Prevalence of the metabolic syndrome in individuals with hyperuricemia

Purpose

The link between hyperuricemia and insulin resistance has been noted, but the prevalence of the metabolic syndrome by recent definitions among individuals with hyperuricemia remains unclear. Our objective was to determine the prevalence of the metabolic syndrome according to serum uric acid levels in a nationally representative sample of US adults.

Methods

By using data from 8669 participants aged 20 years and more in The Third National Health and Nutrition Examination Survey (1988-1994), we determined the prevalence of the metabolic syndrome at different serum uric acid levels. We used both the revised and original National Cholesterol Education Program Adult Treatment Panel (NCEP/ATP) III criteria to define the metabolic syndrome.

Results

The prevalences of the metabolic syndrome according to the revised NCEP/ATP III criteria were 18.9% (95% confidence interval [CI], 16.8-21.0) for uric acid levels less than 6 mg/dL, 36.0% (95% CI, 32.5-39.6) for uric acid levels from 6 to 6.9 mg/dL, 40.8% (95% CI, 35.3-46.4) for uric acid levels from 7 to 7.9 mg/dL, 59.7% (95% CI, 53.0-66.4) for uric acid levels from 8 to 8.9 mg/dL, 62.0% (95% CI, 53.0-66.4) for uric acid levels from 9 to 9.9 mg/dL, and 70.7% for uric acid levels of 10 mg/dL or greater. The increasing trends persisted in subgroups stratified by sex, age group, alcohol intake, body mass index, hypertension, and diabetes. For example, among individuals with normal body mass index (<25 kg/m²), the prevalence increased from 5.9% (95% CI, 4.8-7.0), for a uric acid level of less than 6 mg/dL, to 59.0%, (95% CI, 20.1-97.9) for a uric acid level of 10 mg/dL or greater. With the original NCEP/ATP criteria, the corresponding prevalences were slightly lower.

Conclusions

These findings from a nationally representative sample of US adults indicate that the prevalence of the metabolic syndrome increases substantially with increasing levels of serum uric acid. Physicians should recognize the metabolic syndrome as a frequent comorbidity of hyperuricemia and treat it to prevent serious complications.     

代谢综合征患者尿路结石危险因素分析

目的 分析代谢综合征(MS)患者合并尿路结石的特点,试图找到MS患者罹患尿路结石的相关危险因素.方法 选取MS合并尿路结石患者85例,MS排除结石患者80例作为对照组.测定两组人群血清同型半胱氨酸(Hcy)、血尿酸(SUA)、24小时尿酸(aliA)、空腹和餐后2小时血糖、胰岛素、24小时尿微量自蛋白(TUP)等.以上危险因素为自变量,有无尿路结石为应变量做Logistic多元逐步回归.结果 TUA、SUA、胰岛素抵抗指数、Hcy、TUP进入回归模型(R2＝0.823,P＝0.002).结论 高尿酸排泄、血尿酸水平增高、胰岛素抵抗、血Hcy增高等是MS患者罹患尿路结石的危险因素;降低血尿酸水平、改善胰岛素抵抗对于减少MS尿路结石的发生具有重要意义.     

非酒精性脂肪性肝病与代谢综合征

非酒精性脂肪性肝病(NAFLD)是一种包括从单纯的肝脂肪变性到非酒精性脂肪性肝炎,以致最终发展为肝硬化的一组肝脏慢性广谱性临床病理综合征。近年来大量研究表明,NAFLD与代谢综合征(MS)的各个组分密切伴随,甚至有学者将其作为MS的组分之一,并发现胰岛素抵抗在NAFLD发病机制中起关键作用。迄今对NAFLD的发病机制还了解甚少,目前广泛接受的一个理论是“二次打击”假说。脂肪酸和甘油三酯在肝脏沉积造成的“第一次打击”之后,肝细胞对氧化应激和炎症因子作用导致的“第二次打击”的敏感性增加而引起肝损害。本文主要目的是对NAFLD的临床病理特点、与胰岛素抵抗及MS的关系以及可能的分子机制进行综述,同时也介绍了目前预防和治疗NAFLD的策略。     

代谢综合征的诊断问题

复习了几种代谢综合征的定义,并对其组分进行了讨论。目前最新的是2005年4月提出的国际糖尿病联盟(IDF)定义。我国于2004年也有一定义。还介绍了最近对代谢综合征诊断的争论。美国糖尿病学会(ADA)及欧洲糖尿病学会(EASD)认为目前此诊断尚不成熟,但IDF定义制定者予以坚决反驳。     

The relationship between hyperuricemia and anemia and metabolic syndrome in Korean adults: The Korea National Health and Nutrition Examination Survey 2019

