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Chapter 13
Agents Used to Treat Hyperuricemia and Gout
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Copyright 2007 Thomson Delmar Learning, a division of Thomson Learning Inc. All rights reserved.
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Gout
Gout is a metabolic disease associated with the development of high uric acid in the blood.
It is a metabolic defect and is not caused by excessive intake of meat and alcohol.
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Uric Acid
Uric acid is formed from the breakdown of proteins.
The accumulation of uric acid causes a problem in the joints and kidneys:
Kidney stones Kidney failure Gouty arthritis Hyperuricemia
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Acute Attacks
Acute attacks of gout are treated with: Nonsteroidal anti-inflammatory drugs
(NSAIDs) Corticosteroids Colchicine: intravenously or orally
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Agents Used
Corticosteroids and NSAIDs actions Produce anti-inflammatory effects Produce analgesic effects
Colchicine’s action is unclear Reduces leukocyte production of lactic acid Reduces phagocytic activity
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Colchicine
Not a first-line agent because of its adverse side effects
(continues)
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Colchicine
Major adverse effects: Nausea, vomiting, and diarrhea Gastrointestinal bleeding Neuritis Myopathy Alopecia Bone marrow depression
(continued)
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Long-term Control
Most commonly used agent for gout: Allopurinol: prevents formation of uric acid
Adverse effects: hepatotoxicity and skin rash
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Gouty Arthritis
Most commonly used agent NSAIDs
Indomethacin (Indocin) Naproxen (Aleve) Sulindac (Clinoril)
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Uricosuric Agents
Increase excretion of uric acid Probenecid (Benemid)
Side effects• Headaches• Dizziness
(continues)
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Uricosuric Agents
Sulfinpyrazone (Anturane) Side effects
• Nausea and vomiting• Diarrhea
(continued)
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Therapeutic Effects
Monitor for: Decreased inflammation Decreased pain Ease of movement
Monitor lab values of uric acid Monitor urine output