSAIDs .  At high doses, side effects (primarily gastrointestinal upset) limit its usage. At lower doses, which are still effective, it is well tolerated.

Glucocorticoids

Glucocorticoids have been found to be as effective as NSAIDs and may be used if contraindications exist for NSAIDs. They also lead to improvement when injected into the joint .

Prognosis

Without treatment, an acute attack of gout usually resolves in five to seven days; however, 60% of people have a second attack within one year.

Those with gout are at increased risk of hypertension , diabetes mellitus , metabolic syndrome , and kidney and cardiovascular disease and thus are at increased risk of death. It is unclear whether medications that lower urate affect cardiovascular disease risks. This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.

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