Asymptomatic hyperuricemia: are we passing the problem?

Abstract

Hyperuricemia is a laboratory phenomenon of persistent increase in serum uric acid concentration (above 420 μmol/l). This condition precedes gout, but only in every 5 cases does hyperuricemia develop into gout. The main pathogenic factor in this disease is not uric acid, but the enzyme xanthine oxidase. In treatment, it is important to block it as a source of free radicals, and then we can improve the prognosis in patients. Today, there is no doubt about the association of hyperuricemia with obesity, metabolic syndrome, diabetes, heart failure, hyperlipidemia and hypertension. For example, hypertension in healthy patients occurs with a frequency of 6.39 %, with hyperuricemia, this figure increases to almost 50 %, and in patients with gout – up to 73.9 %. Asymptomatic hyperuricemia is not considered treatable, although ultrasound studies have shown that sodium monourate crystals (MUN) are deposited in soft tissues and joints. Their presence is a marker of asymptomatic hyperuricemia. Therefore, experts have recently begun to talk about a new stage of gout. If earlier we listed asymptomatic hyperuricemia, acute gout attack, intermittent gout and chronic tofus gout, now we are talking about an additional second stage - asymptomatic hyperuricemia with the deposition of MUN crystals. The path from hyperuricemia to chronic gout can take up to 11 years, but after 4 years can develop kidney damage and decreased glomerular filtration rate, after 6 years - hypertension, and after 10 years – heart failure. So is it worth waiting for the development of chronic gout or perhaps you should start treatment for hyperuricemia earlier?