URATE CRYSTAL DEPOSITIONS ARE ASSOCIATED WITH INFLAMMATORY MARKERS AND CAROTID PLAQUES INDICATING SUBCLINICAL INFLAMMATION IN GOUT; BASELINE RESULTS FROM THE NOR-GOUT STUDY
Authors: H. B. Hammer et al.
Gout may be associated with atherosclerotic disease which might be related to low-grade inflammation. Calprotectin is a major granulocyte protein reflecting the level of systemic inflammation.
The baseline data from NOR-GOUT, a prospective study of patients with crystal-proven gout with increased serum urate levels (>360 μmol/L), were used. In all patients sum scores of the ultrasound elementary lesions for MSU depositions (bilateral assessment of wrist, MCP2, knee, ankle, MTP1 and insertions of triceps, quadriceps, proximal/distal patellar and Achilles tendons) were calculated and the associations with calprotectin, CRP level, carotid plaques and carotid intima-media thickness (cIMT) in bilateral B-mode US was explored.
Significant correlations were found between the MSU depositions and the inflammatory markers as well as cIMT.
In asymptomatic gout patients, higher load of MSU crystal depositions was associated with increased levels of inflammatory markers, cIMT and the presence of atherosclerotic plaques in the carotid arteries. This may indicate that crystal depositions cause subclinical inflammation with subsequent systemic implications. These findings demonstrate once more that treatment of hyperuricemia in patients with gout is essential to prevent or reverse urate crystal deposition. Optimal therapy not only prevents gouty attacks but also could prevent atherosclerotic disease.