Objective: To investigate the relationship between metabolic syndrome and hyperuricemia. Methods: A total of 2 subjects who received health examination. Introduction: Metabolic syndrome and hyperuricemia are important risk factors for cardiovascular disease. Objective: To assess the association. Background. Associations between hyperuricemia, metabolic syndrome, cardiovascular disease and diabetes have been reported. Limited information, however.
Remarkably when uric acid elevation was prevented by treating with allopurinol or with a uricosuric agent, the development of hypertension could be abrogated [ 16 ]. This study supports the hypothesis that there exists a direct causative role for uric acid in the development of hypertension. Collectively, these data strongly suggest that uric acid may have a pathogenic role in the development of metabolic syndrome and associated cardiovascular disease, rather than simply functioning as a surrogate marker for such disorders.
Hyperuricemia in Rheumatic Diseases Other Than Gout An association between hyperuricemia and rheumatic diseases, besides gouty arthritis, has been observed in epidemiologic studies.
Furthermore, among patients with RA, one study has shown that SUA levels are correlated with the risk of renal dysfunction.
SUA, independent of GFR, age, systolic blood pressure, total cholesterol, triglycerides, and RA duration, was determined to be a risk factor for kidney disease [ 18 ]. Similarly, Yang et al. The authors found that SUA is independently associated with the development of lupus nephritis in SLE patients [ 19 ]. There are also reports showing an association between uric acid and osteoarthritis OA.
One study in OA patients with hip replacement found that elevated SUA concentrations were associated with the presence of multijoint hand OA [ 20 ]. Another study has shown the occurrence of gout attacks in joint sites that demonstrated radiographical OA such as big toe, midfoot, knee, and distal finger joints. It is possible that OA may facilitate the localized deposition of urate crystals [ 21 ].
More recently, Denoble et al. These findings suggest that synovial fluid UA is a risk marker for OA severity. The association of synovial fluid IL with OA progression also suggests the possibility that UA is a risk factor promoting the pathological process of OA possibly through activation of the inflammasome.
Biochemistry and Biological Actions of Uric Acid Uric acid is the end product of purine metabolism in humans and is generated by the action of the enzyme, xanthine oxidase XOwhich catalyzes the last two steps of uric acid conversion: For many years, uric acid was regarded as a metabolically inert substance. However, there is ample evidence that uric acid has multiple actions impacting cellular metabolism.
For example, uric acid can act as an endogenous antioxidant and a powerful scavenger of single oxygen peroxyl ROS and hydroxyl radicals OH [ 23 ]. Uric acid reacts with peroxynitrite and stabilizes endothelial nitric oxide synthase eNOS activity [ 24 ]. Its chemical limitations include the fact that uric acid cannot scavenge superoxide and that the presence of ascorbic acid in the plasma is required for its antioxidant effect. Finally, uric acid paradoxically behaves as a prooxidant and proinflammatory factor.
A few points should be emphasized to better understand this apparent contradiction. First, uric acid functions differently inside cells versus the extracellular milieu, where it is present in soluble form [ 25 ]. Although it is a potent antioxidant in extracellular fluid, uric acid exerts prooxidative effects once inside the cell [ 26 ]. It has been demonstrated that plasma uric acid is a circulating marker of oxidant damage in a variety of pathological conditions, including, among others, ischemic liver injury, ischemic-reperfusion injury, hyperlipidemia, chronic heart failure, atherosclerosis, and diabetes [ 27 — 31 ].
Hyperuricemia and Atherosclerosis Serum uric acid levels have an association with surrogate markers of atherosclerosis in a number of studies.
Surrogate markers of atherosclerosis shown to have an association with hyperuricemia include carotid intima-media thickness C-IMT [ 1132 — 36 ], ankle brachial index [ 34 ], coronary artery calcification [ 37 ], and brachial-ankle pulse wave velocity baPWV [ 38 ].
In addition, many studies suggest an independent effect of elevated serum uric acid on atherosclerosis as measured by these surrogate markers after adjusting for the influence of metabolic syndrome and other factors [ 11333539 ]. In particular, there is evidence that uric acid has direct effects on key processes involved in endothelial function and vascular remodeling [ 40 ].
Xanthine oxidoreductase has two forms. Under ischemic conditions, xanthine dehydrogenase is converted to xanthine oxidase. It is unclear whether the resulting inflammation and arterial wall damage associated with hyperuricemia are related to the free radicals formed or to the uric acid itself [ 41 ]. As noted above, uric acid has both prooxidant and antioxidant activity. When acting an antioxidant, it chelates metals and scavenges oxygen radicals [ 42 ].
As a prooxidant, uric acid oxidizes lipids [ 43 ], reduces nitric oxide availability in endothelial cells [ 44 ], and increases reactive oxygen species [ 45 ].
Furthermore, as a prooxidant, high levels of serum uric acid cause increased lipid oxidation [ 43 ]. The resultant inflammation would be expected to disrupt reverse cholesterol transport, a function that is important to reduce cardiovascular risk [ 46 ].
Oxidants also cause endothelial dysfunction by reacting with and removing NO, thereby preventing vasodilation of the endothelium. Decreased NO and increased reactive oxygen species may promote a proinflammatory state that causes endothelial dysfunction and contributes to atherosclerosis and cardiovascular disease [ 47 ]. Finally, uric acid inhibits endothelial cell proliferation and stimulates C-reactive protein production in endothelial cells [ 48 ].
At the level of vascular smooth muscle cells, uric acid stimulates the production of monocyte chemoattractant protein-1 MCP-1a key chemokine implicated in atherosclerosis and chronic kidney disease.
