by Nathan Wei, MD, FACP, FACR
Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.
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Gout is a disease caused by inflammation produced as a result of deposits of crystals of monosodium urate (uric acid) in body tissue.
Gout comes is caused by having too much uric acid in the blood. Uric acid is produced when purines- a constituent of many types of foods- are metabolized into uric acid.
Uric acid is excreted by the body in two different ways. Two-thirds of uric acid is excreted by the kidneys and one-third by the intestine.
Elevated blood uric acid occurs either because the body makes too much… or because the kidneys don’t rid of it fast enough. This second situation is more common.
Gout develops when crystals of monosodium urate accumulate in tissue and the body responds with an acute inflammatory response. When white blood cells come into the area and ingest the crystals, the crystals cause the inflammatory cells to rupture and release enzymes that increase inflammation.
Factors that induce gout include diets high in purine containing foods, trauma, surgery, medical illness, starvation, drugs that elevate uric acid levels, and alcohol, particularly beer and red wine.
Uric acid deposits in joint cartilage, soft tissues next to joints, and the kidney. When crystals accumulate over a period of time, they form a mass called a tophus. Joints affected by gout can develop erosion of cartilage and bone as well as inflammation of the synovium (lining of the joint). Deposits in the kidneys lead to tissue damage.
Gout occurs twice as often in men as in women. The risk of developing gout increases with increased levels of blood uric acid. Women rarely develop gout before menopause. Peak incidence for gout in men is the fifth decade.
Medical conditions associated with gout include obesity, hyperlipidemia, diabetes, hypertension, excessive alcohol ingestion, and some malignancies.
Interestingly, gout is also associated with lead poisoning. Gout is more common in African Americans, probably because of the increased incidence of hypertension and obesity.
Acute gout is the most common early manifestation of gout. The most common site for an attack is the big toe. Involvement of this joint is called podagra.
The big toe is affected between 75-90 per cent of the time with more than 50 per cent of patients experiencing their first attack in this area. Eighty per cent of attacks involve a single joint, usually the foot, ankle, or knee. The onset is generally at night or very early in the morning and the joint becomes swollen, red, warm, and very painful. Fever may occur and an infected joint should be ruled out. Early attacks subside over 3 to 10 days. The skin overlying the joint may peel. Attacks that come on subsequently tend to last longer, involve more joints, and occur more often. In those patients where the disease is poorly controlled, attacks may begin to affect multiple joints.
The period between acute attacks is called the intercritical period. Most patients who are not treated for gout will have another attack within two years of the first one. Sometimes, if a patient has involvement of the hands at this stage, their disease may be confused with rheumatoid arthritis.
Chronic tophaceous gout describes a situation where deposits of uric acid will develop in the ear, elbows, front of the knees, Achilles tendons, and hands. These deposits of uric acid may cause the overlying skin to ulcerate and chalky deposits of uric acid will leak out. Risk factors for the development of tophaceous gout are : early age of onset, inadequate treatment, frequent attacks, very high levels of uric acid in the blood, involvement of the upper extremities, and attacks affecting multiple joints.
Kidney involvement from gout comes in two varieties. The first is uric acid stones. The frequency of stones increases as the serum uric acid increases and as the the amount of uric acid excreted increases.
The second consequence of gout in the kidney is deposits of uric acid in the kidney tissue. Uric acid kidney disease, if it progresses, causes hypertension and protein leaks in the urine. Eventually, it may also cause kidney failure.
Uric acid deposits can occur almost anywhere. One relatively common presentation is for gout to develop in the distal row of finger joints. This can be confused with osteoarthritis. Typically, older women on diuretic therapy present with this syndrome.
A few diagnostic laboratory tests may be helpful. The first is the presence of an elevated serum uric acid level at the time of an attack. A word of warning... patients can have normal serum uric acids at the time of attacks and elevated serum uric acids can occur in other arthritic disease states such as psoriatic arthritis and pseudogout. Certain drugs such as aspirin or diuretics can also raise serum uric acid levels.
Patients may have elevated white blood cell counts and elevated erythrocyte sedimentation rates.
The best method for establishing the diagnosis is to examine fluid aspirated from an acutely inflamed joint. Patients with gout almost always have monosodium urate crystals in the joint fluid. A polarizing microscope must be used and the attack has to be relatively acute. If some time has gone by (more than 3 days after the onset of the attack), crystals may not be evident. An experienced lab tech or rheumatologist should look at the fluid because the crystals are not that easy to identify. The fluid will also have many white blood cells and it’s important to rule out the presence of simultaneous infection.
X-rays will demonstrate soft tissue swelling. With long established gout, bony erosions will occur. Ultraound has been used by some researchers to evaluate gout.
Treatment of the acute attack will depend on the health of the patient. In otherwise healthy patients, oral colchicine or non steroidal anti inflammatory drugs can be used. In older patients with other medical conditions, treatment with this set of drugs needs to be monitored very carefully. Occasionally, oral corticosteroids may be needed.
Commitment to changes in diet is an often forgotten but important part of gout therapy. Foods high in purines such as sweet breads, red meats, sardines, shellfish, turkey, salmon, trout, beans, peas, asparagus, and spinach should be avoided.
Likewise, drugs that elevate blood uric acid levels, such as thiazide diuretics, and low dose aspirin may need to be changed.
Patients with frequent (more than 2 attacks per year) probably should go on uric acid lowering therapy.
Young patients who don’t excrete a lot of uric acid in the urine (less than 800 mg per 24 hours as measured by a 24 hour urine collection) may be treated with probenicid. Probenicid increases the amount of uric acid excreted in the urine. Patients who have abnormal kidney function may not respond to probenicid.
Those patients who already excrete a lot of uric acid in the urine (more than 800 mg per 24 hours) should be treated with allopurinol. This drug reduces the amount of uric acid produced by the body. Allopurinol has many potential side effects associated with it including hepatitis, aplastic anemia, and rashes. This drug needs to be started at a low dose and increased slowly.Alternatively, febuxostat (Uloric) can be used. The mechanism of action is similar to that of allopurinol with fewer potential side effects.
Patients who are started on either probenicid or allopurinol need to be on prophylactic colchicine because there is a tendency for flares to develop in patients during the first six months of uric acid lowering therapy.
Co-morbid conditions such as hypertension, obesity, hyperlipidemia, etc. need to be addressed and dietary counseling in regards to purine containing foods is advised.
Patients with tophaceous refractory gout can be treated with Krystexxa. This drug administered intravenously converts uric acid to allantoin, an inert ingredient that is excreted through the kidneys.
Kidney transplant patients with gout present a whole host of additional problems. They are often being treated with cyclosporine which can lower kidney blood flow or with azathioprine which has significant interactions with both allopurinol and colchicine.
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