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Clin Chem Lab Med 2011;49(5):909–914
2011 by Walter de Gruyter • Berlin • New York. DOI 10.1515/CCLM.2011.124

An increase in serum uric acid concentrations is associated

with an increase in the Framingham risk score in Korean
adults

Ga-Eun Nam1, Kyung-Shik Lee2, Yong-Gyu Park3, Introduction

Kyung-Hwan Cho1, Seung-Hwan Lee1, Byung-Joon
Ko1 and Do-Hoon Kim4,*
1
Department of Family Medicine, Korea University Anam
Hospital, Seoul, Korea
2
Department of Family Medicine, Gachon University Gil
Medical Center, Incheon, Korea
3
Department of Biostatistics, Catholic University of Korea
College of Medicine, Seoul, Korea
4
Department of Family Medicine, Korea University Ansan
Hospital, Ansan-Si, Gyeonggi-Do, Korea
Abstract
Background: Uric acid is a novel cardiovascular disease
(CVD) factor, but its use as an independent risk factor for
CVD remains controversial. Here, we examined the corre-
lation between Framingham risk score (FRS) and serum uric
acid concentrations in asymptomatic Korean adults.
Methods: This cross-sectional study was performed on 8035
Korean adults. Besides FRS, we measured body mass index,
fasting blood glucose, homeostasis model assessment of
insulin resistance, creatinine, g-glutamyltransferase, the lipid
profile, uric acid, high-sensitive C-reactive protein, and the
white blood cell count. All subjects were placed into one of
three risk groups according to their FRS.
Results: All CVD related factors were significantly different
in the three FRS groups. The increments of uric acid in-
creased significantly FRS from the 10-year risk 0%–9%
group to the )10% group after adjusting for other CVD-
related factors using ordinal logistic regression analysis.
Analyses of the three age groups showed similar effects.
Conclusions: An increased uric acid concentration is asso-
ciated with an increase in coronary heart disease risk calcu-
lated from the FRS, and doctors need to pay attention to this
CVD risk in apparently healthy adults with hyperuricemia.
Keywords: cardiovascular disease; coronary heart disease;
Framingham risk score; risk factors; uric acid.
*Corresponding author: Do-Hoon Kim, MD, PhD, Clinical
Assistant Professor, Department of Family Medicine, Korea
University Ansan Hospital, 516, Gojan1-Dong, Danwon-Gu,
Ansan-Si, Gyeonggi-Do, 425-707, Korea
Phone: q82-11-9636-6567, Fax: q82-31-412-5364,
E-mail: kmcfm@hanmail.net
Received August 3, 2010; accepted November 21, 2010;
previously published online February 3, 2011
Coronary heart disease (CHD) is the leading cause of mor-
tality worldwide. Major independent risk factors for this
lethal disease include hypertension, total cholesterol, low
density lipoprotein (LDL) cholesterol and high density lipo-
protein (HDL) cholesterol concentrations, family history of
a first degree relative with cardiovascular disease (CVD),
smoking, and age (1). Reduced glomerular filtration rate and
increased insulin resistance may also be associated with an
increase in CVD risk (2, 3). In addition, serum g-glutamyl-
transferase (g-GT) has emerged as a predictor of cardiovas-
cular morbidity and mortality (4). Inflammatory markers
related to CVD risk in epidemiological studies or clinical
research include high-sensitive C-reactive protein (hs-CRP),
the white blood cell (WBC) count, neutrophil count, cyto-
kines winterleukin (IL)-1, IL-6, IL-8, IL-10, tumor necrosis
factor (TNF)-ax, and endothelial cell markers (VCAM, ICAM,
E-selectin) (5, 6).
The Framingham risk score (FRS) rates a set of key car-
diovascular risk factors to calculate the 10-year risk for
developing CHD. It enables clinicians to estimate cardiovas-
cular risk worldwide (7). In addition, uric acid is increasingly
gaining acceptance as a novel risk factor of CVD (1, 6, 8).
There may be an association between an increase in serum
uric acid (SUA) concentrations and endothelial dysfunction
or subclinical atherosclerosis (9). Also, uric acid could neg-
atively impact the development or progression of CVD by
stimulating inflammatory responses linked to CVD patho-
genesis (6). There is also a statistically significant relation-
ship between hyperuricemia and cardiovascular risk factors
(10). The association seems to be stronger in people with
hypertension or congestive heart failure compared with the
general population (11). The Losartan Intervention For End-
point reduction in hypertension (LIFE) study proposed asso-
ciations between SUA and cardiovascular events in hyper-
tensive women. The Preventive Cardiology Information Sys-
tem (PreCIS) database study demonstrated that SUA pre-
dicted mortality in type 2 diabetic patients (12) and was an
independent predictor of death in patients at high risk of
CVD (13). However, whether uric acid is an independent
cardiovascular risk factor remains controversial (14).
Past research on the association between SUA concentra-
tions and cardiovascular risk found that an increase in uric
acid is associated with an increased FRS even after adjusting
for well-known cardiovascular risk factors, such as creati-
nine, triglycerides, and hs-CRP (1). However, this study was
confined to subjects aged 65 and above. In Asia-Pacific
regions, including South Korea, several studies have been

