Objective. Atherogenic serum lipid profile possesses pro-inflammatory properties and is associated with more active RA. While prevalent in patients with gout, whether atherogenic lipid profile is associated with gouty flares is unknown. This study aims to investigate whether atherogenic serum lipid predicts gouty flares in patients with gout. Methods. Adult patients (age >21 yrs) who suffered from gout were prospectively followed between September 2006 and November 2007 and their demographic, clinical and laboratory data were collected. Episodes of gouty flares over this observation period were recorded and factors predictive of gouty flares were studied by regression models. Results. Of the 100 patients, 80 were men, 65 were ethnic Chinese, 31 were Malay and the rest were Indian and Caucasian. The mean age and duration of gout (±S.D.) were 61.9 ± 14.0 and 6.6 ± 7.8 yrs, respectively. The mean serum uric acid and creatinine levels were 537.6 ± 142.8 and 173.6 ± 119.9 μmol/l, respectively. In univariate analysis, longer duration of gout, higher adjusted mean serum creatinine, lower adjusted mean fasting serum, total cholesterol and high-density lipoprotein cholesterol (HDL-C) levels were associated with gouty flares. After adjustment for potential confounders in multivariate regression models, longer duration of gout and lower adjusted mean fasting serum HDL-C level remained independently predictive of gouty flares. Conclusions. Low serum high-density lipoprotein cholesterol level was an independent predictor for gouty flares. Whether optimizing serum HDL-C level can benefit patients with gout in terms of reducing gouty flares needs to be addressed by controlled trials. © The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved.
CITATION STYLE
Mak, A., Ho, R. C. M., Tan, J. Y. S., Teng, G. G., Lahiri, M., Lateef, A., … Feng, P. H. (2009). Atherogenic serum lipid profile is an independent predictor for gouty flares in patients with gouty arthropathy. Rheumatology, 48(3), 262–265. https://doi.org/10.1093/rheumatology/ken471
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