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Wednesday, December 29, 2010
Introduction & Epidemiology
Background
Gout is a common disorder of uric acid metabolism that can lead to deposition of monosodium urate (MSU) crystals in soft tissue, recurrent episodes of debilitating joint inflammation, and, if untreated, joint destruction and renal damage. Gout is definitively diagnosed based on the demonstration of urate crystals in aspirated synovial fluid.
Improvements in early diagnosis and the availability of definitive treatment have significantly improved the prognosis of gout, as evidenced by the declining incidence of disabling chronic tophaceous gout. However, tophaceous gout may still develop because of misdiagnosis, poor management, medication intolerances, and/or poor patient compliance.
What is gout? What is hyperuricemia?
Gout is a disease that results from an overload of uric acid in the body. This overload of uric acid leads to the formation of tiny crystals of urate that deposit in tissues of the body, especially the joints. When crystals form in the joints, it causes recurring attacks of joint inflammation (arthritis).
Gout is considered a chronic and progressive disease. Chronic gout can also lead to deposits of hard lumps of uric acid in the tissues, particularly in and around the joints and may cause joint destruction, decreased kidney function, and kidney stones (nephrolithiasis).
Gout has the unique distinction of being one of the most frequently recorded medical illnesses throughout history. It is often related to an inherited abnormality in the body's ability to process uric acid. Uric acid is a breakdown product of purines that are part of many foods we eat. An abnormality in handling uric acid can cause attacks of painful arthritis (gout attack), kidney stones, and blockage of the kidney-filtering tubules with uric acid crystals, leading to kidney failure. On the other hand, some people may only develop elevated blood uric acid levels (hyperuricemia) without having manifestations of gout, such as arthritis or kidney problems.
The state of elevated levels of uric acid in the blood without symptoms is referred to as asymptomatic hyperuricemia. Asymptomatic hyperuricemia is considered a precursor state to the development of gout. The term gout refers the disease that is caused by an overload of uric acid in the body, resulting in painful arthritic attacks and deposits of lumps of uric acid crystals in body tissues.
Gouty arthritis is typically an extremely painful attack with a rapid onset of joint inflammation. The joint inflammation is precipitated by deposits of uric acid crystals in the joint fluid (synovial fluid) and joint lining (synovial lining). Intense joint inflammation occurs as the immune system reacts, causing white blood cells to engulf the uric acid crystals and chemical messengers of inflammation to be released, leading to pain, heat, and redness of the joint tissues. As gout progresses, the attacks of gouty arthritis typically occur more frequently and often in additional joints.
Gout is a common disorder of uric acid metabolism that can lead to deposition of monosodium urate (MSU) crystals in soft tissue, recurrent episodes of debilitating joint inflammation, and, if untreated, joint destruction and renal damage. Gout is definitively diagnosed based on the demonstration of urate crystals in aspirated synovial fluid.
Improvements in early diagnosis and the availability of definitive treatment have significantly improved the prognosis of gout, as evidenced by the declining incidence of disabling chronic tophaceous gout. However, tophaceous gout may still develop because of misdiagnosis, poor management, medication intolerances, and/or poor patient compliance.
What is gout? What is hyperuricemia?
Gout is a disease that results from an overload of uric acid in the body. This overload of uric acid leads to the formation of tiny crystals of urate that deposit in tissues of the body, especially the joints. When crystals form in the joints, it causes recurring attacks of joint inflammation (arthritis).
Gout is considered a chronic and progressive disease. Chronic gout can also lead to deposits of hard lumps of uric acid in the tissues, particularly in and around the joints and may cause joint destruction, decreased kidney function, and kidney stones (nephrolithiasis).
Gout has the unique distinction of being one of the most frequently recorded medical illnesses throughout history. It is often related to an inherited abnormality in the body's ability to process uric acid. Uric acid is a breakdown product of purines that are part of many foods we eat. An abnormality in handling uric acid can cause attacks of painful arthritis (gout attack), kidney stones, and blockage of the kidney-filtering tubules with uric acid crystals, leading to kidney failure. On the other hand, some people may only develop elevated blood uric acid levels (hyperuricemia) without having manifestations of gout, such as arthritis or kidney problems.