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910 Nam et al.: Uric acid and Framingham risk score
conducted on the relationship between SUA concentrations
and the metabolic syndrome (15, 16), a serious cardiovas-
cular risk factor (17). However, no research has been per-
formed on the relationship between SUA concentrations and
CVD risk based on FRS in Korean populations. Here, we
assessed the relationship between SUA concentrations and
the 10-year risk for developing CHD using FRS in healthy
South Korean adults with a wide range of ages.
Materials and methods
Study population
We examined 12,468 Koreans, aged 20–79 years, who were self-
referred and underwent routine health check-ups at the Center for
Health Promotion in the Korea University Anam Hospital located
in Seoul, South Korea, from March 1, 2007, to March 31, 2009.
The subjects filled out self-administered questionnaires. Both smok-
ers and non-smokers were included in this study. Subjects whose
anthropometric measures or blood chemistry results were omitted,
those who did not indicate their medical history and health behavior,
those who were on medication for gout or hyperlipidemia or had
been diagnosed with a CVD, such as CHD or stroke, those who had
been diagnosed with hypertension or diabetes mellitus previously,
and those with health evaluation results suggesting malignancies,
hepatic or renal diseases, acute infections or inflammatory diseases
were excluded. The final study population included 8035 adults
aged 20–79 years. All study participants gave informed written con-
sent, and this study was approved by the Institutional Review Board
at the Korea University Anam Hospital.
Anthropometric measurements
The subjects’ heights and weights were measured and body mass
index (BMI) was calculated using the formula wweight (kg)/height
(m)2x. Blood pressure was measured at the upper arm with an auto-
matic blood pressure monitoring device (MP800, MEKICS, Chun-
cheon, Korea) after subjects had rested for at least 10 min.
Blood chemistry
Before collection of blood, each subject was asked to fast for 10 h
or more. After overnight fasting, a venous blood sample was
obtained between 08:00 and 09:00 am to measure SUA concentra-
tions, fasting blood glucose, creatinine, g-GT, total cholesterol, tri-
glycerides, HDL, LDL cholesterol, hs-CRP, serum insulin, and the
WBC count.
The serum uric acid, creatinine, total cholesterol, triglycerides,
LDL, HDL cholesterol, fasting glucose, and hs-CRP concentrations
were measured using an automated analyzer, TB200FR (Toshiba
Co., Otawara, Japan). SUA concentrations were measured using the
uricase method and fasting blood glucose was measured with the
hexokinase method. Serum creatinine concentrations were measured
using the kinetic alkaline picrate method, and g-GT was measured
using the JSCC (Japan Society of Clinical Chemistry) method. Total
cholesterol and serum triglycerides were measured using enzymatic
colorimetric tests. HDL cholesterol was measured by the selective
inhibition method and LDL cholesterol by a homogenous enzymatic
colorimetric assay. hs-CRP was determined optically by latex agglu-
tination. Fasting insulin concentrations were measured using an
