gout - Signs and symptoms, Diagnosis, Pathogenesis, Stages of gout, Treatment, Diet, Suggestions for pain relief, Additional observations

A disorder arising from a raised concentration of uric acid in the blood, which is deposited in the joints and soft tissues leading to recurrent acute attacks of arthritis, classically affecting the big toe, and accumulations of uric acid in the fingers, ear lobes, and kidneys. The cause is unknown, but affected individuals are typically overweight males.

Gout
Classifications and external resources

Uric acid
ICD-10	M10.
MeSH	D006073

Gout (also called metabolic arthritis) is a disease due to an inborn uric acid metabolism.

Normally, the human bloodstream only carries small amounts of uric acid. However, if the blood has an elevated concentration of uric acid, uric acid crystals are deposited in the cartilage and tissue surrounding joints.

Signs and symptoms

The classic picture is of excruciating and sudden pain, swelling, redness, warmness and stiffness in the joint.

Gout usually attacks the big toe (approximately 75% of first attacks), however it can also affect other joints such as the ankle, heel, instep, knee, wrist, elbow, fingers, and spine. In some cases the condition may appear in the joints of the small toes which have become immobile due to impact injury earlier in life, causing poor blood circulation that leads to gout.

Patients with longstanding hyperuricemia (see below) can have uric acid crystal deposits called tophi (singular: tophus) in other tissues e.g.

Diagnosis

The diagnosis is generally made on a clinical basis, although tests are required to confirm the disease. despite the above, high uric acid level does not necessarily mean a person will develop gout. If gout is suspected, the serum urate should be repeated once the attack has subsided.

A definitive diagnosis of gout is from light microscopy of joint fluid aspirated from the joint (this test may be difficult to perform) to demonstrate intracellular monosodium urate crystals in synovial fluid polymorphonuclear leukocytes.

Pathogenesis

Although the exact cause of gout is not known, it is thought to be linked to defects in purine metabolism. People with primary gout have either an increased production of uric acid or an impaired excretion of uric acid, or a combination of both.

There are also different racial propensities to develop gout. The prevalence of gout is high among the peoples of the Pacific Islands, and the Māori of New Zealand, but rare in the Australian aborigine despite the latter's higher mean concentration of serum uric acid. This explains the increased prevalence of gout among obese individuals.

Many still believe that gout is caused by a combination of dietary factors and "laziness". In particular, many believe that gout develops following several years of excessive alcohol consumption combined with an ongoing lack of physical activity and a diet completely lacking in purine-neutralising foods, such as berries, as well as other specific fruit and vegetables (see below). Others have refined this theory, saying that some are genetically predisposed to gout and some are not. As a result, people who are not predisposed can live over-indulgent lifestyles and not develop gout, while others who are predisposed can develop gout, despite being physically active and having a well-rounded diet. It is known that lead sugar was used to sweeten wine, and that chronic lead poisoning is a cause of gout, which condition is then known as saturnine gout, because of its association with alcohol and excess.

Gout can also develop as co-morbidity of other diseases, including polycythaemia, leukaemia, intake of cytotoxics, obesity, diabetes, hypertension, renal disorders, and hemolytic anemia. This form of gout is often called secondary gout. Diuretics (particularly thiazide diuretics) have traditionally been blamed for precipitating attacks of gout, but a Dutch case-control study from 2006 appears to cast doubt on this.

Stages of gout

Gout has four distinct stages:

asymptomatic, acute, intercritical, chronic.

In the first (asymptomatic) stage, plasma uric acid level increases, but there are no symptoms. The first attack of gout marks the second or acute stage. Most gout patients have their second attack within 6 months to 2 years from their initial episode.

In the last or chronic stage, gout attacks become frequent and become polyarticular (affecting multiple joints at one time). In advanced cases of chronic gout, kidney damage, hypertension and kidney stones can also develop.

Treatment

Attacks

Acutely, first line treatment should be pain relief.

Colchicine was previously the drug of choice in acute attacks of gout. It impairs the motility of granulocytes and can prevent the inflammatory phenomena that initiate an attack of gout. NSAIDs are the preferred form of analgesia for patients with gout. Professional medical care is needed for long term management of gout.

Prevention

Long term treatment (in frequent attacks) is antihyperuricemic therapy.

Dietary change can make a contribution to lowering the plasma urate level if a diet low in purines is maintained, because the body metabolizes purines into uric acid. These might be an especially preferable option to transplant patients, who frequently suffer gout due to increased toxicity and strain on the kidneys due to their immunosuppressant medication.

