Kidney Stones Kidney Stones Kidney stones, also known as "renal calculi" are highly relevant to gout sufferers because of uric acid build up leads to uric acid crystallisation within the joints.In fact, before their first attack of gouty arthritis around ten percent of gout sufferers have had an episode of renal colic due to the formation of a small stone(calculus)within the kidney or the urinary tract. These calculi, which may vary in size from a millimetre to several centimetres, commonly cause intense pain(renal colic)which passes around the loin to the groin on the same side;this may be accompanied by the passage of blood in the urine(haematuria).

Often the stones are small enough to be passed out of the body in the urine without any problem,but occasionally they may be large enough to cause obstruction to urine flow.The other type of stone common in patients with gout is a calcium scale stone.This is usually associated with a very high urinary acid excretion,but the urine need not be unusually acid.Often this high urinary uric acid seems to be caused by a diet high in purines..The reasons why a high urinary uric acid should promote the formation of another type of calculus are complex and involve solubilising factors in the urine which would normally maintain the calcium oxalate in solution. The first thing that a gout sufferer can do to reduce the risk of kidney stones is to maintain a dilute urine, ie, always drink sufficient fluid to have a urine column exceeding 1500 ml/day.Few other techniques have as great an effect upon the uric acid concentration in the urine as the volume passed or the urine flow rate. One home remedy for the supposed elimination of stones is the following.Two ounces of olive oil as well as two ounces of lemon juice which is consumed straight away.Followed by a large glass of water.

This method should be researched thoroughly and we are not advocating it as a definite cure. Uric acid crystal deposition in joint | definition of Uric acid crystal deposition in joint by Medical dictionary Uric acid crystal deposition in joint | definition of Uric acid crystal deposition in joint by Medical dictionary Definition Gout is a form of acute arthritis that causes severe pain and swelling in the joints. It most commonly affects the big toe, but may also affect the heel, ankle, hand, wrist, or elbow. It affects the spine often enough to be a factor in back pain. Gout usually comes on suddenly, goes away after 5-10 days, and can keep recurring. Gout is different from other forms of arthritis because it occurs when there are high levels of uric acid circulating in the blood, which can cause urate crystals to settle in the tissues of the joints. Description Uric acid, which is found naturally in the blood stream, is formed as the body breaks down waste products, mainly those containing purine, a substance that is produced by the body and is also found in high concentrations in some foods, including brains, liver, sardines, anchovies, and dried peas and beans.

Normally, the kidneys filter uric acid out of the blood and excrete it in the urine. Sometimes, however, the body produces too much uric acid or the kidneys aren't efficient enough at filtering it from the blood, and it builds up in the blood stream, a condition known as hyperuricemia. A person's susceptibility to gout may increase because of the inheritance of certain genes or from being overweight and eating a rich diet. In some cases, another disease (such as lymphoma, leukemia, or hemolytic anemia ) may be the underlying cause of the uric acid buildup that results in gout. An additional factor is occupational or environmental; it is now known that chronic exposure to high levels of lead decreases the body's excretion of urates, allowing uric acid to accumulate in the blood. Hyperuricemia doesn't always cause gout. Over the course of years, however, sharp urate crystals build up in the synovial fluid of the joints. Often, some precipitating event, such as an infection, surgery, the stress of hospitalization, a stubbed toe, or even a heavy drinking binge can cause inflammation.

White blood cells, mistaking the urate crystals for a foreign invader, flood into the joint and surround the crystals, causing inflammation—in other words, the redness, swelling, and pain that are the hallmarks of a gout attack. Causes and symptoms As a result of high levels of uric acid in the blood, needle-like urate crystals gradually accumulate in the joints. Urate crystals may be present in the joint for a long time without causing symptoms. Infection, injury to the joint, surgery, drinking too much, or eating the wrong kinds of foods may suddenly bring on the symptoms, which include pain, tenderness, redness, warmth, and swelling of the joint. In many cases, the gout attack begins in the middle of the night. The pain is often so excruciating that the sufferer cannot bear weight on the joint or tolerate the pressure of bedcovers. The inflamed skin over the joint may be red, shiny, and dry, and the inflammation may be accompanied by a mild fever . These symptoms may go away in about a week and disappear for months or years at a time. However, over the course of time, attacks of gout recur more and more frequently, last longer, and affect more joints.

Eventually, stone-like deposits known as tophi may build up in the joints, ligaments, and tendons, leading to permanent joint deformity and decreased motion. (In addition to causing the tophi associated with gout, hyperuricemia can also cause kidney stones , also called renal calculi or uroliths.) Gout affects an estimated one million Americans; according to the National Institutes of Health, it accounts for about 5% of all cases of arthritis. It occurs more often in men than in women; the sex ratio is about 4:1. Uric-acid levels tend to increase in men at puberty , and, because it takes 20 years of hyperuricemia to cause gout symptoms, men commonly develop gout in their late 30s or early 40s. Women more typically develop gout later in life, starting in their 60s. According to some medical experts, estrogen protects against hyperuricemia, and when estrogen levels fall during menopause , urate crystals can begin to build up in the joints.

Excess body weight, regular excessive alcohol intake, the use of blood pressure medications called diuretics , and high levels of certain fatty substances in the blood (serum triglycerides) associated with an increased risk of heart disease can all increase a person's risk of developing gout. Gout appears to be on the increase in the American population. According to a study published in November 2002, there was a twofold increase in the incidence of gout over the 20 years between 1977 and 1997. It is not yet known whether this increase is the result of improved diagnosis or whether it is associated with risk factors that have not yet been identified. Diagnosis Usually, physicians can diagnose gout based on the physical examination and medical history (the patient's description of symptoms and other information). Doctors can also administer a test that measures the level of uric acid in the blood. While normal uric acid levels don't necessarily rule out gout and high levels don't confirm it, the presence of hyperuricemia increases the likelihood of gout. The development of a tophus can confirm the diagnosis of gout.

The most definitive way to diagnose gout is Gout, a form of acute arthritis, most commonly occurs in the big toe. It is caused by high levels of uric acid in the blood, in which urate crystals settle in the tissues of the joints and produce severe pain and swelling. (Illustration by Electronic Illustrators Group.) to take a sample of fluid from the joint and test it for urate crystals. Treatment The goals of treatment for gout consist of alleviating pain, avoiding severe attacks in the future, and preventing long-term joint damage. In addition to taking pain medications as prescribed by their doctors, people having gout attacks are encouraged to rest and to increase the amount of fluids that they drink. Acute attacks of gout can be treated with nonaspirin, nonsteroidal anti-inflammatory drugs (NSAIDs) such as naproxen sodium (Aleve), ibuprofen (Advil), or indomethacin (Indocin). In some cases, these drugs can aggravate a peptic ulcer or existing kidney disease and cannot be used. Doctors sometimes also use colchicine (Colbenemid), especially in cases where nonsteroidal anti-inflammatory drugs cannot be used.