The state of elevated levels of uric acid in the blood without symptoms is referred to as asymptomatic hyperuricemia. Asymptomatic hyperuricemia is considered a precursor state to the development of gout. The term gout refers the disease that is caused by an overload of uric acid in the body, resulting in painful arthritic attacks and deposits of lumps of uric acid crystals in body tissues.
Gouty arthritis is typically an extremely painful attack with a rapid onset of joint inflammation. The joint inflammation is precipitated by deposits of uric acid crystals in the joint fluid (synovial fluid) and joint lining (synovial lining). Intense joint inflammation occurs as the immune system reacts, causing white blood cells to engulf the uric acid crystals and chemical messengers of inflammation to be released, leading to pain, heat, and redness of the joint tissues. As gout progresses, the attacks of gouty arthritis typically occur more frequently and often in additional joints.
Signs & Symptoms
Signs & symptoms of gout
* Sustained high levels of uric acid in the blood is a common gout symptom (also see causes of gout).
* Presence of uric acid crystals in joint fluid (see diagnosis of gout).
* Deposits of uric acid crystals around joints and other areas such as the ears.
* Only one or two joints are affected (initially).
* Common affected areas include the feet, ankles and the ball of the big toe.
* Tenderness around an affected joint.
* The skin around an affected joint is red, shiny and painful to touch- a common gout symptom (see gout pictures).
* Moving the affected limb/s becomes painful.
* Chronic gout can lead to decreased kidney function and kidney stones.
Signs of a gout attack
* A rapid onset usually between 12-24 hours and often occurring overnight whilst an individual is resting.
* Fever or chills developing.
* A fast subsidence. Gout attacks normally subside within hours or days.
Gout presenting in the metatarsal-phalangeal joint of the big toe. Note the slight redness of the skin overlying the joint.
tophus of the knee
Tophus of the toe, and over the external maleolus
* Sustained high levels of uric acid in the blood is a common gout symptom (also see causes of gout).
* Presence of uric acid crystals in joint fluid (see diagnosis of gout).
* Deposits of uric acid crystals around joints and other areas such as the ears.
* Only one or two joints are affected (initially).
* Common affected areas include the feet, ankles and the ball of the big toe.
* Tenderness around an affected joint.
* The skin around an affected joint is red, shiny and painful to touch- a common gout symptom (see gout pictures).
* Moving the affected limb/s becomes painful.
* Chronic gout can lead to decreased kidney function and kidney stones.
Signs of a gout attack
* A rapid onset usually between 12-24 hours and often occurring overnight whilst an individual is resting.
* Fever or chills developing.
* A fast subsidence. Gout attacks normally subside within hours or days.
Gout presenting in the metatarsal-phalangeal joint of the big toe. Note the slight redness of the skin overlying the joint.
tophus of the knee
Tophus of the toe, and over the external maleolus
Pathophysiology
Gout is abnormal accumulation and precipitation of monosodium urate(MSU) crystals into tissue, usually around the joints, causing recurrent acute or chronic arthritis.
Gout is a classic example of the inflammatory response. When the uric acid comes out of solution, it forms crystals in one or several joints. This will attract large numbers of phagocytic white blood cells to that area in order to clear away the crystals. By doing so, the white blood cells release a package of inflammatory mediator substances(will be discussed later) which, in addition to destroying the crystals, also damage the surrounding tissues - hence the pain, swelling and redness occur.
Although the presence of urate crystals in the soft and synovial tissues is a prerequisite for a gouty attack, the fact that urate crystals can also be found in synovial fluid in the absence of joint inflammation suggests that the presence of intrasynovial urate crystals is not sufficient to cause gouty arthritis. This is because clumps or microtophi of highly negatively charged and reactive MSU crystals are normally coated with serum proteins (apolipoprotein [apo] E or apo B) that physically inhibit the binding of MSU crystals to cell receptors. A gout attack may be triggered by either a release of uncoated crystals (for example, due to partial dissolution of a microtophus caused by changing serum urate levels) or precipitation of crystals in a supersaturated microenvironment (for example, release of urate due to cellular damage). Naked urate crystals are then interact with intracellular and surface receptors of local dendritic cells and macrophages, serving as a danger signal to activate the innate immune system of our body.