AimThe present study was conducted to assess the relationship between hyperuricemia and anemia in Korean adults with or without metabolic syndrome (MetS).MethodsData from 6073 adults (age ≥ 20 years) in the Eighth Korean National Health and Nutrition Examination Survey (2019) were analyzed.ResultsSeveral key findings were identified. First, after adjusting for the related variables, the hemoglobin [Hb] level in the hyperuricemia subgroup (uric acid [UA] ≥ 7.0 mg/dL in men or ≥ 6.0 mg/dL in women) was higher than in the normouricemia subgroup (UA < 7.0 mg/dL in men or < 6.0 mg/dL in women) in subjects with non-MetS (p = 0.005), whereas it was lower than in the normouricemia subgroup in subjects with MetS (p = 0.032). Second, after adjusting for the related variables, the odds ratio (OR) of anemia (Hb < 13.0 g/dL in men or < 12 g/dL in women), using the normouricemia subgroup as a reference, was negatively significant for the hyperuricemia subgroup in subjects with non-MetS (OR, 0.478; 95 % CI, 0.300–0.761) but positively significant for the hyperuricemia subgroup in subjects with MetS (OR, 1.765; 95 % CI, 1.160–2.198).ConclusionsHyperuricemia was associated with a decrease in anemia in non-MetS but an increase in anemia in MetS.     

非酒精性脂肪肝、非酒精性脂肪肝合并代谢综合征患者血清脂联素水平及其与胰岛素抵抗程度的相关性分析

目的 研究非酒精性脂肪肝、非酒精性脂肪肝合并代谢综合征患者血清脂联素水平及其与胰岛素抵抗程度的相关性.方法 选取非酒精性脂肪肝106例,非酒精性脂肪肝合并代谢综合征58例,单纯肥胖32例,健康体检42例作为对照组.测定体重指数（BMI）和腰臀比（WHR）,检测空腹血糖（FBS）、丙氨酸氨基转移酶（ALT）、胆固醇（TC）、甘油三脂（TG）和高密度脂蛋自（HDL）等生化指标并行肝脏B超检查.放射免疫法测定空腹胰岛素（FINS）水平,计算胰岛素抵抗指数（HOMA）.同时酶联免疫法测定血清脂联素水平,并用相关及多元回归分析脂联素与各参数的相关性.结果 非酒精性脂肪肝组BMI、ALT、TC、TG、FBS、FINS和HOMA均较正常对照组高,HDL和脂联素水平较正常对照组低;非酒精性脂肪肝合并代谢综合征组胰岛素抵抗程度较非酒精性脂肪肝组更严重,脂联素水平更低.单纯肥胖组ALT、TC高于对照组,脂联素水平有下降趋势.非酒精性脂肪肝ALT异常组与ALT正常组比较,脂联素水平下降.结论 非酒精性脂肪肝存在不同程度胰岛素抵抗,脂联素水平降低;合并代谢综合征者胰岛素抵抗更为严重,脂联素水平更低;合并ALT异常时脂联素水平下降     

慢性阻塞性肺疾病和代谢综合征

慢性阻搴性肺疾病（chronic obstructive puhnonary disease,COPD）和代谢综合征（metabolic syndrome,MS）均是慢性疾病．患病人数多、社会负担重．二者在一定程度上相互影响,发病机制上亦有许多相似之处。吸烟、缺氧、氰化应激、不活动的生活方式、细胞因子、脂肪因子的改变以及糖皮质激素的应用可能是COPD患者中MS高发的原因,而高血糖对感染、免疫及肺功能的影响可能使COPD患者的预后恶化。本文对此方向的研究进展进行综述。     

The link between abdominal obesity, metabolic syndrome and cardiovascular disease

AimThe prevalence of metabolic syndrome has increased dramatically in recent years, and the cluster of metabolic abnormalities it encompasses results in increased cardiovascular morbidity and mortality. The role of abdominal (visceral) obesity and the underlying molecular and cellular mechanisms central to this association have been the subject of intensive research in recent times. The aim of this review is to correlate data in this area, highlighting the central role of excess visceral fat and its secreted adipokines, and to review existing and emerging therapies.Data synthesisData were generated from a search of the PubMed database using the terms ‘abdominal obesity’, ‘metabolic syndrome’, ‘insulin resistance’, ‘adipokines’, ‘interleukin-6 (IL-6)’, ‘adiponectin’, ‘tumour necrosis factor-alpha (TNF-α)’ and ‘cardiovascular disease’.ConclusionMetabolic syndrome is associated with a pro-inflammatory state, and the role of visceral obesity is thought to be central to this. Visceral obesity leads to alteration of the normal physiological balance of adipokines, insulin resistance, endothelial dysfunction and a pro-atherogenic state. In association with this, the presence of conventional cardiovascular risk factors such as hypertension, dyslipidaemia and smoking results in a significantly elevated cardiovascular and metabolic (cardiometabolic) risk. Better understanding of the molecular mechanisms central to this association has led to the development of potential therapeutic agents.     

