Treatment of Gout

Acute Gout Attack

The goal of treatment during an acute gout attack is suppression of inflammation and control of pain. It is important to note, that if a patient is not on uric acid lowering therapy at the time of an acute attack – then this is not the time to initiate such therapy. However, if a patient is on uric acid lowering therapy at the time of an acute attack, it should not be discontinued.

Treatment of pain and inflammation can be achieved with NSAIDs, colchicine, or corticosteroids (systemic or intra-articular). The choice of which treatment is the right one for a particular patient should be made on the basis of the patient’s co-morbid medical conditions, other medications, and side effect profile.

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1. NSAIDS: Commonly used NSAIDs during an acute gout attack include ibuprofen 800 mg three to four times daily or indomethacin 25 to 50 mg four times daily. Treatment should be discontinued when symptoms resolve.
2. Colchicine: Intravenous colchicine is associated with serious toxicities and side effects, so it should be used as an oral formulation only. High dose oral colchicine (1.2 mg followed by 0.6 mg every hour for 6 doses) is generally poorly tolerated because of GI side effects. Lower doses are much better received and may be used in combination with NSAIDs.
3. Corticosteroids: In patients with contraindications to NSAID use, corticosteroids are the next choice. Corticosteroids can be administered as an injection into the effected joint (intra-articular steroids) or given systemically (orally, such as prednisone or medrol). Intra-articular steriods are useful if only one or two joints are affected and the treating physician is proficient in injecting those joints. Oral corticosteroids can be used starting at 30-40 mg daily tapering over 10-14 days.

Treatment: Uric Acid Lowering Therapy

Indications

Patients who have multiple episodes of acute gout attacks per year or who have tophi on exam are candidates for uric acid lowering therapy. Use of uric acid lowering agents will reduce the frequency of gout attacks and over time, reduce tophi formation, and diminish the risk of joint destruction. The following are indications for uric acid lowering therapy:

• tophi or chronic arthritis on exam
• failure of colchicine prophylaxis of acute gouty arthritis
• renal stones
• Prior to chemotherapy as prophylaxis of tumor lysis syndrome
• Extremely high levels of serum uric acid (>12 mg/dl)

Uric acid is the end product of purine (nucleic acid component of DNA) metabolism and is produced normally by the body during tissue remodeling and breakdown. About 20% of uric acid is derived from purines ingested in food. Causes of hyperuricemia can be divided into two major categories: decreased clearance of uric acid from the kidney and increased synthesis of uric acid.

Decreased renal clearance – (90% of patients)

• Intrinsic kidney disease
• heart disease causing decreased blood flow to the kidney
• drugs (loop diuretics, low dose aspirin, cyclosporin)
• genetic predisposition
• age related decrease in glomerulofiltration rate

Increased uric acid synthesis

• Dietary indiscretions
• Genetic predisposition
• Increased tissue turnover-tumors, lymphoproliferative disorders
• Stress induced increased turnover of ATP
• Alcohol induced turnover of ATP

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All patients should be encouraged to modify their lifestyle including limiting alcohol intake, encouraging weight loss where appropriate and decreasing food rich in purines. Co-morbid medical conditions should also be controlled including hypertension, diabetes and hyperlipidemia.

Foods High in Purines

• Very High – Hearts, herring , mussels, yeast , smelt, sardines, sweetbreads
• Moderately High – Anchovies, grouse,mutton, veal, bacon, liver salmon, turkey, kidneys, partridge, trout, goose, haddock, pheasant, scallops

Medication Options for Uric Acid Lowering

It is important to note that whenever starting a uric acid lowering treatment, there is a risk of precipitating a gout flare. A plan should be in place for management if this occurs. This generally can be avoided with the co-administration of prophylactic medications (steroids, colchicine, NSAIDs) along with the uric acid lowering therapy.

