07-06-2009, 06:09 AM
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). Chronic gout can also lead to deposits of hard lumps of uric acid in and around the joints and may cause joint destruction, decreased kidney function, and kidney stones.
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 arthritis or kidney problems. 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 white blood cells engulf the uric acid crystals and chemical messengers of inflammation are released, causing pain, heat, and redness of the joint tissues.
Who is affected by gout?
Approximately 5 million people in the United States suffer from gout. (Did you know that none other than Benjamin Franklin had terrible gouty arthritis!) Gout is nine times more common in men than in women. It predominantly attacks males after puberty, with a peak age of 75. In women, gout attacks usually occur after menopause.
While an elevated blood level of uric acid may indicate an increased risk of gout, the relationship between hyperuricemia and gout is unclear. Many patients with hyperuricemia do not develop gout, while some patients with repeated gout attacks have normal or low blood uric acid levels. In fact, the blood level of uric acid often lowers during an acute attack of gout.
What are the risk factors for gouty arthritis?
In addition to an inherited abnormality in handling uric acid, other risk factors for developing gout include obesity, excessive weight gain (especially in youth), moderate to heavy alcohol intake, high blood pressure, and abnormal kidney function. Certain drugs, such as thiazide diuretics (hydrochlorothiazide [Dyazide]), low-dose aspirin, niacin, cyclosporine, tuberculosis medications (pyrazinamide and ethambutol), and others can also cause elevated uric acid levels in the blood and lead to gout. Furthermore, certain diseases lead to excessive production of uric acid in the body. Examples of these diseases include leukemias, lymphomas, and hemoglobin disorders.
Interestingly, a recent study demonstrated an increased prevalence of abnormally low thyroid hormone levels (hypothyroidism) in patients with gout.
In patients at risk of developing gout, certain conditions can precipitate acute attacks of gout. These conditions include dehydration, injury to the joint, fever, excessive eating, and recent surgery.
What are symptoms of gout?
The 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!
How is gouty arthritis diagnosed?
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.
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 inflammations. X-rays can also be helpful for monitoring the effects of chronic gout on the joints.
How is gout treated?
There 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.
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, 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.
Dietary changes can help reduce uric acid levels in the blood. 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.
http://www.thenews.com.pk/daily_detail.asp?id=186636
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 arthritis or kidney problems. 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 white blood cells engulf the uric acid crystals and chemical messengers of inflammation are released, causing pain, heat, and redness of the joint tissues.
Who is affected by gout?
Approximately 5 million people in the United States suffer from gout. (Did you know that none other than Benjamin Franklin had terrible gouty arthritis!) Gout is nine times more common in men than in women. It predominantly attacks males after puberty, with a peak age of 75. In women, gout attacks usually occur after menopause.
While an elevated blood level of uric acid may indicate an increased risk of gout, the relationship between hyperuricemia and gout is unclear. Many patients with hyperuricemia do not develop gout, while some patients with repeated gout attacks have normal or low blood uric acid levels. In fact, the blood level of uric acid often lowers during an acute attack of gout.
What are the risk factors for gouty arthritis?
In addition to an inherited abnormality in handling uric acid, other risk factors for developing gout include obesity, excessive weight gain (especially in youth), moderate to heavy alcohol intake, high blood pressure, and abnormal kidney function. Certain drugs, such as thiazide diuretics (hydrochlorothiazide [Dyazide]), low-dose aspirin, niacin, cyclosporine, tuberculosis medications (pyrazinamide and ethambutol), and others can also cause elevated uric acid levels in the blood and lead to gout. Furthermore, certain diseases lead to excessive production of uric acid in the body. Examples of these diseases include leukemias, lymphomas, and hemoglobin disorders.
Interestingly, a recent study demonstrated an increased prevalence of abnormally low thyroid hormone levels (hypothyroidism) in patients with gout.
In patients at risk of developing gout, certain conditions can precipitate acute attacks of gout. These conditions include dehydration, injury to the joint, fever, excessive eating, and recent surgery.
What are symptoms of gout?
The 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!
How is gouty arthritis diagnosed?
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.
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 inflammations. X-rays can also be helpful for monitoring the effects of chronic gout on the joints.
How is gout treated?
There 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.
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, 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.
Dietary changes can help reduce uric acid levels in the blood. 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.
http://www.thenews.com.pk/daily_detail.asp?id=186636