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.
http://www.medicinenet.com/gout/article.htmThere are two key concepts essential to treating gout. First, it is critical to stop the acute inflammation of joints affected by gouty arthritis. Second, it is important to address the long-term management of the disease in order to prevent future gouty arthritis attacks and shrink gouty tophi crystal deposits in the tissues.
The treatment of an acute attack of gouty arthritis involves measures and medications that reduce inflammation. Preventing future acute gout attacks is equally as important as treating the acute arthritis. Prevention of acute gout involves maintaining adequate fluid intake, weight reduction, dietary changes, reduction in alcohol consumption, and medications to lower the uric acid level in the blood (reduce hyperuricemia).
Maintaining adequate fluid intake helps prevent acute gout attacks. Adequate fluid intake also decreases the risk of kidney stone formation in patients with gout. Alcohol is known to have diuretic effects that can contribute to dehydration and precipitate acute gout attacks. Alcohol can also affect uric acid metabolism to cause hyperuricemia. Therefore, alcohol has two major effects that worsen gout by impeding (slowing down) the excretion of uric acid from the kidneys as well as by causing dehydration, both of which contribute to the precipitation of uric acid crystals in the joints.
Dietary changes can help reduce uric acid levels in the blood. Since purine chemicals are converted by the body into uric acid, purine-rich foods are avoided. Examples of foods rich in purines include shellfish and organ meats such as liver, brains, kidneys, and sweetbreads. Researchers have reported, in general, that meat or seafood consumption increases the risk of gout attacks, while dairy food consumption seemed to reduce the risk. Protein intake or purine-rich vegetable consumption was not associated with an increased risk of gout. Total alcohol intake was strongly associated with an increased risk of gout (beer and liquor were particularly strong factors). Fructose from the corn syrup in soft drinks also increases the risk of gout.
Weight reduction can be helpful in lowering the risk of recurrent attacks of gout. This is best accomplished by reducing dietary fat and calorie intake, combined with a regular aerobic exercise program.
http://www.medicinenet.com/gout/page4.htmbumpThere are two key concepts essential to treating gout. First, it is critical to stop the acute inflammation of joints affected by gouty arthritis. Second, it is important to address the long-term management of the disease in order to prevent future gouty arthritis attacks and shrink gouty tophi crystal deposits in the tissues.
The treatment of an acute attack of gouty arthritis involves measures and medications that reduce inflammation. Preventing future acute gout attacks is equally as important as treating the acute arthritis. Prevention of acute gout involves maintaining adequate fluid intake, weight reduction, dietary changes, reduction in alcohol consumption, and medications to lower the uric acid level in the blood (reduce hyperuricemia).
Maintaining adequate fluid intake helps prevent acute gout attacks. Adequate fluid intake also decreases the risk of kidney stone formation in patients with gout. Alcohol is known to have diuretic effects that can contribute to dehydration and precipitate acute gout attacks. Alcohol can also affect uric acid metabolism to cause hyperuricemia. Therefore, alcohol has two major effects that worsen gout by impeding (slowing down) the excretion of uric acid from the kidneys as well as by causing dehydration, both of which contribute to the precipitation of uric acid crystals in the joints.
Dietary changes can help reduce uric acid levels in the blood. Since purine chemicals are converted by the body into uric acid, purine-rich foods are avoided. Examples of foods rich in purines include shellfish and organ meats such as liver, brains, kidneys, and sweetbreads. Researchers have reported, in general, that meat or seafood consumption increases the risk of gout attacks, while dairy food consumption seemed to reduce the risk. Protein intake or purine-rich vegetable consumption was not associated with an increased risk of gout. Total alcohol intake was strongly associated with an increased risk of gout (beer and liquor were particularly strong factors). Fructose from the corn syrup in soft drinks also increases the risk of gout.
Weight reduction can be helpful in lowering the risk of recurrent attacks of gout. This is best accomplished by reducing dietary fat and calorie intake, combined with a regular aerobic exercise program.
http://www.medicinenet.com/gout/page4.htmActive research is ongoing in a variety of fields related to gout and hyperuricemia. The management of the chronic gouty disease and its relationship to improving blood pressure and kidney function is becoming better defined.
Scientists recently reported that high animal protein intake slightly increased the risk for gout. Others found that dietary calcium intake may protect patients from getting gout attacks. Vitamin C may also lower blood uric acid levels.