Probenecid

Probenecid may be given to patients with decreased clearance of uric acid by the kidney and normal renal function. In general its use should be limited to patients under the age of 60. Probenecid acts by inhibiting reabsorption of uric acid in the proximal tubules of the kidney. Starting dose is at 500 mg to 1000 mg daily and increased to 1500 mg to 2000 mg as needed. Occasionally higher doses are needed. Probenecid may precipitate renal stone formation and good oral hydration should be encouraged. Probenecid is contraindicated in patients with renal stones (including calcium and uric acid stones) and in patients with urate nephropathy. Probenecid given inappropriately to patients with hyperuricemia due to overproduction of uric acid can cause renal stones and urate nephropathy.

• uricosuric
• decreases uric acid reabsorption at the proximal renal tubules
• useful in patients with decreased renal clearance of uric acid
• can only be used if creatinine clearance >40 cc/min
• must have 24 hour urine for uric acid <800 mg/dl
• can be used in renal failure
• increased risk of renal stones

Allopurinol

Allopurinol is a well tolerated, inexpensive, and commonly used uric acid lowering agent. Allopurinol can be started at doses as low as 100 mg daily (100 mg qod if creatinine clearance < 10 cc/min) and titrated by 100 mg every 10-14 days to achieve a serum uric acid level of 4-5 mg/dl. Liver tests, blood counts, and renal function and should be monitored while on therapy. Toxicites include rash, hepatoxicity, bone marrow suppression and severe hypersensitivity reactions. Medication interactions can occur with allopurinol, warfarin, and theophylline and levels should be monitored. Allopurinol should be avoided in patients on azathiprine, 6-mercaptopurine and cyclophosphamide because of risk for bone marrow toxicity.

• xanthine oxidase inhibitor
• prevents production of uric acid
• useful in both patients with increased synthesis and decreased clearance of uric acid
• no 24 hour urine needed
• can be used in renal failure
• rarely associated with bone marrow suppression, hepatotoxicity, and hypersensitivity reactions

Febuxostat

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In 2009, the FDA approved the use of a new xanthine oxidase inhibitor, febuxostat, for the treatment of hyperuricemia in gout. It has demonstrated a dose-dependent decreasee in serum uric acid (daily doses 80mg or 120mg). Its efficacy has been demonstrated in patients with mild or moderate renal impairment and gout. However, it can cause abnormalities in liver function tests and routine monitoring of bloodwork is recommended. Similar to allopurinol, there are interactions of febuxostat with azathioprine, 6MP, and theophylline.

• xanthine oxidase inhibitor
• prevents production of uric acid
• useful in both patients with increased synthesis and decreased clearance of uric acid
• can be used in mild-moderate renal impairment
• rarely associated with bone marrow suppression and hepatotoxicity

Pegloticase

Uricase is an enzyme that converts poorly soluable urate (uric acid) to the more soluable allantoin (excreted in the urine). Uricase is present in most mammals, and these mammals with uricase do not develop gout. However, humans and some primates lack uricase (because of evoluationary gene inactivation) and lack the ability to make uric acid more soluable and hence, have gout. Pegloticase is a porcine uricase which was approved by the FDA in September 2010 for the treatment of gout in patients who have failed conventional therapy.

Pegloticase is administered by intravenous infusion every 2 weeks. Patients should be treated prophylactically for allergic reations to the infusion with steroids and anti-histamines and monitored closely for the development of an infusion reaction. Caution should be used in prescribing this treatment in patients with a known cardiac history.

• pegylated porcine uricase
• useful in both patients with increased synthesis and decreased clearance of uric acid
• increases solubility of uric acid
• patients should be pre-medicated prior to infusions and monitored for allergic reactions
• caution should be used in patients with known cardiac history

Treatment: Lifestyle

Nutrition / Body Composition

Avoidance of purine rich foods and alcohol may help lower uric acid levels and prevent significant fluctuations in serum uric acid that may precipitate acute attacks. Obesity and increased fat distribution are risk factors for gout.

Eating a healthy balanced diet of low-fat proteins, low-fat dairy and vegetables will help maintain a healthy weight which is beneficial for the prevention of gout attacks as well.

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