Colchicine may cause diarrhea , which tends to go away once the patient stops taking it. Corticosteroids such as prednisone (Deltasone) and adrenocorticotropic hormone (Acthar) may be given orally or may be injected directly into the joint for a more concentrated effect. While all of these drugs have the potential to cause side effects, they are used for only about 48 hours and are not likely to cause major problems. However, aspirin and closely related drugs (salicylates) should be avoided because they can ultimately worsen gout. Once an acute attack has been successfully treated, doctors try to prevent future attacks of gout and long-term joint damage by lowering uric acid levels in the blood. There are two types of drugs for correcting hyperuricemia. Such uricosuric drugs as probenecid (Benemid) and sulfinpyrazone (Anturane) lower the levels of urate in the blood by increasing its removal from the body (excretion) through the urine. These drugs may promote the formation of kidney stones, however, and they may not work for all patients, especially those with kidney disease.

Allopurinol (Zyloprim), a type of drug called a xanthine-oxidase inhibitor, blocks the production of urate in the body, and can dissolve kidney stones as well as treating gout. The potential side effects of allopurinol include rash, a skin condition known as dermatitis , and liver dysfunction. In 2004, the FDA was seeking trial data on a new drug called oxypurinol (Oxyprim) for treating chronic gout. These medications may have to be taken for life to prevent further gout attacks. New quality of care indicators were released in 2004 to improve care for patients with gout. The aim of the guidelines was to prevent repeat gout attacks and to reduce medication errors associated with intravenous colchicine in hospitals. Alternative treatment Alternative approaches to gout focus on correcting hyperuricemia by encouraging weigt loss and limiting the intake of alcohol and purine-rich foods. In addition, consuming garlic (Allium sativum) has been recommended to help prevent gout. Increasing fluid intake, especially by drinking water, is also recommended.

During an acute attack, contrast hydrotherapy (alternating three-minute hot compresses with 30-second cold compresses) can help dissolve the crystals and resolve the pain faster. Prognosis Gout cannot be cured but usually it can be managed successfully. As tophi dissolve, joint mobility generally improves. (In some cases, however, medicines alone do not dissolve the tophi and they must be removed surgically.) Lowering uric acid in the blood also helps to prevent or improve the kidney problems that may accompany gout. Prevention For centuries, gout has been known as a "rich man's disease" or a disease caused by overindulgence in food and drink. While this view is perhaps a little overstated and oversimplified, lifestyle factors clearly influence a person's risk of developing gout. Since obesity and excessive alcohol intake are associated with hyperuricemia and gout, losing weight and limiting alcohol intake can help ward off gout. Dehydration may also promote the formation of urate crystals, so people taking diuretics or "water pills" may be better off switching to another type of blood pressure medication. Everyone should be sure to drink at least six to eight glasses of water each day.

Since purine is broken down in the body into urate, it may also be helpful to avoid foods high in purine, such as organ meats, sardines, anchovies, red meat, gravies, beans, beer, and wine. A 2004 study revealed that eating more low-fat dairy products could reduce risk of developing gout. Key terms Allopurinol — A drug that corrects hyperuricemia by inhibiting urate production. Colchicine — A drug used to treat painful flare-ups of gout. Corticosteroids — Medications related to a natural body hormone called hydrocortisone, which are used to treat inflammation. Hyperuricemia — High levels of a waste product called uric acid in the blood. Probenecid — A drug that corrects hyperuricemia by increasing the urinary excretion of urate. Purine — A substance found in foods that is broken down into urate and may contribute to hyperuricemia and gout. Sulfinpyrazone — A drug that corrects hyperuricemia by increasing the urinary excretion of urate.

Synovial fluid — Fluid surrounding the joints which acts as a lubricant, reducing the friction between the joints. Tophus (plural, tophi) — A chalky deposit of a uric acid compound found in gout. Tophi occur most frequently around joints and in the external ear. Urate crystals — Crystals formed by high levels of uric acid in the blood. Resources Books Parker, James N., M.D., and Philip M. Parker, Ph. D. The 2002 Official Patient's Sourcebook on Gout. San Diego, CA: ICON Health Publications, 2002. Periodicals Arromdee, E., C. J. Michet, C. S. Crowson, et al. "Epidemiology of Gout: Is the Incidence Rising?" Journal of Rheumatology 29 (November 2002): 2403-2406. Coghill, Kim. "FDA Panel Discusses Endpoints for Approval of Gout Products." Bioworld Today (June 3, 2004).

"Dairy-rich Diet May Help Prevent Gout." Tufts University Health & Nutrition Letter (June 2004): 2. Hsu, C. Y., T. T. Shih, K. M. Huang, et al. "Tophaceous Gout of the Spine: MR Imaging Features." Clinical Radiology 57 (October 2002): 919-925. Lin, J. L., D. T. Tan, H. H. Ho, and C. C. Yu. "Environmental Lead Exposure and Urate Excretion in the General Population." American Journal of Medicine 113 (November 2002): 563-568. MacReady, Norma. "New Gout Quality-of-care Standards Take Aim at Medication-related Errors." Internal Medicine News (June 1, 2004): 18. Perez-Ruiz, F., M. Calabozo, G. G. Erauskin, et al.

"Renal Underexcretion of Uric Acid is Present in Patients with Apparent High Urinary Uric Acid Output." Arthritis and Rheumatism 47 (December 15, 2002): 610-613. Raj, J. M., S. Sudhakar, K. Sems, and R. W. Carlson. "Arthritis in the Intensive Care Unit." Critical Care Clinics 18 (October 2002): 767-780. Shekarriz, B., and M. L. Stoller. "Uric Acid Nephrolithiasis: Current Concepts and Controversies." Journal of Urology 168, no. 4, Part 1 (October 2002): 1307-1314. Organizations Arthritis Foundation.1300 W. Peachtree St., Atlanta, GA 30309. (800) 283-7800. National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS).

National Institutes of Health (NIH), 1 AMS Circle, Bethesda, MD 20892-3675. 〈〉. Other National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). Questions and Answers About Gout. Bethesda, MD: NIAMS, 2002. NIH Publication No. 02-5027. 〈〉. gout [gowt] a form of arthritis in which uric acid appears in excessive quantities in the blood and may be deposited in the joints and other tissues. During an acute attack there is swelling, inflammation, and extreme pain in a joint, frequently that of the big toe. After several years of attacks, the chronic form of the disease may set in, permanently damaging and deforming joints and destroying cells of the kidney. Most cases occur in men and the first attack rarely occurs before the age of 30. Causes. The causes of gout include excessive production of uric acid, as an inherited condition or as a side effect of chemotherapy for tumors, and impairment of clearance due to the antihypertensive agent hydrochlorothiazide or to low-dose aspirin . Acute Gout.