This interaction may be enhanced by immunoglobulin G (IgG) binding. Triggering of these receptors, including Toll-like receptors, NALP3 inflammasomes, and the triggering receptors expressed on myeloid cells (TREMs) by MSU, results in the production of interleukin (IL)–1, which in turn initiates the production of a cascade of pro-inflammatory cytokines, including IL-6, IL-8, neutrophil chemotactic factors, and tumor necrosis factor (TNF)–alpha. Neutrophil phagocytosis leads to another burst of inflammatory mediator production.
Subsidence of an acute gout attack is due to multiple mechanisms, including the clearance of damaged neutrophils, recoating of urate crystals, and the production of anti-inflammatory cytokines including, IL-1RA, IL-10, and transforming growth factor (TGF)–beta.
Pathophysiology
The greater the duration and degree of hyperuricemia, the greater is the likelihood of getting gout and the more severe are the symptoms of it. Urate levels in the body can be elevated due to 3 causes which are:
• Decreased renal excretion
• Increased production
• Increased purine intake
Decreased renal excretion is the most common cause of hyperuricemia. It may be hereditary and also occurs in patients who are receiving diuretics and in those with diseases that decrease glomerular filtration rate(GFR).
Besides that, ethanol will also increase purine catabolism in the liver and thus increase the formation of lactic acid, which blocks urate secretion by the renal tubules. Therefore, heavy alcoholic drinkers predispose to gout.
Lead poisoning and cyclosporine, usually given to transplant patients, irreversibly damages renal tubules, leading to urate retention in the body.
Increased production of urate may be caused by increased rates of nucleoprotein turnover in haematological conditions (for example, lymphoma, leukaemia, haemolytic anaemia) and in conditions with increased rates of cellular proliferation and cell death (for example, psoriasis, cytotoxic cancer therapy, radiation therapy).
Increased urate production may also occur as a primary hereditary abnormality, and in obesity as the urate production correlates with body surface area. In most cases, the cause is unknown, but a few cases are attributable to enzyme abnormalities, for example, deficiency of hypoxanthine-guanine phosphoribosyltransferase (complete deficiency in Lesch-Nyhan syndrome) is one of the possible causes.
Increased intake of purine-rich foods (eg, liver, kidney, anchovies, asparagus, consommé, herring, meat gravies and broths, mushrooms, mussels, sardines, sweetbreads) can contribute to hyperuricemia. Foods rich in protein such as red meat, kidney and liver contain a high proportion of nucleic material (purines) that is broken down to uric acid. Some wines and beers are also high in purines. However, a strict low-purine diet lowers serum urate by only about 1 mg/dL.
Urate precipitates as needle-shaped monosodium urate (MSU) crystals, which are deposited extracellularly in avascular tissues (for example, cartilage) or in relatively avascular tissues (for example, tendons, tendon sheaths, ligaments, walls of bursae) and skin around cooler distal joints and tissues (for example, ears).
In severe, long-standing hyperuricemia, MSU crystals may be deposited in larger central joints and in the parenchyma of organs such as the kidney. At the acid pH of urine, urate precipitates readily as small platelike or irregular crystals that may aggregate to form gravel or stones, which may cause obstruction. Tophi are MSU crystal aggregates that most often develop in joint and cutaneous tissue.
Gout is a classic example of the inflammatory response. When the uric acid comes out of solution, it forms crystals in one or several joints. This will attract large numbers of phagocytic white blood cells to that area in order to clear away the crystals. By doing so, the white blood cells release a package of inflammatory mediator substances(will be discussed later) which, in addition to destroying the crystals, also damage the surrounding tissues - hence the pain, swelling and redness occur.
