Key Points • There are a number of in vitro and in vivo models supporting a complex potential relation of hyperuricemia to both cardiovascular and renal outcomes. • Definitive evidence…
Key Points • By far the majority of calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is an idiopathic/sporadic disease with onset in later life, but early-onset familial disease also occurs….
Key Points • Despite the growing prevalence of gout, only a few studies have examined the overall impact of gout on patient’s health-related quality of life (HRQOL). HRQOL refers to…
Key Points • Uricolytic therapy with uricase (urate oxidase) degrades uric acid, ultimately resulting in the production of allantoin, which is much more soluble and readily excreted in the urine…
Key Points • Gout attacks (also called “flares”) are commonly precipitated by factors that induce rapid rise (e.g., diet and alcohol excess, intensive diuresis for congestive heart failure) or decline…
Key Points • Comprehensive management of gout involves identifying and addressing comorbid cause(s) of the hyperuricemia, treating and preventing attacks of gouty inflammation, and lowering serum urate to an appropriate…
Key Points • Xanthine oxidase is a critical enzyme in the metabolism of purines to uric acid. Both allopurinol and febuxostat reduce serum urate concentration through inhibition of xanthine oxidase….
Key Points • Surprisingly, instances of suboptimal treatment of gout remain frequent, even in this era of expanded and well-understood treatment options. These include errors in medication use and dosages…
Key Points • Lifestyle and dietary modifications can influence serum urate levels and the risk of gout and are the only acceptable options when urate-lowering medications are not yet indicated…
Key Points • Inefficient renal excretion of uric acid is the most common cause of hyperuricemia in gout patients. • Uricosuric drugs tend to normalize renal excretion of uric acid…