This form usually strikes without warning. The affected joint, which in 70 per cent of cases is that of the big toe, becomes swollen, inflamed, and very painful. The first attack may follow an operation, infection, or minor irritation such as tight shoes, or it may have no apparent cause. The patient may have a headache or fever, and often cannot walk because of the pain. Without treatment, acute attacks of gout usually last a few days or weeks. The symptoms then disappear completely until the next attack. As the disease progresses, the attacks tend to last longer and the intervals between attacks become shorter. A definite diagnosis of gout is made by identifying needle-shaped sodium urate crystals in the synovial fluid aspirated from an affected joint. The crystals may be seen inside polymorphonuclear leukocytes. Acute gouty arthritis is an example of an acute inflammatory process. Serial serum uric acid levels are also monitored; levels consistently above 8 mg/100 ml are an abnormal finding. Treatment. An acute attack of gout can be treated successfully with any of several medicines.

colchicine has long been used; in most cases it relieves the pain and swelling in 72 hours or less, although it does not affect the high concentration of uric acid. indomethacin is a nonsteroidal antiinflammatory drug that is particularly effective against acute gout and has become the treatment of choice. Aspirin should be avoided during acute attacks. The dietary management of gout is a subject of disagreement among researchers. Chronic Gout. After a number of acute attacks of gout, the patient who goes without medical treatment may develop symptoms of chronic gout. This seldom occurs less than 10 years after the first acute attack. Joints affected by chronic gout degenerate in the same way as those affected by rheumatoid arthritis and may eventually lose their ability to move. Treatment. Chronic gout is treated with probenecid , allopurinol , or other medicines that promote urinary excretion of uric acid. Other treatment may also be necessary if the kidney is involved. With appropriate treatment, gout should be well controlled. Management Between Attacks. If acute gout is recognized at an early stage and treated correctly, the development of the chronic form can generally be prevented.

Weight should be kept within normal limits, and increasing daily intake of liquids is beneficial because it encourages urine production. Gouty arthritis. Deposits of uric acid crystals in the connective tissue have a chemotactic effect and cause exudation of leukocytes into the joint. The inflammation most often affects the metatarsophalangeal joint of the big toe. From Damjanov, 2000. gout (gowt), [MIM*138900] A disorder of purine metabolism, occurring especially in men, characterized by a raised but variable blood uric acid level and severe recurrent acute arthritis of sudden onset resulting from deposition of crystals of sodium urate in connective tissues and articular cartilage; most cases are inherited, resulting from a variety of abnormalities of purine metabolism. The familial aggregation is for the most part galtonian with a threshold of expression determined by the solubility of uric acid. However, gout is also a feature of the Lesch-Nyhan syndrome , an X-linked disorder [MIM*308000]. [L.

gutta, drop] gout (gout) a group of disorders of purine and pyrimidine metabolism, characterized by typhi causing recurrent paroxysmal attacks of acute inflammatory arthritis usually affecting a single peripheral joint, usually responsive to colchicine, and usually followed by complete remission; hyperuricemia and uric acid urolithiasis are also present in fully developed cases.gout´y latent gout , masked gout lithemia without the typical features of gout. gout (gout) n. 1. A disturbance of uric-acid metabolism occurring chiefly in males, characterized by painful inflammation of the joints, especially of the feet and hands, and arthritic attacks resulting from elevated levels of uric acid in the blood and the deposition of urate crystals around the joints. The condition can become chronic and result in deformity. 2. A large blob or clot: "and makes it bleed great gouts of blood" (Oscar Wilde). gout′i·ness n. gout Etymology: L, gutta, drop a disease associated with an inborn error of uric acid metabolism that increases production or interferes with excretion of uric acid.

Excess uric acid is converted to sodium urate crystals that precipitate from the blood and become deposited in joints and other tissues. Men are more often affected than premenopausal women. The great toe is a common site for the accumulation of urate crystals. The condition can cause exceedingly painful swelling of a joint, accompanied by chills and fever. The symptoms are recurrent. Episodes become longer each year. The disorder is disabling and, if untreated, can progress to the development of destructive joint changes, such as tophi. Treatment usually includes administration of colchicine, phenylbutazone, indomethacin, or glucocorticoid drugs and a diet that excludes purine-rich foods such as organ meats. It may include surgical removal of ulcerated tophi. Chronically, probenecid, allopurinol, or colchicine may be used to decrease uric acid levels. Acquired gout is a condition having the signs and symptoms of gout but resulting from another disorder or treatment for a different condition. Diuretic drugs can alter the concentration of uric acid so that uric acid salts precipitate from the blood and are carried to the joints.

See also chondrocalcinosis, Lesch-Nyhan syndrome, tophus . Gout gout A metabolic disorder characterised by increased uric acid in the blood and joints, resulting in recurring painful arthritis and renal dysfunction with deposits of uric acid in the urinary tract, which in some cases is caused by either of two X-linked enzymes. Clinical findings One-half of cases present with the classic “podagra” which affects the metatarsophalangeal joint; up to 90% suffer podagra at some time during their disease. With time, the attacks become polyarticular. Gouty tophi accumulate on the ears and over joints. Patients with gout are at high risk of forming kidney stones, which, in extreme cases, can cause renal failure. Risk factors Alcoholism, hereditary defect of hypoxanthine-guanine phosphoribosyl transferase (HG-PRT), phosphoribosylpyrophosphate synthetase superactivity, obesity, hypertension, renal dysfunction, drugs; family history of gout is present in about half of cases.

Lab Increased uric acid, often ≥ 410 µmol/L–US: 7.0 mg/ml, a level found in a significant minority of men (90% of gout occurs in men). Diagnosis Crystals in joints, body fluids, tissues. Acute treatment Diet, allopurinol, sulfinpyrazone, salicylates.

gout Orthopedics A condition characterized by ↑ uric acid in the blood and joints, resulting in recurring painful arthritis, renal function and deposits of uric acid in the urinary tract, linked to 2 X-linked enzymes Risk factors Hereditary defects of HG-PRT–hypoxanthine-guanine phosphoribosyl transferase, obesity, weight gain, alcohol intake, HTN, renal dysfunction, drugs Lab ↑ uric acid, often ≥ 410 µmol/L–US: 7.0 mg/ml, a level found in a significant minority of ♂–90% of gout occurs in ♂ Diagnosis Crystals in joints, body fluids, tissues; family Hx of gout is present in ±1⁄2 of cases;1⁄2 present with the classic 'podagra'–1st metatarsophalangeal joint; up to 90% suffer podagra at some time during their disease Acute treatment Colchicine, NSAIDs, corticosteroids Interval Diet Chronic Allopurinol, sulfinpyrazone, salicylates. See Congenital gout , PseudoGout , Saturnine gout .

gout (gowt) A disorder of purine metabolism, occurring especially in men, characterized by a raised but variable blood uric acid level and severe recurrent acute arthritis of sudden onset resulting from deposition of crystals of sodium urate in connective tissues and articular cartilage; usually inherited, resulting from a variety of abnormalities of purine metabolism. [L. gutta, drop] (gowt) [Fr. goute, fr L. gutta, a drop] GOUT: Uric acid crystals and white blood cells in synovial fluid (orig. mag. ×500) GOUT A form of arthritis marked by the deposition of monosodium urate crystals in joints and other tissues. Any joint may be affected, but gout usually begins in the knee or the first metatarsophalangeal joint of the foot. Synonym: monosodium urate deposition disease tophus ; Symptoms Most hyperuricemic people are asymptomatic between acute attacks. When an attack of acute gouty arthritis develops, it usually begins at night with moderate pain that increases in intensity to the point where no body position provides relief.