immunoradiometric assay with the INS-IRMA kit (Diasourse,
Nivelles, Belgium) and the WBC count was determined using flow
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cytometry (XE2100; Sysmax, Kobe, Japan). Insulin resistance (IR)
was determined using the homeostasis model assessment of insulin
resistance (HOMA-IR)swfasting insulin (mU/mL)=fasting plasma
glucose (mmol/L)x/22.5 (18).
Definition of the FRS
We used the FRS calculation method described in the Adult Treat-
ment Panel (ATP) III Guidelines announced by the United States
National Cholesterol Education Program (NCEP) (7). Calculation of
the total risk score took into consideration risk factors, such as age,
total cholesterol and HDL cholesterol concentrations, systolic pres-
sure, and whether any anti-hypertensive treatments were prescribed
or any cigarettes had been smoked in the past month. Those subjects
with a 10-year risk below 10%, between 10% and 20%, and above
20% were stratified into the low-risk group, the intermediate-risk
group, and the high-risk group, respectively.
Statistical analysis
Statistical analysis was performed using SAS for Windows (Version
9.1, SAS Institutes Inc., Cary, NC, USA) and two-sided p-values of
-0.05 were considered statistically significant. The social-demo-
graphic, anthropometric, and hematological characteristics of the
subjects are presented as means"standard deviatio (SD), median
(interquartile range) or frequencies. One-way analysis of variance
(one-way ANOVA) with Scheffe’s test, or Kruskal-Wallist test with
Dunn’s post-hoc test was applied to compare the means of cardio-
vascular risk factors as well as SUA concentrations between CHD
risk groups stratified according to the FRS. Ordinal logistic regres-
sion analysis was performed to assess the impact of novel cardio-
vascular risk factors, such as SUA concentrations on the FRS
groups. In addition, subjects were classified into three age groups
(20–39, 40–64, and 65 years or older), and the impact of SUA
concentrations on the FRS groups in each age group was assessed
by means of ordinal logistic regression analysis. Odds ratios were
calculated for every increment of 0.1 mg/dL of creatinine, 1 mg/dL
of uric acid, 1 mg/mL of hs-CRP, 1 kg/m2 of BMI, and for every
increment of 10 years of age or 10 units of LDL cholesterol, tri-
glycerides, g-GT, and the WBC count.
Results
Distribution of subjects based on FRS
Of the 8035 subjects, 4480 subjects (55.8%) were male and
3555 subjects (44.2%) were female. The average age was
47.5"12.1 years. Subjects were stratified based on 10-year
CHD risk values calculated from the FRS into the low-risk
group (0%–9%), the intermediate-risk group (10%–20%),
and the high-risk group (21% or above). The low, interme-
diate, and high-risk groups contained 82.5% (6626), 16.4%
(1316), and 1.2% (93) of the subjects, respectively (Table 1).
Means of cardiovascular risk factors of three risk
groups based on FRS
BMI, WBC count, and the concentrations of LDL cholester-
ol, triglycerides, creatinine, HOMA-IR, g-GT, uric acid and
hs-CRP all showed significant differences between the three
risk groups (p-0.001; Table 2).
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Nam et al.: Uric acid and Framingham risk score 911

