Agents for Acute Gout

HPI KM is a 57-year-old man who presents with severe pain in his right great toe. He states that the pain was first noticeable 2 days ago. This was several days after he stubbed his toe on the leg of the dining room table. He awoke at 3 A.M. with excruciating pain. His toe is swollen, red, and tender to the touch. He states that the pain is constant and does not go away. This is KM s second attack, the first attack occurring 7 months ago, which was successfully treated. The fluid aspirated from the joint is positive for urate crystals. PMH HTN, asthma, family history of gout. Medications Hydrochlorothiazide, beclomethasone inhaler, albuterol inhaler. 

Labs Serum uric acid 11 mg/dL. All other labs within normal limits. 

Uric acid, an end product of protein catabolism, was identified as the cause of gout in the middle of the 19th century. Patients with primary hyperuricemia have elevated serum uric acid levels because of increased production of uric acid or impaired renal excretion of uric acid. 

Overproduction of uric acid can occur due to excessive de novo purine synthesis, excessive dietary purines, or the conversion of tissue nucleic acid to purine nucleotides. When these purines are metabolized, the by-products are converted to uric acid by the enzyme xanthine oxidase. Increased levels of uric acid result if the overproduction exceeds excretion. Underexcretion of uric acid can be due to defects in the renal tubular mechanisms that regulate uric acid levels in the body, causing decreased filtration, decreased secretion, or increased reabsorption. 

Acute attacks of gout are a result of urate crystal deposits in the synovium of joints. Crystal formation is dependent on a constellation of factors, including the degree of hyperuricemia, physical state of the joint, and presence of synovial fluid. Urate crystals present in the joint space can trigger an acute inflammatory response. Prostaglandins 

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