Low-grade fever and joint inflammation (hot, exquisitely tender, dusky-red or cyanotic joints) may be present. See: illustration Treatment Colchicine, nonsteroidal anti-inflammatory agents, or corticosteroids are used to treat acute gouty attacks. Long-term therapy aims at preventing hyperuricemia by giving uricosuric drugs such as probenecid, or xanthine oxidase inhibitors such as allopurinol. Patients with gout have a tendency to form uric acid kidney stones. The diet should be well balanced and devoid of purine-rich foods, e.g., anchovies, sardines, liver, kidneys, sweetbreads, lentils, beer, wine, and other alcoholic beverages, because these raise urate levels. Fluid intake should be encouraged. Patient care During the acute phase, bedrest is prescribed for at least the first 24 hr, and affected joints are elevated, immobilized, and protected by a bed cradle. Analgesics are administered, and hot or cold packs applied, depending on which the patient finds most helpful. The patient is taught about these measures.

Colchicine, nonsteroidal anti-inflammatory agents, prednisone, or other prescribed drugs are administered. Allopurinol may be prescribed as maintenance therapy after acute attacks to suppress uric acid formation and control uric acid levels, thus preventing future attacks. Patients should be warned to report adverse effects of allopurinol, e.g., drowsiness, dizziness, nausea, vomiting, urinary frequency, dermatitis. A low-purine diet is recommended. The importance of gradual weight reduction is explained if obesity, which places additional stress on painful joints, is a factor. If soft-tissue tophi are present, e.g., near joints in fingers, knees, or feet, the patient should wear soft clothing to cover these areas and should use meticulous skin care and sterile dressings to prevent infection of open lesions. Surgery may be required to excise or drain infected or ulcerated tophi, to correct joint deformities, or to improve joint function. Even minor surgery may precipitate gouty attacks (usually within 24 to 96 hr after surgery); therefore, the patient should be instructed about this risk and medications administered as prescribed to prevent acute attacks.

The goal of chronic management of gout is to maintain serum uric acid levels below 6 mg/dl. At these levels chronic complications of gout are limited. abarticular gout Gout that involves structures near the joints. Synonym: abarticular gout Lead gout. tophaceous gout Gout marked by the development of tophi (deposits of sodium urate) in the joints and in the external ear. gout An acute inflammatory joint disorder ( ARTHRITIS ) caused by deposition of monosodium urate monohydrate crystals around joints, tendons and other tissues, especially the near joint of the big toe. This occurs when there is excess uric acid in the body, probably as a result of a genetic abnormality. There is excruciating pain and inflammation. Treatment is by non-steroidal anti-inflammatory drugs ( NSAIDS ), such as indomethacin (indometacin) or naproxen, used early and throughout the attack. Colchicine is also effective. Gout can be prevented by the use of allopurinol which lowers the levels of uric acid in the blood. See also GOUTY TOPHI .

gout ; podagra metabolic disorder, caused by inability to metabolize purines or as a side-effect of drugs (e.g. diuretics) and strongly associated with inflammatory arthropathy of peripheral joints; characterized by raised serum urate levels, birefringent urate crystals in the synovial fluid of affected joints, and ultimately gouty tophus formation; radiographs show marked 'punched-out' marginal erosions within affected joints, with later chronic and marked degenerative arthritis; acute monoarticular gout is treated with high-dose non-steroidal anti-inflammatory drugs (not aspirin), colchicine ± intra-articular injection of corticosteroid; patients with hyperuricaemia and tophus formation require allopurinol or a uricosuric agent gout (gaut), n a type of arthritis, which affects primarily males, that is triggered by increased uric acid in serum and joints. The uric acid forms crystals. A common symptom is intense pain and swelling of the metatarsophalangeal joint of the big toe. Also called rich man's disease.

gout (gowt) [MIM*138900] A disorder of purine metabolism, occurring especially in men, characterized by a raised but variable blood uric acid level and severe recurrent acute arthritis of sudden onset resulting from deposition of crystals of sodium urate in connective tissues and articular cartilage. [L. gutta, drop] gout, n a disease associated with an inborn error of uric acid metabolism that increases production or interferes with the excretion of uric acid. Excess uric acid is converted to sodium urate crystals that precipitate from the blood and become deposited in joints and other tissues. The great toe is a common site for the accumulation of urate crystals. It can be exceedingly painful, with swelling of a joint and may be accompanied by chills and fever. gout a disorder of uric acid metabolism in which there is hyperuricemia and deposition of urates in and around the joints. Occurs in humans and anthropoid apes. Most animals possess the enzyme uricase that converts uric acid to allantoin. Dalmatian dogs excrete large amounts of uric acid in their urine, but the breed is not affected by gout.

A disease called gout occurs in commercial chickens due to feeding of excessive amounts of protein. articular gout caused by gross excesses of protein in the diet. A chronic disease manifested by swelling of the joints which contain a thick white fluid consisting largely of uric acid crystals. visceral gout birds become weak and listless and die. The viscera are covered with a frosting of urea crystals. There is a primary renal disease and a fatal uremia. The high-protein diet exacerbates that original disease. Patient discussion about gout Q. Is gout hereditary? My Mother has gout for a few years now. Is it hereditary? Does this mean I too will get it in the future? A. most likely, yes! If other members of your family have had gout, you’re more likely to develop it also, yet, just because someone in the family suffers from gout does not mean everyone in that family will have the disease. This risk varies from person to person. for further reading , you can visit my blog : Q. How is gout treated? After a lot of tests, my Doctor concluded that I have gout. What treatment should I expect? Is gout curable? A.

There are basically three types of treatment for gout arthritis : corticosteroids, anti-inflammatory drugs (NSAID- ibuprofen, diclofenac, naproxen), and medication that lowers uric acid levels, such as allopurinol (Zylopric) or probenecid, also may be prescribed to help prevent a gout attack. Colchicine is used to treat acute gout attack and usually begins working within few hours of taking it. Low doses of colchicine are also used to prevent attacks. These drugs are recommended for people who have had multiple attacks of gout, kidney stones due to uric acid, or tophi. The goal of lowering the blood uric acid is to slowly dissolve deposits of uric acid in the joint. Q. what is the connection between gout and drinking cokes? There was an article in your magazine earlier this year about how drinking cokes could affect gout....can I get a copy of that artical? A. Men who consume two or more sugary soft drinks a day have an 85% higher risk of gout compared with those who drink less than one a month.

This is because soft drinks contain large quantities of high-fructose corn syrup (HFCS), a common sweetener in soft drinks, which results in Hyperuricemia in blood. Hyperuricemia, in turn predispose the body for gout. (taken from : ) How to Remove Uric Acid Crystalization in Joints (Gout and Joint pain) How to Remove Uric Acid Crystalization in Joints (Gout and Joint pain) POSTED ON September 14, 2014 BY Drew Canole Are you aware that cucumber juice helps bring down body temperature, is highly alkalizing and effective for removing uric acid crystalization in joints, like with gout. There may be a slight pain when drinking this juice – a sign of healing – it is the stirring of the old toxins to be eliminated. The celery and ginger will help reduce inflammation during the cleansing. Perfect combo! Juice the following: How to Remove Uric Acid Crystalization in Joints (Gout and Joint pain) Prepare the ingredients. Clean them thoroughly first. You can use a vegetable wash. Cut the cucumber into smaller pieces based on the capacity of your juicer. Also prepare the celery ribs making sure that there is no accumulation of dirt.