Table 1 Distribution of 8035 study subjects by Framingham risk groups.

Low-risk group Intermediate-risk group High-risk group Total

(0%–9%) (10%–20%) (G21%)
Male, n (%) 3130 (69.9) 1263 (28.2) 87 (1.9) 4480 (100)
Female, n (%) 3496 (98.3) 53 (1.5) 6 (0.2) 3555 (100)
Total, n (%) 6626 (82.5) 1316 (16.4) 93 (1.2) 8035 (100)

Odds ratios for individual cardiovascular risk factors
in relation to 10-year CHD risk groups
The odds ratios for individual cardiovascular risk factors in
Table 3 indicate the risk that a 10-year CHD risk based on
FRS will increase from the 0–9 range to a 10 or above.
Likewise, Table 4 shows odds ratios for individual cardio-
vascular risk factors to indicate the risk of increasing a
10-year risk from the 0–20 range to 21 or above.
The odds ratio of progressing from the low-risk group to
the intermediate-risk group and beyond was 1.169 (95% CI:
1.159–1.180, p-0.001) for age, 1.013 (95% CI: 1.010–
1.015, p-0.001) for LDL cholesterol, 1.004 (95% CI:
1.004–1.005, p-0.001) for triglycerides, 1.649 (95%
CI: 1.562–1.740, p-0.001) for creatinine, 1.003 (95% CI:
1.002–1.004, p-0.001) for g-GT, 1.246 (95% CI:
1.164–1.333, p-0.001) for uric acid, 1.012 (95%
CI: 0.997–1.027, ps0.128) for hs-CRP and 1.315 (95% CI:
1.250–1.383, p-0.001) for the WBC count (Table 3). In
other words, each increment in LDL cholesterol, triglycer-
ides, creatinine, g-GT, and uric acid, as well as in WBC
count, significantly increased the risk of progressing from
the low-risk group to the intermediate-risk group and
beyond. Furthermore, increases in the concentrations of LDL
cholesterol, triglycerides, creatinine, g-GT, and WBC count
significantly increased the risk of progressing from the low-
and intermediate-risk groups to the high-risk group (Table 4).
After adjusting for age and other cardiovascular risk fac-
tors, such as BMI, LDL cholesterol, triglycerides, creatinine,
HOMA-IR, g-GT, hs-CRP, and WBC count, we discovered
that additional increments in SUA concentration increased
the risk of progressing from the low-risk group to the inter-
mediate-risk group and beyond at a statistically significant
level (Table 3).
Relationship between uric acid concentrations and
FRS by age group
The odds ratios for risk that every increment of 1 mg/dL in
the SUA level increase the FRS from the low-risk group to
the intermediate-risk group and beyond are 1.323 for 20–39-
year-olds (95% CI: 1.054–1.660, ps0.016), 1.118 for
40–64-year-olds (95% CI: 1.039–1.204, ps0.003), and
1.268 for 65-year-old and older (95% CI: 1.078–1.490,
ps0.004) (Figure 1). These results demonstrate statistically
significant increases in the 10-year CHD risk from the 0–9
range to 10 or higher with increases in SUA concentrations
across all age groups. However, the odds ratio for how incre-
ments in SUA increase the 10-year CHD risk from 0 to 20
range to 21 or higher was 1.038 for 40–64-year-olds (95%
CI: 0.793–1.360, ps0.784) and 1.224 for 65-year-olds and
older (95% CI: 0.950–1.578, ps0.119), which were not sig-
nificant. We could not apply ordinal logistic regression anal-
ysis to SUA concentration in 20–39-year-olds because the

Table 2 Cardiovascular disease-related factors of the three Framingham risk groupsa.

0–9 Group 10–20 Group G21 Group p-Valueb

Age, years 45.1"11.2 58.6"9.6c 63.8"9.7c,d -0.001
SBP, mm Hg 114.4"13.7 122.9"13.3c 131.3"11.6c,d -0.001
DBP, mm Hg 67.6"10.1 73.5"8.6c 76.7"9.1c,d -0.001
BMI, kg/m2 23.7"3.2 24.8"2.7c 25.0"2.6c -0.001
LDL-C, mg/dLe 107.7"27.9 121.0"29.1c 129.7"34.2c,d -0.001
TG, mg/dLe 104 (74–150) 146 (107–208)c 166 (136–235)c,d -0.001
Creatinine, mg/dLe 0.89"0.17 1.02"0.14c 1.00"0.16c -0.001
HOMA-IR 2.22"1.10 2.52"1.27c 2.70"1.37c -0.001
g-GT, IU/L 23 (15–38) 36 (26–61)c 33 (23–62)c -0.001
Uric acid, mg/dLe 5.08"1.36 5.86"1.30c 5.92"1.22c -0.001
hs-CRP, mg/L 0.544 (0.28–1.197) 0.857 (0.468–1.838)c 1.36 (0.748–3.061)c,d -0.001
WBC, =109/L 5.88"1.56 6.58"1.70c 7.46"1.72c,d -0.001
a
Data is presented by mean"SD or mean (inter-quartile range). bp-Values were obtained by one-way ANOVA or Kruskal-Wallis test.
c,d
p-0.05, significantly different from 0 to 9 group and 10–20 group, respectively, by Scheffe’s or Dunn’s post-hoc analyses. eConversion
factors: for LDL, multiply by 0.0259 to convert from mg/dL to mmol/L; for TG, multiply by 0.0113 to convert from mg/dL to mmol/L;
for creatinine, multiply by 88.4 to convert from mg/dL to mmol/L; for uric acid, multiply by 59.48 to convert from mg/dL to mmol/L.
BMI, body mass index; LDL-C, low-density lipoprotein cholesterol; TG, triglyceride; HOMA-IR, homeostasis model assessment of insulin
resistance; g-GT, g-glutamyltransferase; WBC, white blood cell count; hs-CRP, high-sensitive C-reactive protein.

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912 Nam et al.: Uric acid and Framingham risk score

Table 3 Increments in cardiovascular related risk factors to move from Framingham risk of 0%–9% to 10% or above.

