Gout

Gout
Classification and external resources
Gout, a 1799 caricature by James Gillray
10	M10
9	274.00 274.1 274.8 274.9
OMIM	138900 300323
DiseasesDB	29031
MedlinePlus	000422
eMedicine	emerg/221 med/924 med/1112 oph/506 orthoped/124 radio/313
MeSH	D006073

Gout (also known as podagra when it involves the big toe)^[1] is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint. The metatarsal-phalangeal joint at the base of the big toe is the most commonly affected (approximately 50% of cases). However, it may also present as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood. The uric acid crystallizes, and the crystals deposit in joints, tendons, and surrounding tissues.

Clinical diagnosis is confirmed by seeing the characteristic crystals in joint fluid. Treatment with probenecid provide long-term prevention.

Gout has increased in frequency in recent decades, affecting about 1–2% of the life expectancy and changes in diet. Gout was historically known as “the disease of kings” or “rich man’s disease”.

Contents 1 Signs and symptoms 2 Cause 2.1 Lifestyle 2.2 Genetics 2.3 Medical conditions 2.4 Medication 3 Pathophysiology 4 Diagnosis 4.1 Synovial fluid 4.2 Blood tests 4.3 Differential diagnosis 5 Prevention 6 Treatment 6.1 NSAIDs 6.2 Colchicine 6.3 Steroids 6.4 Pegloticase 6.5 Prophylaxis 7 Prognosis 8 Epidemiology 9 History 10 In other animals 11 Research 12 References 13 External links

Signs and symptoms

Gout can present in a number of ways, although the most usual is a recurrent attack of acute [3]

Long-standing elevated [5]

Cause

[1]

Lifestyle

Dietary causes account for about 12% of gout,^[13]

Genetics

The occurrence of gout is partly genetic, contributing to about 60% of [6]

Medical conditions

Gout frequently occurs in combination with other medical problems. Lesch-Nyhan syndrome is often associated with gouty arthritis.

Medication

[19]

Pathophysiology

Gout is a disorder of [6]

The triggers for precipitation of uric acid are not well understood. While it may crystallize at normal levels, it is more likely to do so as levels increase.^[23]

Diagnosis

Gout may be diagnosed and treated without further investigations in someone with hyperuricemia and the classic podagra. Synovial fluid analysis should be done, however, if the diagnosis is in doubt.^[1] X-rays, while useful for identifying chronic gout, have little utility in acute attacks.^[6]

Synovial fluid

A definitive diagnosis of gout is based upon the identification of [6]

Blood tests

[1]

Differential diagnosis

The most important [30]

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 [33]

Treatment

The initial aim of treatment is to settle the symptoms of an acute attack.^[6]

NSAIDs

NSAIDs are the usual first-line treatment for gout, and no specific agent is significantly more or less effective than any other.^[37]

Colchicine

[38]

Steroids

[2]

Pegloticase

[41]

Prophylaxis

A number of medications are useful for preventing further episodes of gout, including [2]

[43]

Xanthine oxidase inhibitors (including allopurinol and [44]

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.^[45]

Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi.^[6]

• Nodules of the finger and helix of the ear representing gouty tophi

• Tophus of the knee

• Tophus of the toe, and over the external malleolus

• Gout complicated by ruptured tophi (exudate tested positive for uric acid crystals)

Epidemiology

Gout affects around 1–2% of the Western population at some point in their lifetimes, and is becoming more common.^[36]

In the United States, gout is twice as likely in African American males as it is in European Americans.^[48]

History

The word “gout” was initially used by Randolphus of Bocking, around 1200 AD. It is derived from the [50]

Gout has, however, been known since antiquity. Historically, it has been referred to as “the king of diseases and the disease of kings”^{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.^[54]

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.^[55]

The Dutch scientist [56]

In other animals

Gout is rare in most other animals due to their ability to produce [58]

Research

A number of new medications are under study for treating gout, including [1]

References

External links

Wikimedia Commons has media related to: Gout

• Gout at the Open Directory Project

v t e Antigout preparations (M04) Uricosurics primary: Probenecid Sulfinpyrazone Benzbromarone Isobromindione secondary: Amlodipine Atorvastatin Fenofibrate Guaifenesin Losartan Xanthine oxidase inhibitors Allopurinol# Oxypurinol Tisopurine other: Febuxostat Phytic acid Myo-inositol) Mitotic inhibitors Colchicine Other Cinchophen aspirin Sevelamer Rasburicase Pegloticase) #WHO-EM ‡Withdrawn from market Clinical trials: †Phase III §Never to phase III JNT phys noco(injr M4)

v t e 711–719) Arthritis (monoarthritis / polyarthritis) Inflammation (Neutrophilia) Infectious Septic arthritis Tuberculosis arthritis Reactive arthritis (indirectly) Noninfectious Seronegative spondyloarthropathy: Reactive arthritis Psoriatic arthritis Ankylosing spondylitis Juvenile idiopathic arthritis Adult-onset Still’s disease Felty’s syndrome Crystal arthropathy: Gout Chondrocalcinosis Noninflammatory Heberden’s node Bouchard’s nodes Other hemorrhage Hemarthrosis pain Arthralgia Osteophyte villonodular synovitis Pigmented villonodular synovitis Joint stiffness JNT phys noco(injr M4)

v t e 277.2) Purine metabolism Anabolism Adenylosuccinate lyase deficiency Adenosine Monophosphate Deaminase Deficiency type 1 Nucleotide salvage Hyperuricemia Adenine phosphoribosyltransferase deficiency Catabolism Adenosine deaminase deficiency Purine nucleoside phosphorylase deficiency Xanthinuria Gout Mitochondrial neurogastrointestinal encephalopathy syndrome Pyrimidine metabolism Anabolism Orotic aciduria Miller syndrome Catabolism Dihydropyrimidine dehydrogenase deficiency MET m epon m(m)

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