Although the presence of urate crystals in the soft and synovial tissues is a prerequisite for a gouty attack, the fact that urate crystals can also be found in synovial fluid in the absence of joint inflammation suggests that the presence of intrasynovial urate crystals is not sufficient to cause gouty arthritis. This is because clumps or microtophi of highly negatively charged and reactive MSU crystals are normally coated with serum proteins (apolipoprotein [apo] E or apo B) that physically inhibit the binding of MSU crystals to cell receptors. A gout attack may be triggered by either a release of uncoated crystals (for example, due to partial dissolution of a microtophus caused by changing serum urate levels) or precipitation of crystals in a supersaturated microenvironment (for example, release of urate due to cellular damage). Naked urate crystals are then interact with intracellular and surface receptors of local dendritic cells and macrophages, serving as a danger signal to activate the innate immune system of our body.
This interaction may be enhanced by immunoglobulin G (IgG) binding. Triggering of these receptors, including Toll-like receptors, NALP3 inflammasomes, and the triggering receptors expressed on myeloid cells (TREMs) by MSU, results in the production of interleukin (IL)–1, which in turn initiates the production of a cascade of pro-inflammatory cytokines, including IL-6, IL-8, neutrophil chemotactic factors, and tumor necrosis factor (TNF)–alpha. Neutrophil phagocytosis leads to another burst of inflammatory mediator production.
Subsidence of an acute gout attack is due to multiple mechanisms, including the clearance of damaged neutrophils, recoating of urate crystals, and the production of anti-inflammatory cytokines including, IL-1RA, IL-10, and transforming growth factor (TGF)–beta.
Pathophysiology
The greater the duration and degree of hyperuricemia, the greater is the likelihood of getting gout and the more severe are the symptoms of it. Urate levels in the body can be elevated due to 3 causes which are:
• Decreased renal excretion
• Increased production
• Increased purine intake
Decreased renal excretion is the most common cause of hyperuricemia. It may be hereditary and also occurs in patients who are receiving diuretics and in those with diseases that decrease glomerular filtration rate(GFR).
Besides that, ethanol will also increase purine catabolism in the liver and thus increase the formation of lactic acid, which blocks urate secretion by the renal tubules. Therefore, heavy alcoholic drinkers predispose to gout.
Lead poisoning and cyclosporine, usually given to transplant patients, irreversibly damages renal tubules, leading to urate retention in the body.
Increased production of urate may be caused by increased rates of nucleoprotein turnover in haematological conditions (for example, lymphoma, leukaemia, haemolytic anaemia) and in conditions with increased rates of cellular proliferation and cell death (for example, psoriasis, cytotoxic cancer therapy, radiation therapy).
Increased urate production may also occur as a primary hereditary abnormality, and in obesity as the urate production correlates with body surface area. In most cases, the cause is unknown, but a few cases are attributable to enzyme abnormalities, for example, deficiency of hypoxanthine-guanine phosphoribosyltransferase (complete deficiency in Lesch-Nyhan syndrome) is one of the possible causes.
Increased intake of purine-rich foods (eg, liver, kidney, anchovies, asparagus, consommé, herring, meat gravies and broths, mushrooms, mussels, sardines, sweetbreads) can contribute to hyperuricemia. Foods rich in protein such as red meat, kidney and liver contain a high proportion of nucleic material (purines) that is broken down to uric acid. Some wines and beers are also high in purines. However, a strict low-purine diet lowers serum urate by only about 1 mg/dL.
Urate precipitates as needle-shaped monosodium urate (MSU) crystals, which are deposited extracellularly in avascular tissues (for example, cartilage) or in relatively avascular tissues (for example, tendons, tendon sheaths, ligaments, walls of bursae) and skin around cooler distal joints and tissues (for example, ears).
In severe, long-standing hyperuricemia, MSU crystals may be deposited in larger central joints and in the parenchyma of organs such as the kidney. At the acid pH of urine, urate precipitates readily as small platelike or irregular crystals that may aggregate to form gravel or stones, which may cause obstruction. Tophi are MSU crystal aggregates that most often develop in joint and cutaneous tissue.
