Gouty attacks

In elderly patients, gouty attacks may be atypical with insidious onset and polyarticular, often involving hand or wrist joints. 

The major side effects of allopurinol are skin rash, urticaria, leukopenia, GI problems, headache, and increased frequency of acute gouty attacks with the initiation of therapy. An allopurinol hypersensitivity syndrome characterized by fever, eosinophilia, dermatitis, vasculitis, and renal and hepatic dysfunction occurs rarely but is associated with a 20% mortality rate. 

Hyperuricemia - Hyperuricemia may occur or acute gout may be precipitated in certain patients receiving thiazides, even in those patients without a history of gouty attacks. 

Gout Do not start therapy until an acute gouty attack has subsided. However, if an acute attack is precipitated during therapy, probenecid may be continued. Give full therapeutic doses of colchicine or other appropriate therapy to control the acute... 

Probenecid and sulfinpyrazone are uricosuric drugs employed to decrease the body pool of urate in patients with tophaceous gout or in those with increasingly frequent gouty attacks. In a patient who excretes large amounts of uric acid, the uricosuric agents should not be used. 

Pyrazinamide and ethambutol may cause urate retention and gouty attacks. 

Acute gouty attacks can result from a number of conditions, includ- Figure 39.14... 

There are varying opinions on when prophylactic treatment should be initiated after an attack of gout. It is usually recommended that if a patient experiences two or more gouty attacks per year, long-term hypouricaemic agents should be considered. 

Hyperuricemia Thiazide diuretics, furosemide Gouty attack... 

Electrolyte imbalances K+, i Mg +, i Na+, i Cl, T uric acid reabsorption in the proximal tubules can precipitate gouty attacks. Other side effects include rash, T glucose, dizziness, photosensitivity, i BP, headache, T lipids. 

C This patient is a candidate for allopurinol. Allopurinol is the drug of choice for patients with renal impairment. Probenecid is not recommended for patients with a CrCI rate of less than 50 mL/min. Indomethacin, ibuprofen, and colchicine are agents to treat acute gouty attacks. 

Wait until acute gouty attack has subsided. 

A second aspect of the precipitation of acute attacks of gout is related to the inflammatory reaction produced by the injection of sodium urate crystals. The historical background for believing that such materials are related to the occurrence of acute attacks is reviewed by McCarty (MIO). Since synovial fluid from patients with acute attacks contains micro-crystalline sodium urate, it appeared reasonable to believe that the presence of these crystals would cause gouty attacks. A number of investigators showed that administration of a microcrystalline sodium urate resulted in attacks in normal human subjects, in dogs, and in gouty patients in a quiescent phase (FI, H12, M4). 

Allopurinol is the antihyperuricemic drug of choice in patients with a history of urinary stones or impaired renal function, in patients who have lymphoproliferative or myeloproliferative disorders and need pretreatment with a xanthine oxidase inhibitor before initiation of cytotoxic therapy to protect against acute uric acid nephropathy, and in patients with gout who are overproducers of uric acid. The major side effects of allopurinol are skin rash, leukopenia, occasional gastrointestinal toxicity, and increased frequency of acute gouty attacks with the initiation of therapy. An allopurinol hypersensitivity syndrome characterized by fever, eosinophilia, dermatitis, vasculitis, and renal and hepatic dysfunction is a rare side effect, but is associated with a 20% mortality rate. ... 

Colchicine A tricyclic, water-soluble alkaloid isolated from the autumn crocus. Colchicine will inhibit miCTotubule formation and inhibit phagocytosis of urate crystals, thus preventing the inflammatory events associated with a gouty attack. 

Ingestion of alcohol is traditionally considered a predisposing or precipitating factor in the gouty attack Studies performed in man by Lieber et al. (1962) have shown that the administration of ethanol provokes an increase in the serum concentration of uric acid, which was attributed to a decrease in its renal excretion More recently, ethanol infusion has been shown to enhance the production of uric acid by the liver, as measured from arteriovenous concentration differences during hepatic catheterisation in human volunteers (Grunst et al, 1973) ... 

The survey of cases of gout with renal involvement in relation to blood pressure (Table IV) revealed, in the hypertensive secondary renal gout, an earlier age of onset a higher incidence of females a predominance of the acute clinical type and a higher incidence of gouty attacks caused by the admin Istration of diuretic drugs. On the contrary. In the normotensive group, uric acid renal lithiasis and diabetes were more frequent, which confirms the non-specificity of these parameters. 

Kidney transplant was performed In 8 patients of the normo-tenslve group, In whom the hyperuricemia and gouty attacks disappeared. 

Although the etiologic role of microcrystalline monosodium urate monohydrate in the pathogenesis of acute gouty arthritis has been well established, the mechanism by which urate precipitates in joints, soft tissues and the kidneys remains unclear. Some studies have suggested that the solubility of urate is the key factor and that when the solubility of urate in blood synovial fluid and urine is exceeded, urate then precipitates. The question is more complex than this, however, since only approximately 25 per cent of patients with hyperuricemia develop acute gouty arthritis. Furthermore, there is poor correlation between uric acid concentration and the frequency of acute gouty attacks. This has led to speculation that there are factors in serum which are partially responsible for solubilization of urate and that alterations in these factors could be responsible for urate deposition. 

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