Cut the lemon into half. You can put the other one in the fridge. Then carve out the ginger root. 3.2.2807 How long? Drink until you see the results you want (once a day or twice a day to speed up the process) Source: Natural Cures Not Medicine Make use of this information to hype up your very own detoxification! Start now! The detoxification process can also take in the form of a juice fast. Here at FitLife.TV, we recommend people to try the Alpha Reset (AR) . The Alpha Reset is a 5 Day Juice Fast. It is part of the Juice with Drew System . This is the first step in your detoxification process. If you are just starting out with juicing, do not jump right into a juice fast right away. Just try 1 juice per day along with the rest of your nutrition and see how your body responds. If your body responds well to juicing, then ramp up the number of juices per day. These healthy, nutrient-dense juices can replace that coffee you reach for in the morning or that soda in the afternoon. Here are some of our followers that have tried the Alpha Reset!

If you’re ready to take the first step, begin your transformation by clicking the transformations below! Disclaimer: The techniques, strategies, and suggestions expressed here are intended to be used for educational purposes only. The author, Drew Canole, and the associated are not rendering medical advice, nor to diagnose, prescribe, or treat any disease, condition, illness, or injury. It is imperative that before beginning any nutrition or exercise program you receive full medical clearance from a licensed physician. Drew Canole and Fitlife.tv claim no responsibility to any person or entity for any liability, loss, or damage caused or alleged to be caused directly or indirectly as a result of the use, application, or interpretation of the material presented here. Thy Gout be Gone: The Healing Power of Cherries | NZ Health Article Thy Gout be Gone: The Healing Power of Cherries By HealthPost on June 26, 2014 Throughout history gout seemed to be an affliction that affected the wealthy more than their poorer counterparts, as such it came to be known as “the disease of kings” or more poignantly “rich man’s disease”.

But in the last hundred years, with ever increasing life spans and changing diets, gout has moved away from this stereotype and now afflicts a much broader spectrum of the human population. Gout is a very painful form of inflammatory arthritis caused by the crystallisation of uric acid within joints. In just over 50% of all cases of gout, the main joint at the bottom of the big toe is the part of the body that gets afflicted with this acute type of inflammation. But gout can happen in other joints, most commonly the hands, elbows and knees. The crystallised uric acid gets deposited in the surrounding tissues, tendons and joints of the afflicted area. When treating gout, the main aim is to curb inflammation and lower the concentration of uric acid within the tissues affected. Enter the Healing Property of Cherries Tart cherries are full of powerful antioxidants known as anthocyanins, which are coloured compounds that lend cherries their red colour. These anthocyanins have been shown to effectively block pathways involving several key pro-inflammatory compounds in the blood. Cherries have traditionally been used to promote normal levels of uric acid and alleviate the pain associated with gout.

Anecdotal evidence regarding cherries and gout has been around for some time. In the 1950s a physician by the name of Ludwig Blau made the unexpected discovery that cherries could have therapeutic value in gout. A long sufferer himself, Ludwig had noticed that the pain and swelling associated with his gout would significantly subside after he had eaten cherries. When he happened to not eat any cherries at all, the symptoms would reoccur again – leading him to make this anecdotal assumption. Gout is a serious medical condition, it is persistent and if left untreated the acute symptoms can become chronic. If left untreated over several years, gout can transition from an acute condition to a chronic one, with devastating effects felt throughout the whole body. One of the more nasty effects of chronic gout is the development of microlesions called tophus (or tophi – plural) literally anywhere on the body – from the tips of fingers to the earlobe. Not only are these lesions unpleasant to look at, they are also extremely painful and in the worst case scenario, need to be removed via surgery.

Clinical Studies Prove Association between Cherry Consumption and Reduction of Gout Symptoms In one large multicentre study of prospectively recruited patients with pre-existing gout, we found that cherry intake was associated with a 35% lower risk of recurrent gout attacks The first known published study on cherries and gout dates back to 1950 in Texas Reports on Biology and Medicine. Dr. Ludwig W. Blau, the investigator, was himself affected by gout—so much so that he was confined to a wheelchair. After eating cherries, he noticed that his gout pain and swelling were considerably reduced. When he stopped eating cherries, his pain and swelling returned. In a more recent study published in 2003, it was shown that as little as 45 cherries (equivalent of about 280g) decreased blood uric levels by 14% in nearly 5 hours!! It was also shown that the excretion of uric acid was significantly increased in the same time frame. Food and Drink Affect Gout In 2008, findings from a retrospective study were released that investigated the association between soft drinks (with high sugar content) and gout.

This study indicated a direct correlation between sugary drinks and the development of gout. The other risk factor is volume of alcohol intake. The reason for this lies twofold, for one, alcohol in the blood, slows down the body’s natural mechanism for uric acid excretion and secondly, it dehydrates the body leading to an increase in crystal formation in the joints. If you are experiencing gout-like symptoms, you should curb alcohol consumption to a bare minimum. Making sure to hydrate whilst drinking (and even when not drinking alcohol) has been shown to reduce the frequency of recurring gout symptoms. Other risk factors include certain foods known to trigger the crystallisation of uric acid, these include red meat consumption as well aas shellfish and other sea food. Fructose is also known to increase uric acid levels, so try to avoid foods that contain a high amount of fructose (such as dried fruits). Whilst aiming for a gout-free lifestyle, try to eat plenty of vegetables (especially green leafy types such as spinach and kale), fruits, nuts and eggs. Dairy products are known to decrease uric acid formation, crystallisation and subsequent deposition in joints.

Citric acid from fruits such as lemons and limes can lower the uric acid concentration. A glass of warm lemon juice first thing in the morning before breakfast has the ability to set up the body’s metabolism to optimum levels, as well as fending off gout. So try to make this a routine. We'll donate $1 to charity for every web order - you choose the cause! Learn more . Total donated to date: $723,204 Friendly Reminder: The information on this website is intended for your general information. It is not a substitute for medical advice from a health care professional and is not intended to diagnose, treat, cure or prevent any disease. Always consult your doctor or other qualified health care professional with any questions you may have regarding a medical condition. Do not disregard medical advice or postpone consultation with your health care professional because of information that you have read on this website. Always read the label of any supplements or natural health products you purchase and use only as directed. Consult a health care professional if symptoms persist. Customer reviews reflect individual experiences and may not be typical. Individual results may vary.