Laboratory Investigations
There are numbers of significance laboratory investigations that can be carried out in order to diagnose gout in a patient. Below are the numerous tests that can be done:
1) Joint aspiration/arthrocentesis
This is a really important diagnostic investigation especially in ruling out ‘gouty arthritis’ and differentiates it from inflammation that is due to infection in the joint.This test is done by inserting a needle into the joint and withdraw an amount of fluid, in which afterwards being observed under the microscope. The fluid will be examined for any presence of uric acid crystal which is indeed an important marker for gout. Signs of bacterial infection also need to be checked. Other types of crystal can also present in the aspirated fluid, such as calcium pyrophosphate in a condition called ‘pseudogout’ (like gout). Sometimes, gouty arthritis can be diagnosed based on the typical clinical presentation without doing this invasion method.
Arthrocentesis
2) Blood test
This test comprises of full blood count, renal profile, and level of uric acid in the blood.
Full blood count concerned on the white blood cell count, is measured in order to rule out infection as the causes of inflammation. However, the level of uric acid in blood is not reliable in gout diagnosis. Why is this so? This is because approximately 10% patients have a normal uric acid level during an acute attack of gouty arthritis. Besides, in 5-8% out of general population have high uric acid (hyperuricemia) in their blood. Thus, this means that high uric acid in blood does not necessarily mean gout is the cause of inflamed joint. Remarkably, during a flare of inflammatory gouty arthritis, the amount of uric acid in the blood is rather low. So, usually level of uric acid in blood is measured after a flare has resolved when acute inflammation is absence.
3) Radiographs
Patients who had recurrent episodes of gouty arthritis will develop joint damage. In order to assess this underlying damage, x-ray of the joint can be carried out.
X-ray of a foot with numerous interosseous tophi
X-ray of a hand with visible swellings around the affected joints
1) Joint aspiration/arthrocentesis
This is a really important diagnostic investigation especially in ruling out ‘gouty arthritis’ and differentiates it from inflammation that is due to infection in the joint.This test is done by inserting a needle into the joint and withdraw an amount of fluid, in which afterwards being observed under the microscope. The fluid will be examined for any presence of uric acid crystal which is indeed an important marker for gout. Signs of bacterial infection also need to be checked. Other types of crystal can also present in the aspirated fluid, such as calcium pyrophosphate in a condition called ‘pseudogout’ (like gout). Sometimes, gouty arthritis can be diagnosed based on the typical clinical presentation without doing this invasion method.
Arthrocentesis
2) Blood test
This test comprises of full blood count, renal profile, and level of uric acid in the blood.
Full blood count concerned on the white blood cell count, is measured in order to rule out infection as the causes of inflammation. However, the level of uric acid in blood is not reliable in gout diagnosis. Why is this so? This is because approximately 10% patients have a normal uric acid level during an acute attack of gouty arthritis. Besides, in 5-8% out of general population have high uric acid (hyperuricemia) in their blood. Thus, this means that high uric acid in blood does not necessarily mean gout is the cause of inflamed joint. Remarkably, during a flare of inflammatory gouty arthritis, the amount of uric acid in the blood is rather low. So, usually level of uric acid in blood is measured after a flare has resolved when acute inflammation is absence.
3) Radiographs
Patients who had recurrent episodes of gouty arthritis will develop joint damage. In order to assess this underlying damage, x-ray of the joint can be carried out.
X-ray of a foot with numerous interosseous tophi
X-ray of a hand with visible swellings around the affected joints
Treatment
While some medications are used to treat the hot, swollen joint, other medications are used to prevent further attacks of gout. With any of these medications, call your doctor if you think you are having problems from them or if they are not working.