OR 95% CI p-Valuea
Age, 10 years 1.169 1.159–1.180 -0.001
BMI, kg/m2 0.997 0.968–1.027 0.847
LDL-C, mg/dL 1.013 1.010–1.015 -0.001
TG, mg/dL 1.004 1.004–1.005 -0.001
Creatinine, mg/dL 1.649 1.562–1.740 -0.001
HOMA-IR 0.992 0.969–1.024 0.645
g-GT, IU/L 1.003 1.002–1.004 -0.001
Uric acid, mg/dL 1.246 1.164–1.333 -0.001
hs-CRP, mg/L 1.012 0.997–1.027 0.128
WBC, =109/L 1.315 1.250–1.383 -0.001
a
p-Values were obtained by generalized ordinal logistic regression analysis. BMI, body mass index; LDL-C, low-density lipoprotein cho-
lesterol; TG, triglyceride; HOMA-IR, homeostasis model assessment of insulin resistance; g-GT, g-glutamyltransferase; hs-CRP, high-
sensitive C-reactive protein; WBC, white blood cell count; OR, odds ratio; CI, confidence interval.

Table 4 Increments in cardiovascular related risk factors to move from Framingham risk of 0%–20% to 21% or above.

OR 95% CI p-Valuea
Age, 10 years 1.170 1.139–1.201 -0.001
BMI, kg/m2 1.050 0.965–1.143 0.255
LDL-C, mg/dL 1.018 1.010–1.025 -0.001
TG, mg/dL 1.005 1.004–1.007 -0.001
Creatinine, mg/dL 1.219 1.057–1.406 0.007
HOMA-IR 0.977 0.903–1.056 0.533
g-GT, IU/L 1.003 1.001–1.004 0.009
Uric acid, mg/dL 1.134 0.947–1.358 0.170
hs-CRP, mg/L 0.991 0.949–1.035 0.684
WBC, =109/L 1.464 1.298–1.652 -0.001
a
p-Values were obtained by generalized ordinal logistic regression analysis. BMI, body mass index; LDL-C, low-density lipoprotein cho-
lesterol; TG, triglyceride; HOMA-IR, homeostasis model assessment of insulin resistance; g-GT, g-glutamyltransferase; hs-CRP, high-
sensitive C-reactive protein; WBC, white blood cell count; OR, odds ratio; CI, confidence interval.

number of subjects with high CHD risk (G21%) in this age hyperuricemia can result from decreased uric acid excretion
group was too small. due to the use of diuretics or increased uric acid production
due to alcohol intake, tissue ischemia, or oxidative stress
(24).
Discussion Uric acid can influence the development of atherosclero-
sis. When SUA concentrations increase, vascular smooth
In purine metabolism, xanthine oxidase, a form of xanthine muscle cells proliferate, vascular lumen diameters decrease,
oxidoreductase which is associated with oxidative stress and and intravascular inflammatory responses increase (6). An
the development of CVD can produce both xanthine and uric
acid from hypoxanthine (13), with concomitant production
of hydrogen peroxide (19). Superoxides facilitate the creation
of reactive oxygen species, particularly in ischemic cell envi-
ronments. This cascade reaction reduces the biological usa-
bility of nitrogen monoxide (NO), thereby incurring endo-
thelial dysfunction in coronary arteries and a decrease in cor-
onary blood flow (20, 21).
Over 90% of subjects with hyperuricemia have impaired
renal capacity for excreting uric acid (22). In a hypertensive
state, a decrease in renal blood flow facilitates the reabsorp-
tion of uric acid, and hypertensive microvascular injury
results in the release of lactic acid from local ischemic tis-
sues. As a result, excretion of uric acid is hindered in the
proximal renal tubule (23). Hyperinsulinemia due to insulin Figure 1 Increments in uric acid significantly increase the 10-year
resistance can also impair urinary excretion of uric acid, con- CHD risk in progressing from 0%–9% to 10% or above in all age
tributing to the development of hyperuricemia. Moreover, groups (m, j, d – odds ratio for each age group).

