A practical approach to gout

Current management of an 'old' disease

General treatment recommendations

Serum uric acid concentrations may be reduced with nonpharmacologic therapy.

Useful dietary and lifestyle changes include weight reduction, decreased alcohol ingestion, decreased consumption of foods with a high purine content, and control of hyperlipidemia and hypertension. Used alone, however, these measures will probably not reduce serum uric acid levels to normal, which is the treatment goal for the prevention of acute gout attacks. Symptomatic hyperuricemia usually requires medication.

Acute Gouty Arthritis

Three treatments currently available for acute gouty arthritis attacks are nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine and corticosteroids.

NSAIDs. These rapid-acting drugs are currently the most favored treatment for acute gout attacks. Indomethacin (Indocin) is generally the drug of choice, but other NSAIDs can be used. One study reported the achievement of pain relief in patients who presented to an emergency department with acute gouty arthritis who were treated with a 60-mg intramuscular injection of ketorolac (Toradol).

All NSAIDs can have serious gastrointestinal side effects, including bleeding and ulceration. These drugs should therefore be used with caution in patients with a history of peptic ulcer disease, congestive heart failure or chronic renal failure. Discretion should be used in giving NSAIDs to patients who are allergic to aspirin or have asthma or nasal polyps.

Corticosteroids.

Have anti-inflammatory (glucocorticoid) and salt-retaining (mineralocorticoid) properties. Glucocorticoids cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli. Oral corticosteroids may be used for patients with gout or pseudo gout who cannot tolerate NSAIDs. Although there have been case reports of adrenal crisis related to multiple interarticular injections of steroids for gout, this has not been clearly proven.  Monarthric gout responds well to corticosteroids given by intra-articular injection. Systemic corticosteroids (e.g., prednisone [Deltasone], in a dosage of 20 to 30 mg per day) are used only when NSAIDs and colchicine are not effective or are contraindicated.

Long-term therapy is not indicated for a single attack of gout. However, it may be reasonable to identify precipitating factors and to obtain a 24-hour urine collection to determine creatinine clearance and excretion of uric acid. Treatment with allopurinol or a uricosuric drug should be considered in patients who have at least two episodes of gout in 1 year.

Asymptomatic hyperuricemia does not usually produce adverse effects before the development of gout and, therefore, does not require treatment. However, it may be advisable to determine the cause of the hyperuricemia.

Urate-lowering therapy should not be prescribed without concomitant use of an NSAID or low-dose colchicine. Serum urate levels may fluctuate during the initiation of such therapy and induce a gouty flare or prolong an ongoing attack.

Long-term therapy should not be initiated until the patient has returned to baseline in terms of nutrition, activity level, and medication use. Beginning therapy before that time may actually exacerbate a flare or prolong an existing episode.

Prevention of Recurrent Attacks

Hyperuricemic therapy should be initiated in patients with frequent gout attacks, tophi or urate nephropathy.

A low dosage of an NSAID or colchicine is effective in preventing acute gouty attacks.

Hyperuricemic drug therapy should not be started until an acute attack of gouty arthritis has ended, because of the risk of increased mobilization of uric acid stores. A reasonable goal is to reduce the serum uric acid concentration to less than 6 mg per dL (360 µmol per L).

Reduction of serum uric acid levels to normal is the goal of treatment designed to prevent acute attacks of gout.

Uricosuric Drugs. These agents decrease the serum uric acid level by increasing renal excretion.

Probenecid (Benemid) and sulfinpyrazone (Anturane) are used in patients who are considered underexcretors of uric acid. Uricosuric drugs should not be given to patients with a urine output of less than 1 mL per minute, a creatinine clearance of less than 50 mL per minute (0.84 mL per second) or a history of renal calculi. The physiologic decline in renal function that occurs with aging frequently limits the use of uricosuric agents.

Probenecid, in a dosage of 1 to 2 g per day, achieves satisfactory control in 60 to 85 percent of patients.  It is important to note that the drug also blocks the tubular secretion of other organic acids. This may result in increased plasma concentrations of penicillins, cephalosporins, sulfonamides and indomethacin.

Sulfinpyrazone is a uricosuric agent that is related to phenylbutazone. Because it can act as an antiplatelet drug, it should be used cautiously in patients who are anticoagulated or have bleeding problems. Sulfinpyrazone can also cause gastrointestinal problems. Thus, caution should also be exercised in giving this drug to patients with peptic ulcer disease.

Allopurinol. As a xanthine oxidase inhibitor, allopurinol (Zyloprim) impairs the conversion of hypoxanthine to xanthine and the conversion of xanthine to uric acid. The effect of the drug depends on the dosage.

Allopurinol in a dosage of 300 mg per day has been reported to reduce serum urate concentrations to less than 7 mg per dL (420 µmol per L) in 70 percent of patients.24

Allopurinol is the drug of choice in patients with severe tophaceous deposits and in patients with a history of impaired renal function (creatinine clearance of less than 50 mL per minute [0.84 mL per second]), uric acid nephropathy or nephrolithiasis.

The drug is also preferred as a pretreatment agent to protect against uric acid nephropathy in patients with lymphoproliferative or myeloproliferative disorders.

The side effects of allopurinol include skin rash (e.g., Stevens-Johnson syndrome and toxic epidermal necrolysis), leukopenia and gastrointestinal disturbances. The initiation of allopurinol therapy can also precipitate an acute gout attack. The dosage of allopurinol should be adjusted in patients with renal impairment.

Summary

Gouty arthritis is the culmination of a number of physiologic mechanisms that ultimately result in deposition of uric acid within joints and soft tissues.

Decreased uric acid clearance through the kidney is the most common cause of gout. Tophaceous gout occurs in less than 10% of patients.

Acute episodes are treated with NSAIDs or colchicine.

Low-dose therapy with these agents can also prevent recurrent attacks. Most patients with gout need long-term treatment with either uricosuric agents or xanthine oxidase inhibitors.

The above opinionated views and information serves to educated and informed consumer .  The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. .It should not replaced professional advise and consultation.A licensed physician should be consulted for diagnosis and treatment of any and all medical conditions