New medications to increase the elimination of uric acid in the urine (such as benzbromarone) are being evaluated in clinical trials. Researchers are also reporting on experimental drugs that can affect chemical messengers involved in gouty inflammation called interleukins.
The optimal regimens for the treatment of acute gout attacks and chronic gout conditions still require further long-term studies. Research scientists will continue to develop less toxic and more effective medications to battle this "scourge of the ages."
http://www.medicinenet.com/gout/page6.htm
What does the future hold for patients with gout and hyperuricemia?Active research is ongoing in a variety of fields related to gout and hyperuricemia. The management of the chronic gouty disease and its relationship to improving blood pressure and kidney function is becoming better defined. Scientists recently reported that high animal protein intake slightly increased the risk for gout. Others found that dietary calcium intake may protect patients from getting gout attacks. Vitamin C may also lower blood uric acid levels. New medications to increase the elimination of uric acid in the urine (such as benzbromarone) are being evaluated in clinical trials. Researchers are also reporting on experimental drugs that can affect chemical messengers involved in gouty inflammation called interleukins. The optimal regimens for the treatment of acute gout attacks and chronic gout conditions still require further long-term studies. Research scientists will continue to develop less toxic and more effective medications to battle this "scourge of the ages." http://www.medicinenet.com/gout/page6.htm |
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Active research is ongoing in a variety of fields related to gout and hyperuricemia. The management of the chronic gouty disease and its relationship to improving blood pressure and kidney function is becoming better defined.
Scientists recently reported that high animal protein intake slightly increased the risk for gout. Others found that dietary calcium intake may protect patients from getting gout attacks. Vitamin C may also lower blood uric acid levels.
New medications to increase the elimination of uric acid in the urine (such as benzbromarone) are being evaluated in clinical trials. Researchers are also reporting on experimental drugs that can affect chemical messengers involved in gouty inflammation called interleukins.
The optimal regimens for the treatment of acute gout attacks and chronic gout conditions still require further long-term studies. Research scientists will continue to develop less toxic and more effective medications to battle this "scourge of the ages."
http://www.medicinenet.com/gout/page6.htmDietary changes can help reduce uric acid levels in the blood. Since purine chemicals are converted by the body into uric acid, purine-rich foods are avoided. Examples of foods rich in purines include shellfish and organ meats such as liver, brains, kidneys, and sweetbreads. Researchers have reported, in general, that meat or seafood consumption increases the risk of gout attacks, while dairy food consumption seemed to reduce the risk. Protein intake or purine-rich vegetable consumption was not associated with an increased risk of gout. Total alcohol intake was strongly associated with an increased risk of gout (beer and liquor were particularly strong factors). Fructose from the corn syrup in soft drinks also increases the risk of gout.
Weight reduction can be helpful in lowering the risk of recurrent attacks of gout. This is best accomplished by reducing dietary fat and calorie intake, combined with a regular aerobic exercise program.
http://www.medicinenet.com/gout/page4.htmThe small joint at the base of the big toe is the most common site of an acute gout attack of arthritis. An acute attack of gouty arthritis at the base of the big toe is medically referred to as podagra. Other joints that are commonly affected include the ankles, knees, wrists, fingers, and elbows. Acute gout attacks are characterized by a rapid onset of pain in the affected joint followed by warmth, swelling, reddish discoloration, and marked tenderness. Tenderness can be intense so that even a blanket touching the skin over the affected joint can be unbearable. Patients can develop fever with the acute gout attacks. These painful attacks usually subside in hours to days, with or without medication. In rare instances, an attack can last for weeks. Most patients with gout will experience repeated attacks of arthritis over the years.
Uric acid crystals can deposit in tiny fluid-filled sacs (bursae) around the joints. These urate crystals can incite inflammation in the bursae, leading to pain and swelling around the joints (a condition called bursitis). In rare instances, gout leads to a more chronic type of joint inflammation that mimics rheumatoid arthritis.
In chronic (tophaceous) gout, nodular masses of uric acid crystals (tophi) deposit in different soft-tissue areas of the body. Even though they are most commonly found as hard nodules around the fingers, at the tips of the elbows, in the ears, and around the big toe, tophi nodules can appear anywhere in the body. They have been reported in unexpected areas such as in the vocal cords or (rarely) even around the spinal cord. When tophi appear in the tissues, the gout condition is felt to represent a substantial overload of uric acid within the body.