The mainstay of this approach, however, is the drug allopurinol, a xanthine oxidase inhibitor, which directly reduces the production of uric acid. However, allopurinol treatment should not be initiated during an attack of gout, as it can then worsen the attack. Patients have been known to relapse into acute arthritic gout when they stop taking their allopurinol, as the changing of their serum urate levels alone seems to cause crystal precipitation. As arterial hypertension quite often coexists with gout, treating it with losartan, an AT receptor antagonist, might have an additional beneficial effect on uric acid plasma levels. This way losartan can offset the negative side-effect of thiazides (a group of diuretics used for high blood pressure) on uric acid metabolism in patients with gout. It is suspected that in many cases gout may be secondary to untreated sleep apnea, when oxygen-starved cells break down and release purines as a by-product. Treatment for apnea can be effective in lessening incidence of acute gout attacks. A study in 2004 suggests that animal flesh sources of purine, such as beef and seafood, greatly increase the risk of developing gout. Low fat dairy products such as skim milk significantly reduced the chances of gout. The study followed over 40 thousand men over a period of years, in which 1300 cases of gout were reported. Puricase, a poly(ethylene glycol) ("PEG") conjugate of recombinant porcine uricase (urate oxidase), which breaks down the uric acid deposits is being studied in Phase III clinical trials for the treatment of severe, treatment-refractory gout in the United States in 2006.Pipeline

Surgery

For extreme cases of gout, surgery may be necessary to remove large tophi and correct joint deformity.

Diet

The following suggestions do not meet with universal approval among medical practitioners. This will slightly reduce the acidity and thus might reduce the chance of gout.

Low purine diet:

To lower uric acid: cherries have been shown to reduce uric acid strawberries or blueberries (and other dark red/blue berries) are also reputed to be beneficial celery extracts (celery or celery seed either in capsule form or as a tea) is believed by many to reduce uric acid levels (although these are also diuretics). Others claim that red wine is particularly bad for gout, though again it is difficult to find an explanation. Moderate intake of purine-rich vegetables is not associated with increased gout.

Quercetin – inhibits uric acid production Bromelain – anti-inflammatory Vitamin E Flaxseed oil Avoid high doses of vitamin C and niacin (vitamin B-3) - may increase uric acid

Suggestions for pain relief

You may use an ice pack, applied for 20-30 minutes several times a day.

Additional observations

Due to swelling around affected joint for prolonged periods, shedding of skin may occur.

History

Gout was traditionally viewed as a disease of the decadent and indolent, because the foods which contribute to its development were only available in quantity to the wealthy. This stereotype is especially evident when Gout is referred to as "The Disease of Kings".

Perhaps due to the traditional relationship between wealth and literacy, gout is one of the most commonly-reported maladies in history.

The Roman gladiatorial surgeon Galen described gout as a discharge of the four humors of the body in unbalanced amounts into the joints. The Latin term for a drop, as a drop of discharge, is gutta -- the term gout descends from this word.

Famous people who had gout

One of the most famous sufferers of gout was Henry VIII.

The Roman poet Ennius wrote "numquam poetor nisi podager" — "I never write poetry unless I am suffering from gout."

The surgical treatment of his gout led Mel Brooks to create his famous persona, the 2000 Year Old Man.

According to a 1997 paper in Nature, also Sue, the T-Rex, could have suffered from gout.

Gout in fiction

Benjamin Franklin, who was afflicted with gout, wrote a fictionalized account of a conversation he had with a "Madam Gout," where they listed together all the reasons why he was afflicted, in the literary piece Dialogue Between Franklin and The Gout In an episode of King of the Hill, Bobby Hill develops gout in the big toe as a result of eating chopped liver on a daily basis. In an episode of Lost In Space, Will Robinson encounters Hamish Rhu-Glamis, a Scotsman executed in 1497, but who was suffering gout at the time of his death. Will's mother Maureen attempts to treat the gout when Hamish is made living again by passage through a space warp. In George Eliot's Middlemarch, Tertius Lydgate publishes a book on gout. In an episode of Everybody Hates Chris, Chris's father has gout in the episode "Everybody Hates The Gout." In Archie Comics, the school principal Mr. Weatherbee was a long time sufferer of gout. In an episode (Angel Gabriel Blue) of Keeping Up Appearances, Richard has a fungus infection on his feet, but Hyacinth prefers to tell everyone it's gout because it "afflicts those who over-indulge on finer living". Jiggs ate large amounts of wonderfully rich food, especially corned beef and cabbage, bringing on very painful attacks of gout in the foot. 1750 novel 'Humphry Clinker', suffers from a number of ailments, including gout. In Jane Austen's last novel, Persuasion, Admiral Croft, arrives at Bath with orders "to walk to keep off the gout." In the Epic Fantasy series "A Song of Ice and Fire", Prince Doran Martell suffers from a chronic case of gout. In Charles Dicken's Bleak House, the stereotype of Gout associated with the aristocracy, is reinforced through the character Lord Dedlock, and the male line of ancestors in the Dedlock family, and is repeatedly referred to as the "family gout" In the Adam Sandler song Lunch Lady Land are these lyrics: "I wear this hair net because my red hairs are falling out. / I wear these brown orthopedic shoes because I've got a bad case of gout!".