代谢综合征患者血尿酸水平与冠心病的关系

将 769例不同程度代谢异常患者分为冠心病组和非冠心病组,分析血尿酸在不同代谢异常状态下与冠心病的关系。结果显示,在缺乏其他代谢因素影响时,尿酸可能与冠心病的发生有一定关联,但并非冠心病的独立危险因素。     

剖析代谢综合征组分间的内在联系

代谢综合征(MS)表现为一组心血管疾病危险因素的聚集,因其严重威胁人类健康而越来越受到关注.其发病机制末完全明确,围绕Ms还存在诸多争议.目前其定义并不统一,但涉及的组分相同.既往MS曾被称作胰岛素抵抗综合征,随着研究的深入,发现这种称谓并不恰当.胰岛素抵抗(IR)在MS的发生、发展中起了最为重要的作用,而并非MS的唯一病理生理机制.腹型肥胖与IR、血脂紊乱、高血压、高血糖、炎性反应状态密切相关.     

对胰岛素抵抗在代谢综合征中作用的新认识

代谢综合征(MS)是以中心性肥胖、高血压、脂质代谢异常、微量蛋白尿、葡萄糖耐量受损和(或)糖尿病等为特征的一组临床综合征,是导致糖尿病、心脑血管疾病的危险因素。1999年WHO将其正式命名为MS,并做了工作定义。2005年国际糖尿病联盟(IDF)对其提出了新的工作定义,进而达成全球共识。胰岛素抵抗是指机体对一定量胰岛素的生物学反应低于预计正常水平的一种现象,是导致MS发病的主要机制,其与MS各组分之间密切相关,但机制尚未完全阐明。本文就MS的定义及有关胰岛素抵抗在MS发生中的作用机制的研究的新进展做简要综述。     

The metabolic syndrome: time for a critical appraisal

Background The term metabolic syndrome refers to a clustering of specific cardiovascular disease (CVD) risk factors whose underlying pathophysiology is thought to be related to insulin resistance.Methods Since the term is widely used in research and clinical practice, we undertook an extensive review of the literature in relation to the syndromes definition, underlying pathogenesis, association with cardiovascular disease and to the goals and impact of treatment.Discussion While there is no question that certain CVD risk factors are prone to cluster, we found that the metabolic syndrome has been imprecisely defined, there is a lack of certainty regarding its pathogenesis, and there is considerable doubt regarding its value as a CVD risk marker. Our analysis indicates that too much critically important information is missing to warrant its designation as a syndrome.Conclusion Until much-needed research is completed, clinicians should evaluate and treat all CVD risk factors without regard to whether a patient meets the criteria for diagnosis of the metabolic syndrome.This statement was reviewed and approved by the Professional Practice Committee of the American Diabetes Association and by an ad hoc committee of the European Association for the Study of Diabetes (members: H. Beck-Nielsen [Odense, Denmark], K. Borch-Johnsen [Gentofte, Denmark], E. A. M. Gale [Bristol, UK], L. Groop [Malmö, Sweden], H.-U. Häring [Tübingen, Germany], R. J. Heine [Amsterdam, The Netherlands], and D. R. Matthews [Oxford, UK]).Simultaneous publication: This article is being simultaneously published in 2005 in Diabetes Care and Diabetologia by the American Diabetes Association and the European Association for the Study of Diabetes.Copyright 2005 by the American Diabetes Association, Inc. and Springer-Verlag. Copying with attribution allowed for any noncommercial use of the work.     

Non-alcoholic fatty liver disease and the metabolic syndrome： An update

Sedentary lifestyle and poor dietary choices are leading to a weight gain epidemic in westernized countries, subsequently increasing the risk for developing the metabolic syndrome and nonalcoholic fatty liver disease （NAFLD）. NAFLD is estimated to affect approximate 30% of the general US population and is considered the hepatic manifestation of the metabolic syndrome. Recent findings linking the components of the metabolic syndrome with NAFLD and the progression to nonalcoholic steatohepatitis （NASH） will be reviewed; in particular, the role of visceral adipose tissue, insulin resistance, and adipocytokines in the exacerbation of these conditions. While no therapy has been proven effective for treating NAFLD/NASH, common recommendations will be discussed.     

代谢综合征与抑郁症的相关性

近年来随着代谢综合征发病率的升高,其并发抑郁症的人数也相应增加.代谢综合征中的胰岛素抵抗、皮质醇增多、肥胖和非酒精性脂肪肝与抑郁症的发生有关,而抑郁症患者的不健康生活习惯又是发生代谢综合征的原因.而且两种疾病的治疗也存在交叉.探索二者之间的关系,有助于进一步研究其发病机制,预防和治疗代谢综合征相关性抑郁症.     

