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Irene Petrides, PharmD

Management and Treatment of Gout

2016 07 15 8 42 15Gout is a syndrome of acute or chronic recurrent arthritis and pain. The incidence of this condition continues to rise with increasing age. Therefore, this condition is a common comorbidity for many hospice patients. Reviewing the characteristics of gout and how to most appropriately manage this condition can help us to also best manage our hospice patients.  

Gout is characterized by having chronic hyperuricemia. Hyperuricemia is defined as having urate levels greater than 6.8 mg/dl which is considered the level at which the physiological saturation threshold is exceeded.5 Hyperuricemia is the result of overproduction or underexcretion of uric acid. Increased production of uric acid is less common but is seen in myeloproliferative disorders or lymphoproliferative disorders.1 The risk of developing gout can be associated with medications, renal disease, obesity, and hypothyroidism.2 Medication that are most frequently associated with gout are thiazide and loop diuretics. Stress, trauma or alcohol ingestion may also result in an acute gout attack. Due to multiple comorbid conditions with combination of medication use, the elderly have an increased occurrence of developing gout.5

The clinical presentation of an acute gouty attack includes the abrupt onset of joint inflammation causing pain and swelling. This can occur at any time of the day be seems to present most often during the night. Gout commonly affects the first metatarsophalangeal joint and can also affect the feet, ankles, heels, knees wrist, fingers, and elbows. Symptoms include fever, chills, warmth, swelling, erythema, and intense pain of the involved joint.2 An untreated, mild gout attack will usually subside within 3 to 10 days. However, nephrolithiasis, nephropathy, or urate deposits in affected joints can occur in severe cases.1 Treatment of an acute gout attack should start immediately following symptoms and include the use of nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and/or corticosteroids.2

Due to excellent efficacy NSAIDs are considered first line therapy for gout management. Indomethacin, naproxen, and sulindac are approved for labeling by the Food and Drug administration for the treatment of gout. Note other NSAIDs can be used in the treatment of gout but they do not all have the labeled indication for treating gout. Therapeutic success is based on how quickly the drug is initiated. High dose therapy should be initiated and continued for 24 hours after complete resolution of gout and then taper down over 2 to 3 days. After initiating therapy, resolution of gout should occur within 5 to 8 days.2 NSAIDs should be monitored closely or avoided in patients with cardiovascular disease, severe chronic kidney disease, and peptic ulcer disease. Common adverse effects include gastrointestinal intolerance and worsening of renal function.

Colchicine is a medication which is highly effective at treating an acute gout attack and produces a response within hours of administration. Colchicine should be reserved for patients who are unable to take NSAID therapy. However, if colchicine is not administered within the first 48 hours of onset of an acute attack, then efficacy is substantially diminished.  Abdominal cramping and diarrhea may be reported with colchicine therapy. Recommendation include to start colchicine therapy at initial dose of 1.2mg followed 1 hour later by another 0.6mg and not to exceed 1.8mg on the first day of therapy. Therapy with continue at a dose of 0.6mg daily or twice daily until gout attack resolves.2 Due to multiple drug interactions including lipid lower agents, colchicine should be used with extreme caution due to risk of toxicity. Therefore, colchicine should be avoided in patients with renal or hepatic disease and would not be the drug of choice.

Corticosteroids are reserved for patients where NSAID therapy and colchicine therapy are contraindicated or in patients who do not have clinical response to NSAIDs or colchicine.1,4 Patients with gout in multiple joints may benefit from the use of an oral corticosteroid.2 High dose therapy is initiated at onset of gout for 3 to 5 days and then should be tapered gradually over 10 to 14 days in order to avoid a rebound attack. Although most patients tolerate oral corticosteroids, common adverse effects may include mood changes, flood retention, hyperglycemia and increased blood pressure.5

Allopurinol is indicated for prophylactic therapy. Allopurinol is usually initiated after the first gout attack or after the passage of the first renal stone. If the first gout attack was mild and quickly responded to therapy, allopurinol does not need to be initiated.2 Initial dose of allopurinol is 100mg per day and titrated up 100mg per week to achieve a uric acid level of 6 mg/dL or less with a maximum dose of 800mg per day. Adverse effects include skin rash, leukopenia, gastrointestinal problems, headache and urticarial.4

When treating gout, a comprehensive treatment strategy is required. This includes lifestyle changes including a restricted diet. Comorbidity and medication use need to be taken into account. Initiate immediate treatment of acute gout flares with NSAIDS, colchicine or corticosteroids. When indicated, initiate uric acid lowering therapy (allopurinol) at the proper time usually weeks after an acute flare is subsided. Recognizing the signs and symptoms of gout in a timely manner is the primary contributing factor to a desired therapeutic outcome. The goal of therapy is to reduce pain and disability with minimal adverse effects.


  1. Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi, T. Terkeltaub, R. (2012). 2012 American College of Rheumatology guidelines for management of gout. Part 1: Systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res Arthritis Care & Research, 64(10), 1431-1446.

  2. Khanna D, Khanna PP, Fitzgerald JD, Singh MK, Bae S, Neogi T, Terkeltaub, R. (2012). 2012 American College of Rheumatology guidelines for management of gout. Part 2: Therapy and antiinflammatory prophylaxis of acute gouty arthritis. Arthritis Care Res Arthritis Care & Research, 64(10), 1447-1461.

  3. Edwards N, Sundy J, Forsythe A, Blume S, Pan F, Becker M. (2010). Work productivity loss due to flares in patients with chronic gout refractory to conventional therapy. Journal of Medical Economics, 14(1), 10-15.

  4. Edwards N, Sundy J, Forsythe A, Blume S, Pan F, Becker M. (2010). Work productivity loss due to flares in patients with chronic gout refractory to conventional therapy. Journal of Medical Economics, 14(1), 10-15.

  5. Mandell, BF. (2008). Clinical manifestations of hyperuricemia and gout. Cleveland Clinic Journal of Medicine, 75(Suppl_5).

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