© HealthPost 1000+ images about Gout on Pinterest | Cherry drink, Pain d'epices and Juice recipes Forward Cucumber juice helps bring down body temperature, is highly alkalizing and effective for removing uric acid crystalization in joints, like in the case of GOUT. There may be a slight pain when drinking this juice – it is the stirring of the old toxins to be eliminated. The celery and ginger will help reduce inflammation during the cleansing. Perfect combo! See More Gout - The Medical Nutritional Institute Gout Gout What Is Gout? Gout is a form of arthritis caused by the slow but progressive accumulation of uric acid crystals within joints spaces as well as the surrounding soft tissues. For several reasons, the presence of these crystals has the ability to provoke the immune system and activate severe bouts of inflammation, often at a rapid rate. What are the symptoms of gout? As compared to other causes of joint inflammation, acute attacks of gout are characterised by agonising pain. The most common symptom of gout is pain and swelling in the first joint of the big toe. This symptom is called ‘podagra’ in medical terms and occurs in about 50% of cases of gout.

Other regions that gout may affect are the insteps, ankles, heels, knees, wrists, fingers, and elbows. Episodes of pain are intermittent, and may take weeks or months to reoccur. In a more advanced stage, gout may become chronic and cause permanent symptoms. What is uric acid? Uric acid is a natural by-product of the metabolic breakdown of purines, protein-based substance found in DNA and RNA. Uric acid on its own may not pose a problem, but the crystallisation of uric acid within a joint or the adjacent soft tissue leads to gout. This process is directly dependant on blood uric acid levels. What influences blood uric acid levels? After production, uric acid is dissolved in the blood and passed through the kidneys where it is eliminated from the body as a natural waste product. If there is an increase in the rate of production of uric acid, or if the kidneys do not eliminate enough uric acid from the body, uric acid blood levels increase, resulting in a condition called hyperuricemia. Uric acid blood levels are therefore dependent on both the production as well as excretion of uric acid. What causes high blood levels?

Under-excretion of uric acid by the kidney is by far the primary cause of high blood uric acid levels (hyperuricemia) and accounts for about 90% of cases. Various factors contribute to under-excretion, including genetics, diet and certain medication. Overproduction only causes about 10% of cases of hyperuricemia. In this case hyperuricemia may result when a person eats too much high-purine containing food, or eats too much food in general. How does gout develop? Based on the blood uric acid levels and the presence of symptoms, gout can be divided into stages: Stage 1 – Asymptomatic hyperuricemia. (meaning without symptoms) This is the early stage where a person has elevated uric acid blood levels (hyperuricemia), but displays no other symptoms suggestive of gout. Depending on blood uric acid levels, treatment is usually not required at this stage. This is because hyperuricemia is not considered a disease in itself and may not pose a health risk until symptoms develop. Stage 2 – Acute gout / acute gouty arthritis.

By now chronically elevated uric acid blood levels has led to the deposition and crystallisation of uric acid within the joint spaces and surrounding soft tissues. This triggers bouts of severe inflammation resulting in intense pain of sudden onset. Acute attacks commonly occur at night and can be triggered by a variety of factors including stressful events, a minor injury, excess alcohol intake, certain medication, or the presence of another illness. Attacks usually subside within 3 to 10 days, even without treatment, and the next attack may not occur for months or even years. As increasing quantities of uric acid crystals start to accumulate within joints and soft tissues over time, attacks occur more frequently and last longer, and may eventually become persisting and chronic. If left untreated, recurrent bouts of inflammation triggered by gout will cause progressive and permanent damage to a joint. Stage 3 – Chronic tophaceous gout. If preventative treatment of stage 1 and 2 gout is neglected, the accumulation of uric acid crystals may progress to such a degree that visible lumps of uric acid deposits start forming under the skin. This may also lead to the distortion of a joint.

Subcutaneous uric acid deposits are called tophi, hence the term tophaceous gout. When surgically drained, tophi exude a chalky white substance similar to toothpaste in consistency. Chronic tophaceous gout is the most disabling stage of gout. At this stage the disease would most likely have caused permanent damage to the affected joints. High uric acid levels may also affect the kidneys where uric acid kidney stones are formed. What is “Pseudo-gout”? Gout is sometimes confused with other forms of arthritis because the symptoms are very similar. One of these conditions is “pseudo-gout” where the pain, swelling, and inflammation also presents in a sudden and severe manner, and thus mimics the symptoms of gout. However, pseudo-gout is caused by the accumulation of calcium phosphate crystals within a joint, not uric acid. What are the risk factors for gout? A number of risk factors are associated with hyperuricemia and gout. They include: Genetics – There is a strong family history of the disease. In most of these cases these individuals excrete less uric acid via their kidneys. Gender – Men are more commonly affected than women.

Weight – Being overweight increases the risk of developing hyperuricemia and gout through providing more tissue for turnover or breakdown, leading to excess uric acid production. Alcohol consumption – Too much alcohol can lead to hyperuricemia, since alcohol blocks uric acid excretion by the kidneys. Diet – Eating too many foods that are rich in purines or eating too much food in general can increase blood uric acid content. (See below) Medical Conditions – Some diseases may cause an excessively rapid turnover of cells, increasing uric acid waste. Some examples are psoriasis, haemolytic anaemia and some forms of cancer. Medications – Diuretics, aspirin, cyclosporine and levodopa may affect uric acid excretion by the kidneys Which foods are high in purine content? Purines are found in high concentration in meat and meat products, especially internal organs. In general, plant-based diets are low in purines. Specific examples of high-purine foods include anchovies, sardines, herring, mackerel, scallops, liver, kidneys, brains, meat extracts (e.g., Oxo, Bovril), game meats, beer (from the yeast), and gravy.

A moderate amount of purine is also contained in beef, pork, poultry, other fish and seafood, asparagus, cauliflower, spinach, mushrooms, green peas, lentils, dried peas, beans, oatmeal, wheat bran and wheat germ. How is gout treated? With proper treatment, most people who experience gout are able to control their symptoms and prevent further deterioration. Treatment aims to ease the pain associated with acute attacks as well as to prevent future episodes. Since gout may also lead to the formation of tophi and kidney stones, focus should also be placed on avoiding the development of these conditions. Step I – dealing with acute attacks Prescription medication The severe pain caused by acute attack of gout can be treated with nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or colchicine. In severe cases these can be used in combination. Although effective with reducing inflammation and controlling pain caused by the deposition of uric acid crystals, these drugs have no effect on the amount of uric acid present with the blood stream, soft tissue or joints.

Step 2 – preventing future attacks and protecting your joints from permanent damage Prescription medication Since hyperuricemia and gout are chronic conditions, the ideal approach is to lower uric acid levels through either increasing the rate of excretion of uric acid by the kidney, or by lowering the production of uric acid in the body. The drugs probenecid and allopurinol are commonly used for this purpose. Supplements that help prevent inflammation In addition to lowering blood uric acid levels with prescription drugs, several natural molecules derived from plants are highly effective in suppressing certain pathways involved in chronic inflammation. These generally have a low side-effect risk, making them ab attractive approach when compared to other pharmaceuticals. RheumaLin™ is a novel multi-modal, multi-target anti-inflammatory supplement that consists of two plant extracts, Boswellia bark extract and resveratrol. These naturally derived phytochemical (plant based) compounds are widely recognised. They combat inflammation via biochemical mechanisms that are different to those of existing anti-inflammatory drugs. Effective Gout Diet - ThePaleoDiet.co.za Select Page Effective Gout Diet Build An Effective Gout Diet Believe it or not, simple changes to your diet can prevent this from happening… What causes gout?

