Treatment for gout

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Treatment for gout step by step

The therapeutic aims in treatment for gout are as follows:

To terminate the acute attack as promptly and gently as possible
To prevent recurrences of acute gouty arthritis
To prevent or reverse complications of the disease resulting from the deposition of sodium urate or uric acid crystals in joints, kidneys, or other sites
To prevent or reverse associated features of the illness those are deleterious, such as obesity, hypertriglyceridemia, and hypertension.

To achieve above goals we must assess the individualized condition of the person to give treatment for gout. Following approach may be helpful for treatment for gout.

Asymptomatic Hyperuricemia

When no symptom of gout appear besides lab report it is asymptomatic hyperuricemia. The presence of hyperuricemia is rarely an indication for specific antihyperuricemic drug therapy. Rather, the finding of hyperuricemia should cause the following questions to be addressed:

What is the cause of the hyperuricemia?
Are associated findings present?
Has damage to tissues or organs occurred as a result?
What, if anything, should be done?

Hyperuricemia may be the initial clue to the presence of a previously unsuspected disorder. In 70% of hyperuricemic patients, an underlying cause can be readily defined by history and physical examination. The nature of the underlying cause may be useful in predicting the potential consequences. Therefore, an underlying cause should be sought in every patient with hyperuricemia.

It seems prudent not to treat hyperuricemia with specific antihyperuricemic agents until symptoms develop. Rare exceptions include individuals with a known hereditary cause of uric acid overproduction or patients at risk for acute uric acid nephropathy.

It is, however, strongly recommended that the cause of hyperuricemia be determined and any associated factors related to the process, such as obesity, hyper lipidemia, alcoholism, and, especially, hypertension, be addressed. Fenofibrate and losartan might be appropriate agents for the treatment of hypertriglyceridemia and hypertension, respectively, in hyperuricemic individuals, because each has modest uricosuric effects.

 Acute Attack:

Arthritis is treated first and hyperuricemia weeks or months later, if at all. Sudden reduction of serum uric acid often precipitates further episodes of gouty arthritis.


These drugs are the treatment of choice for acute gout. Traditionally, indomethacin has been the most frequently used agent, but all of the other newer NSAIDs are probably equally effective. Indomethacin is initiated at a dosage of 25–50 mg orally every 8 hours and continued until the symptoms have resolved (usually 5–10 days). Active peptic ulcer disease, impaired kidney function, and a history of allergic reaction to NSAIDs are contraindications. For patients at high risk for upper gastrointestinal bleeding, a cyclooxygenase type 2 (COX-2) inhibitor may be an appropriate first choice for management of an acute gout attack. Long-term use of COX-2 inhibitors is not advised because of the association with increased risk of cardiovascular events, which has led to the removal of some drugs from the US market (eg, rofecoxib and valdecoxib).


Neither oral nor intravenous colchicine should be used for the treatment of acute gout flares. The use of oral colchicine during the intercritical period to prevent gout attacks is discussed below.


Corticosteroids often give dramatic symptomatic relief in acute episodes of gout and will control most attacks. They are most useful in patients with contraindications to the use of NSAIDs. If the patient’s gout is monarticular, intra-articular administration (eg, triamcinolone, 10–40 mg depending on the size of the joint) is most effective. For polyarticular gout, corticosteroids may be given intravenously (eg, methylprednisolone, 40 mg/d tapered over 7 days) or orally (eg, prednisone, 40–60 mg/d tapered over 7 days). Gouty and septic arthritis can coexist, albeit rarely. Therefore, joint aspiration and Gram stain with culture of synovial fluid should be performed before corticosteroids are given.

Management between attacks:

Treatment during symptom-free periods is intended to minimize urate deposition in tissues. Thereby prevent tophi and to reduce the frequency and severity of recurrences. These aims to alleviate the causes of gout.

Diet for gout

Potentially reversible causes of hyperuricemia are a high-purine diet, obesity, alcohol consumption, and use of certain medications. Beer consumption appears to confer a higher risk of gout than does whiskey or wine. Higher levels of meat and seafood consumption are associated with increased risks of gout, whereas a higher level of dairy products consumption is associated with a decreased risk. Although dietary purines usually contribute only 1 mg/dL to the serum uric acid level, moderation in eating foods with high purine content is advisable. A high liquid intake and, more importantly, a daily urinary output of 2 L or more will aid urate excretion and minimize urate precipitation in the urinary tract.

Purine contents of foods
Low-purine foods
  Refined cereals and cereal products, cornflakes, white bread, pasta, flour, arrowroot, sago, tapioca, cakes
  Milk, milk products, and eggs
  Sugar, sweets, and gelatin
  Butter, polyunsaturated margarine, and all other fats
  Fruit, nuts, and peanut butter
  Lettuce, tomatoes, and green vegetables (except those listed below)
  Cream soups made with low-purine vegetables but without meat or meat stock
  Water, fruit juice, cordials, and carbonated drinks
High-purine foods
  All meats, including organ meats, and seafood
  Meat extracts and gravies
  Yeast and yeast extracts, beer, and other alcoholic beverages
  Beans, peas, lentils, oatmeal, spinach, asparagus, cauliflower, and mushrooms

Avoidance of hyperuricemic medications:

Thiazide and loop diuretics inhibit renal excretion of uric acid and should be avoided in patients with gout. Similarly, low doses of aspirin aggravate hyperuricemia, as does niacin.

Treatment of chronic gout


Patients with a single episode of gout who are willing to lose weight and stop drinking alcohol are at low risk for another attack and unlikely to benefit from chronic medical therapy. In contrast, older individuals with mild chronic kidney disease who require diuretic use and have a history of multiple attacks of gout are more likely to benefit from pharmacologic treatment. In general, the higher the uric acid level and the more frequent the attacks, the more likely that chronic medical therapy will be beneficial.