Medicines used to treat acute gout and/or prevent further attacks are as follows:
(1) Nonsteroidal anti-inflammatory drugs (NSAIDs)
o Examples include indomethacin (Indocin), ibuprofen (Advil), and naproxen (Aleve). Newer drugs such as celecoxib (Celebrex) can also be used. Aspirin should not be used for this condition.
o High doses of anti-inflammatory medications are needed to control the inflammation and can be tapered off within a couple of weeks.
o Tell your doctor about your other health problems, particularly if you have a history of peptic ulcer disease or intestinal bleeding, if you are taking warfarin (Coumadin), or if you have problems with your kidney function.
o The primary complications of these medications include upset stomach, bleeding ulcers, and decreased kidney function.
(2) Colchicine
o This medication is given in two different ways, either to treat the acute attack of arthritis or to prevent recurring attacks.
o To treat the hot, swollen joint, colchicine is given rapidly (up to once an hour until symptoms improve, side effects develop, or a maximum of 10 doses is reached). While this approach is often effective, most people develop nausea, vomiting, or diarrhea and so it is currently seldom used for this purpose.
o To help prevent an attack from coming back, colchicine can be given once or twice a day. At this frequency, diarrhea is much less likely to occur. While the chronic use of colchicine can reduce the attacks of gout, it does not prevent the accumulation of uric acid that can lead to joint damage even without attacks of hot, swollen joints.
o Tell your doctor if you have any problems with your kidney or liver function.
(3) Corticosteroids
o Corticosteroids such as prednisone are generally given when your doctor feels this is a safer approach than using NSAIDs.
o When given by mouth, a high dose is used initially and is tapered off within a couple of weeks. It is important to take these medications as prescribed to avoid problems.
o Some complications with the short-term use of corticosteroids include altered mood, elevated blood pressure, and problems with control of glucose in patients with diabetes.
o Corticosteroids can also be injected into the swollen joint. Resting the joint temporarily, after it is injected with steroids, can be helpful.
o Occasionally, corticosteroids or a related compound, corticotropin (ACTH), can also be injected into the muscle or given intravenously.
Medicines in addition to low-dose colchicine used to prevent further attacks of gout and lower the level of uric acid in the blood include the following.
(4) Probenecid
o This medication helps the body eliminate excess uric acid through the kidneys and into the urine.
o You should drink at least 2 liters of fluid a day while taking this medication (to help prevent uric acid kidney stones from forming).
o Advise your doctor if you have kidney problems or a history of kidney stones or if you are taking aspirin. You may need to take allopurinol instead.
o There are a number of drug interactions with probenecid, so you should advise your doctor of your other medications. If you are prescribed a new medication, let your doctor know that you are taking probenecid.
(5) Allopurinol
o This medication decreases the formation of uric acid by the body and is a very reliable way to lower the blood uric acid level. Allopurinol is currently the gold standard of maintenance therapy.
o Advise your doctor if you have kidney problems. Allopurinol can be still used, but the dose may need to be adjusted.
o Common side effects include stomach pain, headache, diarrhea, and rash.
o Discontinue allopurinol if you develop a rash or a fever, and call your doctor.
o A very rare risk of allopurinol hypersensitivity exists. This problem can cause a severe skin rash, fever, kidney failure, liver failure, bone marrow failure, and can be fatal.
o Advise your doctor if you are taking azathioprine, 6-mercaptopurine, or cyclophosphamide; dose adjustments of allopurinol may be needed.
o Ampicillin is more likely to cause a rash if you are taking allopurinol.
(6) Febuxostat (Uloric)
o Febuxostat is first new medication developed specifically for the control of gout in over 40 years.
o Febuxostat decreases the formation of uric acid by the body and is a very reliable way to lower the blood uric acid level.
o Febuxostat can be used in patients with mild to moderate kidney impairment.
o Febuxostat should not be taken with theophylline, 6-mercaptopurine (6-MP), or azathioprine.
It is important to understand that these maintenance medications are used to lower the uric acid well below normal to prevent recurrent gouty arthritis attacks. Generally, doctors want the blood uric acid level to be below 6.0 mg/dL.
