[Gout and comorbidities associated with hyperuricemia].

Ann Acad Med Stetin

Katedra i Klinika Reumatologii i Układowych Chorób Tkanki Łacznej Uniwersytetu Medycznego w Lublinie ul. Jaczewskiego 8, 20-954 Lublin.

Published: May 2011

Gout is a condition presenting with inflammatory arthritis caused by crystallization and phagocytosis of monosodium urate in synovial fluid. It is the most common form of arthritis in men above the age of 40 years. Four clinical stages of gout have been distinguished: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout, and chronic gout. Experimental and epidemiologic studies provide growing evidence that hyperuricemia is not only the driving force behind symptoms attributed to the deposition of monosodium urate in the musculoskeletal system but also the important etiological factor in common morbidities of modern societies such as arterial hypertension, cardiovascular disease, chronic kidney disease, and type 2 diabetes mellitus. Today, the majority of gout cases demonstrate clinical features of the metabolic syndrome. Recommendations of the European League Against Rheumatism (EULAR) published in 2006 address key issues in the diagnosis of gout, as well as in the nonpharmacologic and pharmacologic management with regard to the clinical condition and comorbidities of the individual patient. Routinely used antihyperuricemic drugs include allopurinol, colchicine, and uricosuric agents. New agents have recently been introduced into clinical practice, like pegylated uricase and febuxostat, a nonpurine inhibitor analog of xanthine oxidase. Thus, novel therapeutic options are now available to combat this chronic illness which often leads to significant disability.

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