Gout is suspected when a patient reports a history of attacks of painful arthritis, particularly at the base of the toes. Ankles and knees are the next most commonly involved joints in gout. Gout usually attacks one joint at a time, while other arthritis conditions, such as systemic lupus and rheumatoid arthritis, usually attack multiple joints simultaneously.
The most reliable test for gout is finding uric acid crystals in a sample of the joint fluid obtained by joint aspiration (arthrocentesis). Arthrocentesis is a common office procedure performed under local anesthesia. Using sterile technique, fluid is withdrawn (aspirated) from the inflamed joint using a syringe and needle. The joint fluid is then analyzed for uric acid crystals and for infection. Shiny, needle-like uric acid crystals are best viewed with a special polarizing microscope. The diagnosis of gout can also be made by finding these urate crystals from material aspirated from tophi nodules and bursitis fluid. Although many doctors can do the procedure, rheumatologists are specialists who are particularly trained in this evaluation.
Sometimes, patients with a classic history and symptoms of gout can be successfully treated and presumed to have gout without undergoing arthrocentesis. However, establishing a firm diagnosis is still preferable since other conditions can mimic gout. These include another crystal-induced arthritis called pseudogout, psoriatic arthritis, rheumatoid arthritis, and even infection in the joint.
X-rays can sometimes be helpful and may show tophi-crystal deposits and bone damage as a result of repeated bouts of inflammation. X-rays can also be helpful for monitoring the effects of chronic gout on the joints.
http://www.medicinenet.com/gout/page3.htmbumpThe small joint at the base of the big toe is the most common site of an acute gout attack of arthritis. An acute attack of gouty arthritis at the base of the big toe is medically referred to as podagra. Other joints that are commonly affected include the ankles, knees, wrists, fingers, and elbows. Acute gout attacks are characterized by a rapid onset of pain in the affected joint followed by warmth, swelling, reddish discoloration, and marked tenderness. Tenderness can be intense so that even a blanket touching the skin over the affected joint can be unbearable. Patients can develop fever with the acute gout attacks. These painful attacks usually subside in hours to days, with or without medication. In rare instances, an attack can last for weeks. Most patients with gout will experience repeated attacks of arthritis over the years.
Uric acid crystals can deposit in tiny fluid-filled sacs (bursae) around the joints. These urate crystals can incite inflammation in the bursae, leading to pain and swelling around the joints (a condition called bursitis). In rare instances, gout leads to a more chronic type of joint inflammation that mimics rheumatoid arthritis.
In chronic (tophaceous) gout, nodular masses of uric acid crystals (tophi) deposit in different soft-tissue areas of the body. Even though they are most commonly found as hard nodules around the fingers, at the tips of the elbows, in the ears, and around the big toe, tophi nodules can appear anywhere in the body. They have been reported in unexpected areas such as in the vocal cords or (rarely) even around the spinal cord. When tophi appear in the tissues, the gout condition is felt to represent a substantial overload of uric acid within the body.
Gout is suspected when a patient reports a history of attacks of painful arthritis, particularly at the base of the toes. Ankles and knees are the next most commonly involved joints in gout. Gout usually attacks one joint at a time, while other arthritis conditions, such as systemic lupus and rheumatoid arthritis, usually attack multiple joints simultaneously.
The most reliable test for gout is finding uric acid crystals in a sample of the joint fluid obtained by joint aspiration (arthrocentesis). Arthrocentesis is a common office procedure performed under local anesthesia. Using sterile technique, fluid is withdrawn (aspirated) from the inflamed joint using a syringe and needle. The joint fluid is then analyzed for uric acid crystals and for infection. Shiny, needle-like uric acid crystals are best viewed with a special polarizing microscope. The diagnosis of gout can also be made by finding these urate crystals from material aspirated from tophi nodules and bursitis fluid. Although many doctors can do the procedure, rheumatologists are specialists who are particularly trained in this evaluation.
Sometimes, patients with a classic history and symptoms of gout can be successfully treated and presumed to have gout without undergoing arthrocentesis. However, establishing a firm diagnosis is still preferable since other conditions can mimic gout. These include another crystal-induced arthritis called pseudogout, psoriatic arthritis, rheumatoid arthritis, and even infection in the joint.
X-rays can sometimes be helpful and may show tophi-crystal deposits and bone damage as a result of repeated bouts of inflammation. X-rays can also be helpful for monitoring the effects of chronic gout on the joints.
http://www.medicinenet.com/gout/page3.htmGout 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.
http://www.medicinenet.com/gout/article.htm