Gout is a state of joint inflammation and is caused primarily by uric acid crystallising in joints and other supporting tissues. This crystallisation occurs when uric acids exists in high volume in the blood. This state of high blood uric acid concentrations is called hyperuricemia or gout. What produces uric acid in the body? When foods and cells are broken down in the body, purines are metabolised and broken down. Part of the products of the process is uric acid. Uric acid is a very beneficial substance in the body, and is a potent anti-oxidant and aids in blood vessel protection from damage. So remove purine containing food, prevent gout? Not so easy, I’m afraid. Purines exist in almost all foods. Simply trying to remove purines by not eating foods which contain them would be next to impossible, and would pose difficulties for a person to obtain enough nutrition to be healthy. Having said that, what common “healthy” foods contain uric acid causing purines?

The humble little apple could be crystallising your joints… Fructose Fructose, a sugar (a carbohydrate ) found mainly in fruits and to some extent vegetables, when ingested in fairly low concentrations of around 0.5g per kg of body weight, retards the metabolism of purines, and so uric acid levels spike. On top of those, fructose also decreases the excretion of uric acid in urine. A double attack then from fructose. It both increases the levels of uric acid in the blood, and reduces the rate of its excretion. Carbohydrate Sensitivity/insulin resistance Carbohydrate sensitivity or insulin resistance is a condition where a person’s insulin regulation and ultimately the effect of insulin in their body is out of whack with what is normal behaviour. Diabetes is the final product of insulin related issues, and this sensitivity and imbalance of blood sugar can also retard the expulsion of uric acid in urine. People who suffer from gout are also primed to and often do display symptoms of insulin problems. It is very common for those suffering from gout to also be sufferers of diabetes. What diet will reduce gout?

In this study (click here to view) , it becomes evident that a big contributor to gout and joint inflammation is alcohol and fructose, rather than other influences, such as a high-purine diet. By default, Paleo is an effective gout diet and removes pretty much all the offending foods which cause gout. Cut out the booze and you’ll cut out pain, too… “Alcohol intake, whether alone or with a purine-rich meal, produces greater effects on serum urate levels than a high purine diet.” “There is growing evidence that a low energy, calorie restricted, low carbohydrate (40% of energy), high protein (120 g/day, or 30% of energy) diet, with unsaturated fat (30% of energy) and high dietary fiber, is more beneficial in terms of lowering serum urate, insulin, LDL-C, and triglyceride levels, and hence reducing CAD risk, than the conventional low purine diet…” It appears that a great solution to reducing gout causing uric acid is to eat according to the paleo diet’s eating principles.

The paleo diet focuses on high quality foods and promotes the health benefits of eating a low-carbohydrate, high protein, high fat diet. So what is the answer to the question of what makes up an effective gout, or shall we say, anti-gout diet? Eat well (eat paleo), and make sure that you encourage your body to cycle through blood glycogen by exercising at intense levels, and avoid sugars and alcohol. You should aim to increase your insulin sensitivity in order to “teach” your body how to effectively manage both blood sugar levels resulting from food eaten as well as actual insulin levels in the blood. For more information on how you can develop a safe, effective eating plan which is focused around preventing the development of gout or reducing the severity of its symptoms, check out the 7 Paleo Concepts Course below! Hold up, before you read another article... Receive your FREE copy of the 7 Steps To Paleo guide by clicking below! Recent Articles Colchicine - Molecule of the Month - April 2015 (HTML version) Molecule of the Month April 2015 Also available: JSMol version. That�s a scary picture � what is it?

It�s an image of gout, drawn by the famous English satirical artist, James Gillray (1757-1815). Ouch! It really looks painful � what causes it? Gout is caused by crystallisation of uric acid in the joints - often for some reason in the big toe - and is a type of inflammatory arthritis. Uric acid is naturally formed in the body by breakdown of purine bases (adenine, guanine) via xanthine. It is mainly removed via the kidneys, but sometimes there is more than a body can cope with, and the excess build up as small, irritating crystals in joints. Uric acid And there�s a good treatment? Traditionally colchicine is used. And it works? Perhaps the best testimony is due to the Rev.

Sydney Smith (1771-1845, image right), the famous writer and wit (who once said "I never read a book before reviewing it; it prejudices a man so.") In a letter dated December 1838 he wrote: "On Sunday I was on crutches utterly unable to put foot on the ground, on Tuesday I walked 4 miles - such is the power of Colchicum." It was Smith who commented that gout was "the only enemy that I do not wish to have at my feet". On another occasion, observing some of his autumn crocuses in flower, he remarked, "There, who would guess the virtue of that little plant? But I find the power of Colchicum so great that if I feel a little gout coming on, I go into the garden and hold out my little toe to that plant, and it gets well immediately". What does colchicine look like? Structure of colchicine That�s an unusual looking molecule. How do you mean? Well it has seven-membered rings. That's right, and it was years before the structure of colchicine was sorted out.

It was first isolated in 1820 by two French chemists Pierre Joseph Pelletier and Jean Bienaim� Caventou. They are better known for their isolation of quinine (as well as strychnine). Windaus' proposed, but incorrect, structure of colchicine Originally a structure based on six-membered rings (above) was suggested by Windaus, and it was not until 1945 that M.J.S. Dewar (correctly) suggested the presence of seven-membered rings, confirmed subsequently by X-ray diffraction. And it is an alkaloid? If you define alkaloids as �nitrogenous organic compounds of plant origin� (made from breakdown of amino acids), the answer is yes. Some people expect all alkaloids to be basic. Colchinine�s nitrogen atom is part of an amide group, which means that it can�t be protonated, so colchicine is not a base, and by this count not an alkaloid. Where does the name come from?

It comes from the autumn crocus, or meadow saffron (Colchicum autumnale), which in turn originates in the Colchis region (Greek Koλξoζ) on the Black Sea coast of what is now Georgia. A few other plants contain it, such as Gloriosa superba (glory lily). Meadow saffron (Colchicum autumnale) Glory lily (Gloriosa superba) Colchis is famous in classical literature and mythology. Colchicum autumnale, the yellow crocus of Colchis, is associated in legend with Medea, the sorceress daughter of Ae�tes, King of Colchis. She used the poison from its roots � which included colchicine � among her potions. The goddess Aphrodite made Medea fall in love with Jason, leader of the Argonauts, who relied on her assistance in his quest for the Golden Fleece in overcoming the tasks set for him by the king. Some have identified Colchicum autumnale with the Golden Fleece itself.

Jason and Medea sailed off together into the sunset, but the story does not have a happy ending, as subsequently Jason dumps Medea for a younger woman, Glauce (daughter of the King of Corinth). In revenge, Medea killed Glauce with a poisoned dress and also in some accounts killed her children with colchicine. Painting of Jason and Medea by John William Waterhouse (1907) Engaving of Jason on the Douris cup (5th century BC) being regurgitatedby the snake guarding the Golden Fleece. So colchicine is a poison? Indeed. Several people have died through mistaking the autumn crocus for wild garlic. According to some accounts, the symptoms are similar to cholera. The lethal dose varies, with some people killed by as little as 7 mg, others surviving doses of 60 mg. It has also been used as a poison and as an instrument of suicide. Arkady Vaksberg has alleged that the influential Russian businessman Roman Tsepov died in 2004 of colchicine poisoning, and Catherine Wilson , the last woman to be hanged publicly in the UK (1862), used colchicine as her preferred weapon of death.

