Gout is a fairly common arthritic disorder, and is characterized by acute attacks of extremely severe swelling, redness, pain, warmth and limited mobility of a joint, classically the big toe. It can, however, affect any joint of the upper or lower extremities, and it is often so painful that the area cannot even be touched slightly. When one examines the involved joint, it is easy to see a bright red-hot area of inflammation. The cause of gout may be a hereditary problem in the handling of uric acid. Most people with gout have problems in excretion of the uric acid in the kidney. When uric acid levels build up above a certain amount in the blood stream, a state is reached where some of the uric acid cannot be dissolved and therefore crystallizes. These crystals are the source of acute inflammatory arthritic attacks, as well as leading to a buildup in tissues in the form of nodules, called tophi. Also crystals form in the kidney and can lead to acute attacks of kidney stones. Although usually just one joint is involved at a time during attacks of gout, there can be cases of severe gout that lead to inflammation and arthritis of multiple joints over the body on a chronic basis. These latter conditions can often mimic rheumatoid arthritis, and it is extremely important to differentiate the two conditions, since the treatment in each situation may differ.

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Physical findings of gout include a severely inflamed joint with warmth, redness, tenderness and marked limitation of motion. The more frequent and chronic attacks that occur in a specific joint can lead to deformity of that joint. Also if uric acid deposits build up in the skin, then the tophi can form especially around knees, elbows or even on the ear lobes. These nodules are nontender and firm. At times they may become ulcerated and drain a thick yellowish or cream-colored material.

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The diagnosis of gout is made by finding the crystals of uric acid, called monosodium urate, within white blood cells of material taken from the joint or from a skin nodule. An elevated level of uric acid in the blood is consistent with gout, but it is not diagnostic. The physician must see the crystals on a specimen of fluid or tissue in order to make an absolute diagnosis. X-rays may be normal early on in an attack of gout, but as more and more attacks occur in a specific joint, then destructive changes of the joint may occur on an x-ray.

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The diagnosis of gout is made specifically by finding the characteristic crystals when viewing fluid or tissue under a polarizing microscope. The diagnosis is not made on the basis of a blood test alone or on the clinical findings. There are cases where there is some confusion occasionally between the diagnosis of rheumatoid arthritis and gout when multiple joints are involved. That is why documentation of crystals in joint fluid is extremely important in helping to form a correct diagnosis and choose the correct treatment program for these patients.

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The treatment of gout includes the use of anti-inflammatory medicine during an acute attack. Some of the more potent anti-inflammatories, such as Indocin have been used extensively to help calm down an acute attack of gout, but it is sometimes difficult to use Indocin on a long-term basis due to side-effects in the stomach or central nervous system. Other NSAIDs can also be helpful. At times local steroid injection or steroid tablets may be used in more severe cases. Colchicine is another agent that helps control the inflammation of acute gouty arthritis. It has side effects, however, including abdominal cramping or diarrhea which can be dose related and may limit its use. If a patient just has a rare or occasional attack of gout and no evidence of buildup of uric acid in the kidney with kidney stones, then it is not necessary to maintain the patient on any long-term medication to lower uric acid levels. When frequent attacks occur, however, or if a high load of uric acid is going through the kidneys, it is necessary to treat the patient on a permanent basis with medication daily to help lower the uric acid level down to a low normal range. This may eventually prevent further attacks of gout. The medication most frequently used to lower the uric acid level is called allopurinol (Zyloprim). It is not used during an acute attack, since it may actually prolong or aggravate the attack. It is best used after the acute attack has subsided. Diet may be a contributing factor in some cases if excess alcohol is present. It can lead to increased levels of uric acid. Anchovies, sardines, and certain meats that are high in purine content may contribute to uric acid buildup. The best advice on diet is to never overindulge in food or excessive alcohol. Another important factor in the management of gout is to avoid dehydration. Dehydration can sometimes contribute to an attack of gout. Injuries can also sometimes lead to a gouty flare-up as well. It is also important to note that even though treatment with allopurinol lowers uric acid, it may take six months or more for all of the excess uric acid deposits throughout the body to be absorbed. In view of this, it is important not to give up or lose hope if attacks of gout occur even after starting on allopurinol therapy. The simultaneous use of colchicine with allopurinol can often prevent these acute attacks of gout from occurring for the first 3 to 6 months of allopurinol treatment.

Gout is one form of arthritis which can be completely controlled on the right medical regimen. There are a lot of misconceptions about gout and its treatment, so it is extremely important to follow-up with the plan laid out by your primary care physician or rheumatologist.