1032 is an article reporting that 86% of patients with gout have metabolic syndrome (15). As discussed in this report, this difference in prevalence may reflect a difference between diverse ethnic populations. Our results were remarkably sim- ilar to the results of that of the single-center study (7), and they suggest that gout is associated with metabolic syn- drome as there is a much higher prevalence of metabolic syndrome in patients with gout than in the general popula- tion. This is true even when comparing with a study from a middle-aged Korean population (17.6%) (16), which age distribution may match the gout-prevalent ages. The major- ity of patients with gout (>70%) had at least two metabolic risk factors, suggesting that these patients may have a higher risk for cardiovascular complications than normal individuals. Obesity (or hypertension) may have stronger effects on the development of metabolic syndrome in gout than the other components. However, the urate levels, and more importantly, alcohol consumption did not have significant effects on the occurrence of metabolic syndrome in patients with gout. This has significance in terms of the effects of alcohol on the lipid levels. Alcohol consumption has been recently confirmed to have an effect on the development of gout (17). Also, such alcohol consumption could lead to higher triglyceride levels and lower HDL levels, which may lead to an increased preva- lence of metabolic syndrome. However, this was not the case in our study. Because the prevalence of metabolic syndrome did not differ across the levels of alcohol consumption, and also because the triglyceride and HDL variables, even when they were adjusted for alcohol consumption, remained sig- nificant on the multivariate analysis, the effects of alcohol on metabolic syndrome in patients with gout does not seem to be significant. As the effects of alcohol consumption on the development of metabolic syndrome or insulin resistance are not consistent, as was shown in previous studies (18-22), interpretation of our results should be done cautiously. We give the meanings that alcohol consumption did not influ- ence metabolic factors such as lipid levels to make more cases of the metabolic syndrome, and so did not confound us that gout has more individuals with metabolic syndrome through alcohol consumption. Although gout seems to be associated with metabolic syndrome due to its higher prevalence, serum urate did not play a significant role in the development of metabolic syndrome in our patients. This might have hap- pened due to the fact that many of the patients should have been on hypouricemic therapy, and more importantly, since virtually all patients with gout are hyperuricemic, it may be expected to have made no differences. However, uric acid was included in the model for the purpose of controlling for possible confounding, and the results are the same without the urate variable. Therefore, a more generalized case-control study might indicate the significance of uric acid in metabolic syndrome. There is a study that uric acid is related to the components of the metabolic syndrome in the Korean pop- ulation. (23) Y.H. Rho, S.J. Choi, Y.H. Lee, et al. This study might have some weakness, as there were 7 cases (4.2%) missing from the waist data and 2 cases (1.2%) missing from the blood pressure data. However, as the miss- ing values were negatively coded, these should not have had an influence on our conclusions. The significance of obesity and HDL as the strongest positive and negative factors for metabolic syndrome in gout patients should be revalidated and if it is so, this may give insights into the development of hyperuricemia and gout and hopefully, lead to its effective management. Obesity, as well as low HDL levels combined with hypertriglyceridemia are suggested to be associated with insulin resistance (24-26), and as they were the variables with the strongest effects on metabolic syndrome in patients with gout, our data indicates that gout (or hyperuricemia) is more related with dyslipidemia and obesity rather that hypergly- cemia or hypertension. As patients with gout are essentially a subgroup of hyperuricemic individuals, larger samples are needed to generalize to, or to compare with the asymptomatic hyperuricemic individuals, who in fact represent the major- ity of the hyperuricemic population. The results from such studies may give more perspectives on the development of hyperuricemia. REFERENCES 1. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Cir- culation 2002; 106: 3143-421. 2. Cigolini M, Targher G, Tonoli M, Manara F, Muggeo M, De Sandre G. Hyperuricaemia: relationships to body fat distribution and other components of the insulin resistance syndrome in 38-year-old healthy men and women. Int J Obes Relat Metab Disord 1995; 19: 92-6. 3. Bonora E, Targher G, Zenere MB, Saggiani F, Cacciatori V, Tosi F, Travia D, Zenti MG, Branzi P, Santi L, Muggeo M. Relationship of uric acid concentration to cardiovascular risk factors in young men. Role of obesity and central fat distribution. The Verona Young Men Atherosclerosis Risk Factors Study. Int J Obes Relat Metab Disord 1996; 20: 975-80. 4. Rathmann W, Funkhouser E, Dyer AR, Roseman JM. Relations of hyperuricemia with the various components of the insulin resistance syndrome in young black and white adults: the CARDIA study. Ann Epidemiol 1998; 8: 250-61. 5. Emmerson B. Hyperlipidaemia in hyperuricaemia and gout. Ann Rheum Dis 1998; 57: 509-10. 6. Fam AG. Gout, diet, and the insulin resistance syndrome. J Rheuma- tol 2002; 29: 1350-5. 7. Rho YH, Choi SJ, Lee YH, Ji JD, Choi KM, Baik SH, Song GG. Prevalence of the metabolic syndrome in patients with gout. J Kore- an Rheum Assoc 2004; 11: 349-57. 8. Wallace SL, Robinson H, Masi AT, Decker JL, McCarty DJ, Yu TF. Preliminary criteria for the classification of the acute arthritis of pri- mary gout. Arthritis Rheum 1977; 20: 895-900.