She is believed to have carried out at least seven murders. A few other cases are known of homicide by colchicine. Newspaper article describing the public execution of Catherine Wilson for murder in London in 1862 [ Harvard University Library ]. How long back does its use go? Colchicine has been around for some 3000 years � it was described by ancient Greek writers. It is said that it was introduced into the USA by Benjamin Franklin, who had taken it while in Paris. Mind you, it took the American Food and Drug Administration (FDA) until 2009 to "confirm" that it was an effective treatment for gout. How does it work as a medicine? Colchicine binds to β-tubulin, a protein that joins with α-tubulin forming a dimer. When colchicine is bound, the dimer is curved, not linear as usual, and this inhibits the process of assembly of tubulin into microtubules, the key components of the cytoskeleton. In turn, this affects the formation of the spindle in the nucleus of eukaryotic cells, stopping mitosis from occurring and leading to cell death.

One consequence of this which has attracted attention is the fact that cancer cells undergo mitosis significantly faster than normal cells so that cancer cells are more liable to be poisoned by colchicine than normal cells. But its high toxicity is one factor mitigating against the potential of colchicine as an anticancer drug. References Chapman and Hall Combined Chemical Dictionary compound code number: CFR10-M (props, bibliography) History of colchicine P. J. Pelletier and J. B. Caventou, Ann. Chim. Phys., 1820, 14, 69-81 (isolation) A. Windaus and H. Schiele, J. Liebigs Ann. Chem., 1924, 439, 54-68 (incorrect structure) M. Del�pine, J. Chem. Ed., 1951, 28, 454-461 (biographies of Pelletier and Caventou) M. J. S. Dewar, Nature, 1945, 155, 141-142 (structure) M. V. King, J.

L. De Vries and R. Pepinsky, Acta Cryst., 1952, 5, 437-440 (crystal structure) O. J. Eigsti and P. Dustin, Colchicine in Agriculture, Medicine, Biology, and Chemistry, The Iowa State College Press, Ames, Iowa, 1955. T. Graening and H.-G. Schmalz, Angew. Chem. Int. Ed., 2004, 43, 3230 � 3256 (review of syntheses) Colchicine poisoning B. Weakley-Jones, J. Gerber and G. Biggs, Am. J. Forensic Med. Pathol., 2001, 22, 203-206 (two homicides with colchicine) M. J. Maxwell, P. Muthu and P. E. Pritty, Emerg. Med. J., 2002, 19, 265�267 (accidental fatal overdose) M. Brvar, T. Ploj, G.

Kozelj, M. Mozina, M. Noc and M. Bunc, Critical Care, 2004, 8, R56-R59; Z. Sundov, Z. Nincevic, M. Definis-Gojanovic, M. Glavina-Durdov, I. Jukic, N. Hulina and A. Tonkic, Forensic Sci. Int., 2005, 149, 253�256; F. Wehner, F. Musshoff, M. M. Schulz, D. D. Martin and H.-D. Wehner, Forensic Sci., Medicine, and Pathology, 2006, 2, 193-197; M. Amrollahi-Sharifabadi, A. Seghatoleslami, M. Amrollahi-Sharifabadi, F. Bayani and M. Mirjalili, Am. J. Forensic Med.

Pathol., 2013, 34, 295-298 (accidental fatal poisoning from autumn crocus) L. Gussow, Emergency Medicine News, Sept 2009, 14 (fatal dose of 7.2 mg) Y. Finkelstein, S. E. Aks, J. R. Hutson et al., Clin. Toxicol. 2010, 48, 407-414 (�Colchicine poisoning: the dark side of an ancient drug�) K.R. Nagesh, R. G. Menezes, P. Rastogi, N.R. Naik, J. M. Rasquinha, S. Senthilkumaran and A. Fazil, J. Forensic Leg. Med., 2011, 18, 285-287 (suicide) A.

Vaksberg, Toxic Politics: The Secret History of the Kremlin's Poison Laboratory - From the Special Cabinet to the Death of Litvinenko, Santa Barbara, Praeger Publishers, 2011, pp 184-186. Best Practice Journal New Zealand, 2014, 63, 58-60 (toxicity of colchicine) Colchicine in medicine E. F. Hartung, Ann. Rheum. Dis., 1954, 13, 190-200 (gout treatment) M. Levy, M. Spino and S. E. Read, Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy, 1991, 11, 196�211 (review) R. Porter and G. S. Rousseau, Gout: The Patrician Malady, Yale University Press, 1998, pp. 2, 135 and 166 (Smith quotations) B. Bhattacharyya, D. Panda, S. Gupta and M. Banerjee, Med. Res.

Rev., 2008, 28, 155-183. (colchicine as anti-cancer drug) R. A. Terkeltaub, New Engl. J. Med., 2003, 349, 1647-1655 (treatment of gout) G. Weissmann, FASEB J., 2009, 23, 2791-2794 (review of colchicine in medicine) R. A. Terkeltaub, D. E. Furst, K. Bennett, K. A. Kook, R. S. Crockett and M. W. Davis, Arthritis & Rheumatism, 2010, 62, 1060�1068. S. M. Nidorf, J. W. Eikelboom, C. A. Budgeon and P.L. Thompson, J. Am. Coll. Cardiol., 2013, 61, 404-410. (colchicine for secondary prevention of cardiovascular disease) S.

Deftereos, G. Giannopoulos, N. Papoutsidakis, V. Panagopoulou, C. Kossyvakis, K. Raisakis, M. W. Cleman and C. Stefanadis, J. Am. Coll. Cardiol., 2013, 62, 1817-1825. (colchicine in cardiovascular medicine) F. Roubille, E. Kritikou, D. Busseuil, S. Barrere-Lemaire and J-C. Tardif, Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry, 2014, 12, 14-23 How colchicine works S. B. Hastie, Pharmac. Ther., 1991, 51, 377-401. (review of binding to tubulin) R. B. G. Ravelli, B. Gigant, P. A. Curmi, I. Jourdain, S. Lachkar, A. Sobel and M.

Knossow, Nature, 2004, 428, 194-198; A. Dorl�ans, B. Gigant, R. B. G. Ravelli, P. Mailliet, V. Mikol, and M. Knossow, Proc. Natl. Acad. Sci. U.S.A, 2009, 106, 13775�13779 (structure of colchicine-tubulin complex) B. Bhattacharyya, D. Panda, S. Gupta and M. Banerjee, Med. Res. Rev., 2008, 28, 155-183. (colchicine and its binding to tubulin) Y. Lu, J. Chen, M. Xiao, W. Li and D. D. Miller, Pharm Res., 2012, 29, 2943�2971 (tubulin inhibitors)

Question: Gout is caused by the crystallisation of which acid in the, body?
Answer: URIC