Gout is characterized by precipitation of monosodium urate crystals. The precipitations in soft tissue are called tophi. By local pressure, crystal precipitation in and around the joints can cause joint damage as well as acute gout attacks, which are very painful. Gout mainly affects men between the ages of 40-55 years, and postmenopausal women.
Uric acid is the end product of the metabolism of purines, derived from DNA. The enzyme xanthine-oxidase converts purine to hypoxanthine, then to xanthine and finally to uric acid. Uric acid is excreted via the kidney.
Normally, the uric acid production and secretion are in balance. Uric acid levels are below concentrations at which precipitate and crystals are formed. In case of gout, there can be an overproduction of uric acid (10% of the cases) or reduced
renal clearance of uric acid (90% of the cases). Hyperuricemia is associated with obesity, diabetes mellitus, hypertension, renal insufficiency, and drugs (thiazide diuretics, low-dose salicylates) and can be entirely asymptomatic.
Treatment is aimed at prevention and treatment of painful attacks and if present, the elimination of tophi. NSAIDs (indomethacin, diclofenac, naproxen) and colchicine are indicated for acute gout. For the prophylaxis of gout and elimination of tophi xanthine-oxidase inhibitors (allopurinol) or uricosurics can be used.
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Appropriate treatment for acute gouty arthritis in a man with congestive heart failure and renal insufficiency might include:
Extra info: Renal insufficiency is a relative contraindication for the use of allopurinol and due to its side effects (hypertension) also the corticosteroids. Colchicine is a better option, since it is eliminated via the liver. Indomethacin has interactions with many drugs, including anti-coagulants, ACE-inhibitors, β-blockers and diuretics. The patient utilizes probably one or more of these drugs.