Increased production of MCP-1 by uric acid appears to be mediated via activation of mitogen-activated protein MAP kinase and cyclooxygenase-2, leading to increased cell proliferation and production of CRP and other inflammatory mediators [ 48 ]. Taken together, it is not surprising that several studies show that elevated serum uric acid levels are predictive of atherosclerosis or cardiovascular disease.
Hyperuricemia, per se, was found to be an independent predictor for atherosclerosis in patients with hypertension [ 33 ]. In another clinical study, serum uric acid was found to be associated with subclinical atherosclerosis in men with type II diabetes mellitus [ 3449 ].
Serum uric acid levels were also higher in patients with rheumatoid arthritis RA and cardiovascular disease than in those without cardiovascular disease despite the fact that RA is not usually associated with high serum uric acid levels [ 50 ]. Such findings do not appear to be limited by gender.
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In women with systemic lupus erythematosus, serum uric acid was found to be associated with arterial stiffness and of potential use as an indicator of subclinical atherosclerosis, although it was not independent of age and homocysteine levels [ 51 ], nor is it likely the situation that an absolute level of uric acid elevation is necessary for injurious outcome.
This was seen in a population of psoriatic arthritis patients with subclinical atherosclerosis [ 52 ]. Of note, most of the patients in this study had serum uric acid levels that were in the normal reference range even though there remained a link between subclinical atherosclerosis and serum uric acid concentration [ 52 ]. This may mean that the reference ranges for patients with chronic inflammatory diseases may need to be adjusted.
At the very least, elevated levels of serum uric acid, even if within the reference range, may need to be considered more carefully in populations at higher risk for cardiovascular disease. In summary, while it may be true that, under normal physiologic conditions, uric acid functions as an antioxidant and protects against atherosclerosis, it appears that, under ischemic conditions, it becomes a prooxidant and increases the risk of atherosclerosis [ 41 ].
Hence, it is as yet unclear what the role of lowering uric acid may be in reducing cardiovascular disease risk.
Further study is needed to show if lowering serum uric acid will also lower the incidence of atherosclerosis and cardiovascular disease. Gout is not considered as a simple joint disease and is associated with obesity, cardiovascular disease, hypertension, and MetS with increased mortality [ 9 — 11 ].
There is a tendency for younger individuals to have MetS. Also, MetS is closely related to the occurrence and mortality of chronic conditions such as cardiovascular diseases CVDcardiac diseases, diabetes mellitus DMand hypertension [ 12 — 14 ]. Epidemiological studies on MetS in different countries and regions show drastically different results. The primary reasons for such drastic differences can be the different characteristics of the participants e. Previous epidemiological surveys showed that the hyperuricemia is related to the prevalence of MetS [ 1718 ].
However, previous studies, for the most part, recruited the general public as research participants and few studies investigated worker populations.
Review of Hyperuricemia as New Marker for Metabolic Syndrome
Therefore, the purpose of this study was to investigate the relationship between hyperuricemia and MetS in a labor force population.
Thus, identifying asymptomatic individuals with a high risk of developing MetS may lead to improvements in prevention and treatment of the condition and of subsequent cardiovascular events and gouty arthritis. The physical examination document includes physical examination and biochemical blood tests. The total sample size was 33, with a valid sample size of 21, after excluding those with incomplete data on physical examination and biochemical blood tests.
Definition of terms is as follows. We utilized previously established modifications for Asian populations, using waist circumference WC cut-off points [ 24 ].
Any three of the following five criteria were grounds for identifying MetS: The physical examination comprised BP and anthropometric measurements, including height, weight, and body mass index BMI.
Height was measured to the nearest 0. Weight was measured in light clothing, without shoes, using a beam balance scale, and was recorded to the nearest 0. BMI was calculated as weight kg divided by height2 m2.
The average of the two closest readings was calculated to determine the reported BP for each participant.
The sample was venous blood drawn after 8 hours of fasting and was sent to the lab within an hour and analyzed by a Hitachi biochemical analyzer. Data in the present study were analyzed using SPSS Descriptive statistics used the average value, the standard deviation, the frequency distribution, and the percentage criterion.
Inferential statistics used the Chi-square and multiple logistic regression models for analysis. Results Study participants included 21, individuals aged over 21 who were receiving a worker health examination in Changhua County.
The mean age waswith 4, individuals The majority of the participants were male, with 13, males Demographic characteristics such as age and gender differed significantly between individuals with and without MetS. Individuals at an older age had high prevalence of MetS, and males had higher prevalence of MetS than females The ratio of hyperuricemia in individuals with MetS was In addition, we divided SUA concentration into 4 groups, and we found that Quartile 4 had a significantly and abnormally high ratio of SUA compared to Quartile 1 In this study, we added variables that were statistically significant by univariate analysis i.
With increased age, the ORs of having MetS increased accordingly. For example, the OR of individuals over 51 years old having MetS was 4. These ORs are all statistically significant. With increased age, the odds of MetS increased 2. As for gender as a risk factor, males had a risk of developing MetS that was 1.
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Regression analysis of risk factors of metabolic syndrome. Discussion Studies show that hyperuricemia not only can cause gout, but also is a high risk factor for atherosclerotic diseases such as CVD and carotid atherosclerosis [ 25 ], hypertension [ 26 ], DM [ 27 ], MetS [ 28 ], and cardiac diseases and chronic diseases such as cerebral vascular diseases.
Our study shows that MetS is associated with age, and increased age is associated with a higher rate of MetS. We observed that individuals over 51 years old had the prevalence rate of Our result is consistent with many previous studies that show that the prevalence of MetS increases with increased age [ 30 ].
We also found that males have a higher rate of MetS than females For example, Balkau et al. The prevalence rates were