Medicines used to treat acute gout and/or prevent further attacks are as follows:
(1) Nonsteroidal anti-inflammatory drugs (NSAIDs)
o Examples include indomethacin (Indocin), ibuprofen (Advil), and naproxen (Aleve). Newer drugs such as celecoxib (Celebrex) can also be used. Aspirin should not be used for this condition.
o High doses of anti-inflammatory medications are needed to control the inflammation and can be tapered off within a couple of weeks.
o Tell your doctor about your other health problems, particularly if you have a history of peptic ulcer disease or intestinal bleeding, if you are taking warfarin (Coumadin), or if you have problems with your kidney function.
o The primary complications of these medications include upset stomach, bleeding ulcers, and decreased kidney function.
(2) Colchicine
o This medication is given in two different ways, either to treat the acute attack of arthritis or to prevent recurring attacks.
o To treat the hot, swollen joint, colchicine is given rapidly (up to once an hour until symptoms improve, side effects develop, or a maximum of 10 doses is reached). While this approach is often effective, most people develop nausea, vomiting, or diarrhea and so it is currently seldom used for this purpose.
o To help prevent an attack from coming back, colchicine can be given once or twice a day. At this frequency, diarrhea is much less likely to occur. While the chronic use of colchicine can reduce the attacks of gout, it does not prevent the accumulation of uric acid that can lead to joint damage even without attacks of hot, swollen joints.
o Tell your doctor if you have any problems with your kidney or liver function.
(3) Corticosteroids
o Corticosteroids such as prednisone are generally given when your doctor feels this is a safer approach than using NSAIDs.
o When given by mouth, a high dose is used initially and is tapered off within a couple of weeks. It is important to take these medications as prescribed to avoid problems.
o Some complications with the short-term use of corticosteroids include altered mood, elevated blood pressure, and problems with control of glucose in patients with diabetes.
o Corticosteroids can also be injected into the swollen joint. Resting the joint temporarily, after it is injected with steroids, can be helpful.
o Occasionally, corticosteroids or a related compound, corticotropin (ACTH), can also be injected into the muscle or given intravenously.
Medicines in addition to low-dose colchicine used to prevent further attacks of gout and lower the level of uric acid in the blood include the following.
(4) Probenecid
o This medication helps the body eliminate excess uric acid through the kidneys and into the urine.
o You should drink at least 2 liters of fluid a day while taking this medication (to help prevent uric acid kidney stones from forming).
o Advise your doctor if you have kidney problems or a history of kidney stones or if you are taking aspirin. You may need to take allopurinol instead.
o There are a number of drug interactions with probenecid, so you should advise your doctor of your other medications. If you are prescribed a new medication, let your doctor know that you are taking probenecid.
(5) Allopurinol
o This medication decreases the formation of uric acid by the body and is a very reliable way to lower the blood uric acid level. Allopurinol is currently the gold standard of maintenance therapy.
o Advise your doctor if you have kidney problems. Allopurinol can be still used, but the dose may need to be adjusted.
o Common side effects include stomach pain, headache, diarrhea, and rash.
o Discontinue allopurinol if you develop a rash or a fever, and call your doctor.
o A very rare risk of allopurinol hypersensitivity exists. This problem can cause a severe skin rash, fever, kidney failure, liver failure, bone marrow failure, and can be fatal.
o Advise your doctor if you are taking azathioprine, 6-mercaptopurine, or cyclophosphamide; dose adjustments of allopurinol may be needed.
o Ampicillin is more likely to cause a rash if you are taking allopurinol.
(6) Febuxostat (Uloric)
o Febuxostat is first new medication developed specifically for the control of gout in over 40 years.
o Febuxostat decreases the formation of uric acid by the body and is a very reliable way to lower the blood uric acid level.
o Febuxostat can be used in patients with mild to moderate kidney impairment.
o Febuxostat should not be taken with theophylline, 6-mercaptopurine (6-MP), or azathioprine.
It is important to understand that these maintenance medications are used to lower the uric acid well below normal to prevent recurrent gouty arthritis attacks. Generally, doctors want the blood uric acid level to be below 6.0 mg/dL.
