Gout
INTRODUCTION:
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 which crystallizes and the crystals are deposited in joints, tendons, and surrounding tissues.
History
The word gout was initially used by Randolphus of Bocking, around 1200 AD. It is derived from theLatin word gutta, meaning "a drop" (of liquid).[48] 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".[49]
Gout has, however, been known since antiquity. Historically, it has been referred to as "the king of diseases and the disease of kings"[6][50] or "rich man's disease".[51] The first documentation of the disease is from Egypt in 2,600 BC in a description of arthritis of the big toe. The Greek physicianHippocrates around 400 BC commented on it in his Aphorisms, noting its absence in eunuchs andpremenopausal women.[48][52] 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.[53]
While 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.
INTRODUCTION:
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 which crystallizes and the crystals are deposited in joints, tendons, and surrounding tissues.
Gout has increased in frequency in recent decades affecting approximately one to two percent of the Western population at some point in their lives. The increase is believed to be due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancyand changes in diet. Gout was historically known as "the disease of kings" or "rich man's disease".
Frequently Asked Questions about Gouty Arthritis
What is gouty arthritis?
Gout is a painful form of inflammatory arthritis caused by an accumulation of uric acid crystals in the joints. Crystals form when there are supraphysiologic levels of serum uric acid.
How common is gout?
Gout affects more than 8.3 million people in the United States today; a sharp increase from only 5 million suffers just a few years ago.
What symptoms would my patient suffer?
Gout is characterized by sudden, severe pain in the affected joint. Half of all first-time gout attacks occur in the large joint of the patient’s great toe, but many other joints can be affected as well, particularly the forefoot, ankle, knee and wrist. Tenderness, redness, stiffness and/or swelling of the joint occur.
The first gout attack can seem like an isolated incident, but will recur within a year in at least 20 percent of individuals.
What are the key risk factors for gout?
- Hyperuricemia
- Metabolic syndrome
- Binge drinking, particularly beer
- Family history of gout
- Persons who have received transplants and are on cyclosporin
Signs and symptoms
Gout can present in a number of ways, although the most usual is a recurrent attack of acuteinflammatory arthritis (a red, tender, hot, swollen joint).[2] The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases.[3] Other joints, such as the heels, knees, wrists and fingers, may also be affected.[3] Joint pain usually begins over 2–4 hours and during the night.[3] The reason for onset at night is due to the lower body temperature then.[1]Other symptoms that may occur along with the joint pain include fatigue and a high fever.[1][3]
Long-standing elevated uric acid levels (hyperuricemia) may result in other symptomatology, including hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion.[4] Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.[5]
Cause
Hyperuricemia is the underlying cause of gout. This can occur for a number of reasons, including diet, genetic predisposition, or underexcretion of urate, the salts of uric acid.[2] Renal underexcretion of uric acid is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%.[6] About 10% of people with hyperuricemia develop gout at some point in their lifetimes.[7] The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 μmol/L (7 and 8.9 mg/dL), the risk is 0.5% per year, while in those with a level greater than 535 μmol/L (9 mg/dL), the risk is 4.5% per year.[1]
Lifestyle
Dietary causes account for about 12% of gout,[2] and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood.[4][8] Other triggers include physical trauma and surgery.[6] Recent studies have found dietary factors once believed to be associated are, in fact, not; including the intake of purine-rich vegetables (e.g., beans, peas, lentils, and spinach) and total protein.[9][10]The consumption of coffee, vitamin C and dairy products as well as physical fitness appear to decrease the risk.[11][12][13] This is believed to be partly due to their effect in reducing insulin resistance.[13]
Genetics
The occurrence of gout is partly genetic, contributing to about 60% of variability in uric acid level.[6] Two genes called SLC2A9 and ABCG2have been found to commonly be associated with gout and variations in them can approximately double the risk.[14] A few rare genetic disorders, including familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetasesuperactivity, and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch-Nyhan syndrome, are complicated by gout.[6]
Medical conditions
Gout frequently occurs in combination with other medical problems. Metabolic syndrome, a combination of abdominal obesity, hypertension,insulin resistance and abnormal lipid levels occurs in nearly 75% of cases.[3] Other conditions that are commonly complicated by gout include: polycythemia, lead poisoning, renal failure, hemolytic anemia, psoriasis, and solid organ transplants.[6][15] A body mass indexgreater than or equal to 35 increases a male's risk of gout threefold.[10] Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function.[16] Lesch-Nyhan syndrome is often associated with gouty arthritis.
Medication
Diuretics have been associated with attacks of gout. However, a low dose of hydrochlorothiazide does not seem to increase the risk.[17]Other medicines that have been associated include niacin and aspirin (acetylsalicylic acid).[4] The immunosuppressive drugs ciclosporin andtacrolimus are also associated with gout,[6] the former particularly when used in combination with hydrochlorothiazide.[18]
Pathophysiology
Gout is a disorder of purine metabolism,[6] and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating in joints, on tendons, and in the surrounding tissues.[4] These crystals then trigger a local immune-mediated inflammatoryreaction[4] with one of the key proteins in the inflammatory cascade being interleukin 1β.[6] An evolutionary loss of uricase, which breaks down uric acid, in humans and higher primates is what has made this condition so common.[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.[4][19] Other factors believed to be important in triggering an acute episode of arthritis include cool temperatures, rapid changes in uric acid levels,acidosis,[20][21] articular hydration, and extracellular matrix proteins, such as proteoglycans,collagens, and chondroitin sulfate.[6] The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected.[2] Rapid changes in uric acid may occur due to a number of factors, including trauma, surgery, chemotherapy, diuretics, and stopping or starting allopurinol.[1] Calcium channel blockers and losartan are associated with a lower risk of gout as compared to other medications for hypertension. [22]
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 vitamin C, limiting alcohol and fructose consumption, and avoiding obesity.[2] A low-calorie diet in obese men decreased uric acid levels by 100 µmol/L (1.7 mg/dL).[17] Vitamin C intake of 1,500 mg per day decreases the risk of gout by 45%.[30] Coffee, but not tea, consumption is associated with a lower risk of gout.[31] 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.[32]
Prognosis
Without treatment, an acute attack of gout will usually resolve in 5 to 7 days. However, 60% of people will have a second attack within one year.[1] Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and renal and cardiovascular diseaseand thus at increased risk of death.[6][44] This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.[44]
Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi.[6] These tophi occur in 30% of those who are untreated for five years, often in the helix of the ear, over the olecranon processes, or on the Achilles tendons.[6] With aggressive treatment, they may dissolve. Kidney stones also frequently complicate gout, affecting between 10 and 40% of people, and occur due to low urine pH promoting the precipitation of uric acid.[6] Other forms of chronic renal dysfunction may occur.[6]
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