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increase in SUA concentrations also activates blood platelets
and induces their aggregation, which facilitates the formation
of blood clots (20). Furthermore, higher concentrations of
SUA contribute to the oxidation of LDL cholesterol and
facilitate vascular lesions and fibrosis, ultimately exacerbat-
ing CVD (21). Inflammation plays a key role in the devel-
opment and progression of atherosclerosis, a major cause of
CHD, and in the erosion and rupture of atherosclerotic
plaques. The systemic inflammatory markers present in
blood (e.g., hs-CRP, WBC count, IL-1, IL-6, etc.) increase
with the progression of atherosclerosis and are therefore pre-
dictive indices for CHD risk (6, 25). Uric acid relates to
concentrations of inflammatory markers, along with homo-
cysteine and liver enzymes, such as alanine-aminotransfer-
ase, and g-GT (5, 9). However, the role of uric acid in the
pathogenesis of atherosclerosis or CHD is unclear because
of its conflicting reported roles in oxidative stress. Uric acid
has been reported to act as an oxidant at increased concen-
trations and also as an antioxidant with a potential therapeu-
tic role (6, 26). Increased SUA may be an independent
pro-atherogenic factor or could be a counteractive response
against elevated oxidative stress (27, 28). It may also be a
marker associated with well-known CHD risk factors, such
as insulin resistance, inflammation, and renal dysfunction
(27, 28).
Studies on the relationship between SUA and CVD in
healthy adults have shown conflicting results (29, 30), with
insufficient evidence in Koreans. The FRS was first devised
to assess the 10-year risk for CHD in white males 30 years
of age or older. The revised Framingham risk score, with the
purpose of primary prevention of CHD, gives scores to adults
from 20 to 79 years of age according to gender based on
such independent cardiovascular risk factors as age, smok-
ing, and levels of systolic blood pressure, total cholesterol,
and HDL cholesterol. It then sums each risk factor’s score
to compute the 10-year risk (%) for developing CHD (25).
Previous research on the association between uric acid and
FRS was confined to subjects aged 65 years or older. How-
ever, we evaluated adult subjects with a wide range of ages.
In fact, the revised FRS by NCEP ATP III places all men
75 years of age or older into the intermediate- and high-risk
groups for CHD. Therefore, we required a wide age range
to clarify the relationship between uric acid concentrations
and FRS. We measured well-known cardiovascular risk fac-
tors, such as BMI, LDL cholesterol, triglycerides, creatinine,
insulin sensitivity, g-GT, hs-CRP, and WBC count, not all of
which are components of the FRS, and these risk factors all
showed significant differences between the three FRS risk
groups. Even after adjusting for such factors, we found that
increments in SUA concentrations increased the 10-year
CHD risk from the 0–9 range to 10 or higher in all age
groups. These results suggest that increased SUA concentra-
tions may be a risk factor for CHD. Since increased SUA is
very common, especially in routine health check-up pro-
grams for apparently healthy adults, it is important for pri-
mary CHD prevention that doctors evaluate concealed risk
of CHD.
This study has limitations in terms of being representative
of the entire population of South Korea as it evaluated only
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Nam et al.: Uric acid and Framingham risk score 913
subjects undergoing a health check-up who visited a single
center. As a cross-sectional study, it cannot explain a causal
relationship between SUA concentrations and CHD risk.
Although the FRS is a generalized tool, its direct application
in some populations may overestimate CHD risk, especially
in Asian-Pacific populations, such as the Japanese and the
Chinese (25, 31). However, at present, there is no other vali-
dated and reliable CHD risk assessment tool for Koreans,
and many Korean doctors utilize the FRS. In the future, reca-
librating the FRS may improve its usefulness for risk assess-
ment in Koreans. Other limitations of this study include not
considering such factors as family history of CHD, exercise,
drug use (for example, b-blockers and diuretics), as well as
dietary habits that may affect SUA concentrations (for exam-
ple, high purine diets and alcohol). Prospective research on
Asian-Pacific populations should be performed to verify the
causal relationship between uric acid concentration and
CVDs, and to determine whether uric acid concentrations can
predict cardiovascular mortality.
In conclusion, CHD risk based on FRS increases as SUA
rises in asymptomatic Korean adults in all age groups. This
finding suggests that uric acid is an independent CVD risk
factor in adults and warrants further prospective study to
assess the predictability of uric acid in CHD and whether a
causal relationship exists. The risk of CHD as well as gout
needs to be considered in asymptomatic healthy people when
their SUA concentrations increase.
Acknowledgments
The authors thank Korea University Anam hospital health promo-
tion center for data collection and management.
Conflict of interest statement
Authors’ conflict of interest disclosure: The authors state that
there are no conflicts of interest regarding the publication of this
article.
Research funding: None declared.
Employment or leadership: None declared.
Honorarium: None declared.
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