Prevention
(1)Proper diet
• Restrict foods high in purine (a substance that produces uric acid when broken down) such as sardines, anchovies, brains, liver, kidneys, tripe, sweetbreads, tongue, shellfish (mussels and oysters), fish roe, scallops, peas, lentils, beans and an excessive amount of red meat.
• People with gout should eat more raw fruit, vegetables, grains, seeds and nuts. Cherries and strawberries are recommended. Uric acid and vinegar based foods should be avoided.
• Increase intake of dairy products, such as nonfat milk and yogurt, because they can lower the frequency of gout attacks.
• Avoid fructose, such as in corn syrup and diet sodas.
(2)Healthy lifestyle
• Exercise regularly and maintain a healthy body weight. Lose weight if you are overweight, but do not go on diets designed for quick or extreme loss of weight because they increase uric acid levels in the blood. Losing weight too rapidly can occasionally precipitate gout attacks.
(3)Reduce alcohol intake.
• Alcohol especially taken in the form of beer and wine can increase uric acid levels. Limit alcoholic drinks to one or two measures a day. Drinking plenty of water helps prevent further attacks.
(4)Drink plenty of fluids
• Drinking plenty of fluids especially water helps eliminate uric acid from the body.
(5)Avoid stress
• Avoiding stress is an important preventive measure against future gout attacks. A healthy mind often means a healthy body.
• By adopting a ‘gout diet’, taking regular exercise, drinking plenty of fluids whilst reducing alcohol intake, further gout attacks can be avoided.
• Restrict foods high in purine (a substance that produces uric acid when broken down) such as sardines, anchovies, brains, liver, kidneys, tripe, sweetbreads, tongue, shellfish (mussels and oysters), fish roe, scallops, peas, lentils, beans and an excessive amount of red meat.
• People with gout should eat more raw fruit, vegetables, grains, seeds and nuts. Cherries and strawberries are recommended. Uric acid and vinegar based foods should be avoided.
• Increase intake of dairy products, such as nonfat milk and yogurt, because they can lower the frequency of gout attacks.
• Avoid fructose, such as in corn syrup and diet sodas.
(2)Healthy lifestyle
• Exercise regularly and maintain a healthy body weight. Lose weight if you are overweight, but do not go on diets designed for quick or extreme loss of weight because they increase uric acid levels in the blood. Losing weight too rapidly can occasionally precipitate gout attacks.
(3)Reduce alcohol intake.
• Alcohol especially taken in the form of beer and wine can increase uric acid levels. Limit alcoholic drinks to one or two measures a day. Drinking plenty of water helps prevent further attacks.
(4)Drink plenty of fluids
• Drinking plenty of fluids especially water helps eliminate uric acid from the body.
(5)Avoid stress
• Avoiding stress is an important preventive measure against future gout attacks. A healthy mind often means a healthy body.
• By adopting a ‘gout diet’, taking regular exercise, drinking plenty of fluids whilst reducing alcohol intake, further gout attacks can be avoided.
Prognosis
In patient untreated with uric acid lowering drugs ,the risk of recurrence after the first attack
1st year : 62%
2nd year: 78%
3rd year: 84%
In untreated gout, about 2% of patient developed severe arthritis usually 20 years after the first attack
People with untreated gout, tophi will also occur about 50% after 10 years and 72% after 20 years.
Appropriate treatment can suppress gout attacks and their recurrence, and prevent long-term consequences of the disease. If left untreated, gout can lead to kidney damage and to severe joint destruction that may require reconstructive surgery of the affected joint(s).
1st year : 62%
2nd year: 78%
3rd year: 84%
In untreated gout, about 2% of patient developed severe arthritis usually 20 years after the first attack
People with untreated gout, tophi will also occur about 50% after 10 years and 72% after 20 years.
Appropriate treatment can suppress gout attacks and their recurrence, and prevent long-term consequences of the disease. If left untreated, gout can lead to kidney damage and to severe joint destruction that may require reconstructive surgery of the affected joint(s).
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