Antigout medications

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Antigout medications


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Antigout medications

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A 57-year-old man comes to the emergency department due to severe right ankle pain. The pain developed overnight and woke him up from his sleep. He has not traveled recently and has no history of recent trauma. Medical history is significant for hypertension, hyperlipidemia, and chronic kidney disease secondary to type II diabetes mellitus. Current medications include metformin, lisinopril and atorvastatin. Family history is significant for osteoarthritis in the patient’s mother. Temperature is 37.0°C (98.6°F), pulse is 90/min, respirations are 18/min, and blood pressure is 140/75 mmHg. Physical examination shows a moderate-sized effusion of the right ankle with surrounding erythema and warmth. Serum creatinine is 3.5 mg/dL. Microscopic examination of the synovial fluid aspirate is shown below. Which of the following best describes the mechanism of action of the drug indicated to treat this patient’s condition?  

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External References

First Aid









for gout p. 477, 500

gout p. 726

kidney stones p. 628

Lesch-Nyhan syndrome p. 35

rash with p. 251


allopurinol and p. 500

Leukemias p. 440

allopurinol for p. 501


allopurinol p. 501

6-mercaptopurine p. 448

allopurinol and p. 501


Antigout medications, as their name implies, are medications used to treat gout, which is a form of inflammatory arthritis.

The underlying cause of gout is hyperuricemia - which is too much uric acid in the blood, resulting in the formation of monosodium urate crystals.

These sharp, needle-like crystals deposit in areas of slow blood flow, such as joint spaces, or kidney filtration tubules.

Antigout medications work by preventing the buildup of uric acid, or by reducing inflammation.

Now, uric acid is a natural waste product of purines, which are one of the building blocks of DNA and RNA.

During their metabolism, purines are first degraded to hypoxanthine, which is then oxidized twice by xanthine oxidase; first to become xanthine, and then finally, to uric acid.

Uric acid circulates in the bloodstream until it reaches the kidneys where it’s secreted into the proximal tubules, and eventually excreted in the urine.

Now, hyperuricemia occurs when levels of circulating uric acid exceed normal levels, which is around 1.5-6 mg/dL for women and 2.5-8 mg/dL for men.

Urate crystal deposition occurs when concentration of circulating uric acid exceeds its rate of solubility, which is about 6.8 mg/dL.

Now, antigout medications are subdivided into two main groups: chronic gout medications, which are used to prevent the buildup of uric acid in the blood; and acute gout medications, which are used to reduce inflammation.

Chronic gout medications include xanthine oxidase inhibitors, such as allopurinol and febuxostat; uricosuric medications, such as probenecid and sulfinpyrazone; and recombinant urate oxidases, such as rasburicase and pegloticase.

On the other hand, acute gout medications include non-steroidal anti-inflammatory drugs (or NSAIDs), glucocorticoids, and colchicine.


  1. "Katzung & Trevor's Pharmacology Examination and Board Review,12th Edition" McGraw-Hill Education / Medical (2018)
  2. "Rang and Dale's Pharmacology" Elsevier (2019)
  3. "Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th Edition" McGraw-Hill Education / Medical (2017)
  4. "DOES COLCHICINE WORK? THE RESULTS OF THE FIRST CONTROLLED STUDY IN ACUTE GOUT" Australian and New Zealand Journal of Medicine (1987)
  5. "2012 American College of Rheumatology guidelines for management of gout. Part 2: therapy and antiinflammatory prophylaxis of acute gouty arthritis" Arthritis Care Res (Hoboken) (2012)
  6. "Colchicine for acute gout" Cochrane Database Syst Rev (2014)
  7. "Febuxostat for the treatment of hyperuricaemia in gout" Expert Opin Pharmacother (2018)

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