There are two indications for daily colchicine administration. First, colchicine can be used to prevent future attacks. For the person who has mild hyperuricemia and occasional attacks of gouty arthritis, chronic colchicine prophylaxis may be all that is needed. The usual dose is 0.6 mg either once or twice a day. Patients who have coexisting moderate chronic kidney disease or heart failure should take colchicine only once a day in order to avoid the peripheral neuromyopathy that can complicate the use of higher doses. Second, colchicine can also be used when uricosuric drugs or allopurinol are started, to suppress attacks precipitated by abrupt changes in the serum uric acid level.

Reduction of serum uric acid:

Indications for a urate lowering intervention include frequent acute arthritis not controlled by colchicine prophylaxis, tophaceous deposits, or kidney damage. Hyperuricemia with infrequent attacks of arthritis may not require treatment. If instituted, the goal of medical treatment is to maintain the serum uric acid at or below 5 mg/dL, which should prevent crystallization of urate.

Two classes of agents may be used to lower the serum uric acid—the uricosuric drugs and allopurinol (neither is of value in the treatment of acute gout). The choice of one or the other depends on the result of a 24-hour urine uric acid determination. A value under 800 mg/d indicates undersecretion of uric acid. Here we must consider uricosuric agents, if kidney function is preserved or consider allopurinol, if kidney function is limited. Patients with > 800 mg of uric acid in a 24-hour urine collection are overproducers and require allopurinol.

Uricosuric drugs

These block the tubular reabsorption of filtered urate thereby reducing the metabolic urate pool, prevent the formation of new tophi and reduce the size of those already present. When administered concomitantly with colchicine, they may lessen the frequency of recurrences of acute gout. The indication for uricosuric treatment is the increasing frequency or severity of acute attacks. These agents are ineffective in patients with chronic kidney disease, with a serum creatinine of > 2 mg/dL.

The following uricosuric drugs may be used: (1) Probenecid, 0.5 g orally daily initially, with gradual increase to 1–2 g daily; or (2) sulfinpyrazone, 50–100 mg orally twice daily initially, with gradual increase to 200–400 mg twice daily. Hypersensitivity to either with fever and rash occurs in 5% of cases; gastrointestinal complaints are observed in 10%. Probenecid also inhibits the excretion of penicillin, indomethacin, dapsone, and acetazolamide.

Precautions with uricosuric drugs include maintaining a daily urinary output of 2000 mL or more in order to minimize the precipitation of uric acid in the urinary tract. This can be further prevented by giving alkalinizing agents (eg, potassium citrate, 30–80 mEq/d orally) to maintain a urine pH of > 6.0. This drugs should not be used in patients with a history of uric acid nephrolithiasis. Aspirin in moderate doses antagonizes the action of these agents, but low doses (325 mg or less per day) do not; doses of aspirin > 3 g daily are themselves uricosuric.

Xanthine oxidase inhibitors

They promptly lower plasma urate and urinary uric acid concentrations and facilitates tophus mobilization.

Inhibitors of xanthine oxidase are of special value in:-

-uric acid overproducers;

-in tophaceous gout;

-in patients unresponsive to the uricosuric regimen;

-and in gouty patients with uric acid renal calculi.

Two FDA-approved xanthine oxidase inhibitors are available for treating chronic gout, allopurinol and febuxostat. One or the other should be chosen; allopurinol and febuxostat are not to be used together. The most frequent adverse effect with either medication is the precipitation of an acute gouty attack. Hypersensitivity to allopurinol occurs in 2% of cases and can be life-threatening. The most common sign of hypersensitivity is a pruritic rash that may progress to toxic epidermal necrolysis, particularly if allopurinol is continued; vasculitis and hepatitis are other manifestations. Febuxostat apparently does not cause the hypersensitivity reactions. This can be given without dose adjustment to patients with mild to moderate renal disease. However, febuxostat may increase liver function tests in 2-3% of patients.

Allopurinol can be used in chronic kidney disease, but the dose must be reduced to decrease the chance of side effects.

Allopurinol interacts with other drugs. The combined use of allopurinol and ampicillin causes a drug rash in 20% of patients. Allopurinol can increase the half-life of probenecid, while probenecid increases the excretion of allopurinol. Thus, a patient taking both drugs may need to use slightly higher than usual doses of allopurinol and lower doses of probenecid.

Chronic tophaceous arthritis

With rigorous medical compliance, allopurinol or febuxostat shrinks tophi and in time can lead to their disappearance. Resorption of extensive tophi requires maintaining a serum uric acid below 5 mg/dL. Surgical excision of large tophi offers mechanical improvement in selected deformities.

Newer treatment for gout

Adrenocorticotropic Hormone

Single injections of intramuscular ACTH gel (25 to 80 IU) can terminate an acute gout attack. More often, however, repeated administration is required every 24 to 72 hours. This treatment is effective postoperatively and may be more effective than glucocorticoids, possibly related to the mechanism of action. In addition to stimulating the adrenal cortex to produce corticosteroids, ACTH interferes with the acute inflammatory response through activation of melanocortin receptor-3.

Biological agent

Pegloticase is a biological treatment in which the enzyme uricase has been conjugated to monomethoxy polyethylene glycol. It is indicated for the treatment of tophaceous gout  resistant  to  standard  therapy  and  is administered as an intravenous infusion every 2 weeks for up to 6 months. It is highly effective at controlling hyperuricaemia and  causes  regression  of  tophi.  The main  adverse  effects  are  infusion  reactions  and flares of gout  during  the  first  3  months  of  therapy. This can be overcome by using antihistamines or steroids.

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