Low serum uric acid concentration augments insulin effects on the prevalence of metabolic syndrome

Aim

Insulin and uric acid were shown affect the prevalence of Metabolic Syndrome (MetS), but no studies examine their interaction. Therefore, we conducted this study to determine their biological interaction in subjects from central Mexico.

尿酸与腹型肥胖及代谢综合征相关性研究

 目的 探讨血清尿酸(UA)水平的变化与腹型肥胖及代谢综合征(MS)的相关性。方法 875例40~65岁杭州社区居民进入研究,其中男350例,女525例。对所有研究对象均进行问卷调查、体检和血清学检查,并进行腹部MRI扫描,测量腹内脂肪面积和皮下脂肪面积,分析UA水平与腹型肥胖和MS的相关性,并确定UA作为MS诊断的参考指标的最佳界值。结果 该人群中随着 UA 水平增加,腹型肥胖(男性OR=4.35,95%CI 1.91~9.90;女性OR=5.44,95%CI 2.41~12.31) 和MS(男性OR=4.47,95%CI 2.08~9.62;女性OR=11.62,95%CI 3.43~39.37)风险增加。多项logistic 回归分析显示,UA 是TG升高(男性OR=2.23,95%CI 1.02~4.87;女性OR=3.04,95%CI 1.49~6.23)、女性腹型肥胖(OR=3.23,95%CI 1.32~7.91)和血压升高(OR=2.35,95%CI 1.37~4.05)的独立危险因素。在女性中,根据腹内脂肪面积建立多元线性回归模型,UA的最佳切点为244.0 μmol/L,而通过受试者ROC曲线获得MS诊断的最佳界值为258.8 μmol/L。结论 在我国中年人群中,UA与腹型肥胖和MS密切相关。UA水平升高是女性腹型肥胖和MS的独立危险因素。     

睾酮与男性代谢综合征

男性血清睾酮水平与代谢综合征的发生、发展密切相关.低睾酮水平可能导致腹型肥胖、糖代谢异常、血脂紊乱及高血压,给予睾酮水平低下者睾酮替代治疗(TRT)能明显改善其相关代谢指标.同时,腹型肥胖、糖代谢异常也可通过抑制Leydig细胞功能、增加芳香化酶活性等引起睾酮水平下降.     

血尿酸水平与冠状动脉病变及代谢综合征的关系

目的 探讨血尿酸水平变化与冠状动脉病变程度、代谢综合征及其相关组分的关系.方法 343例(男性223例,女性120例)接受冠状动脉造影检查的患者,应用冠脉狭窄指数(CSI)评价冠状动脉病变严重程度.结果 (1)女性血尿酸水平显著低于男性[(306.3±76.9对358.9±85.2)μmol/L,P＜0.01],而男女性代谢综合征及各组分的患病率未见明显差异.(2)女性≥3项代谢异常亚组血清尿酸水平显著高于1项代谢异常亚组(P＜0.01)及2项代谢异常亚组(P＜0.05),而男性尿酸水平与代谢异常数目无明显关系.(3)将男、女人群的尿酸值分为4分位数,女性位于上1/4位点者的CSI评分高于下1/4位点者[7.0(2.5～12.0)对2.0(0.0～6.0),P=0.025].女性多支病变组血尿酸水平明显高于无病变组[(327.0±81.9对284.9±78.6)μmol/L,P=0.033].(4)Logistic回归显示年龄(β=0.042,P=0.007)和血脂异常(β=0.836,P=0.037)为男性冠脉病变的独立危险因素,而女性人群中血压异常(β=1.127,P=0.039)及血脂异常(β=0.901,P=0.009)为影响冠脉病变的主要因素.结论 血尿酸水平较高的女性,代谢异常组分聚集较多,其冠状动脉病变程度较重,故尿酸水平可作为女性动脉粥样硬化的标志.

Abstract：

Objective To analyze the association of blood uric acid level with the severity of coronary artery stenotic changes, metabolic syndrome (MS), and its components. Methods A total of 343 individuals ( male 223,female 120) who underwent coronary angiography and had complete data on MS and serum uric acid were collected. The severity of coronary artery disease (CAD) was assessed by the coronary stenesis index (CSI). MS was diagnosed according to the Guideline on Prevention and Treatment of Blood Lipid Abnormality in Chinese Adults. Results (1)The mean uric acid level was significantly lower in women than in men [ ( 306.3±76.9 vs 358.9±85.2 ) μmol/L, P＜0.01 ]. The prevalence of MS and its components showed no difference between men and women. (2) The uric acid level in women with 3 components was higher than those with1( P＜0. 01 ) or 2 ( P＜0.05 ) components of metabolic disorders, but not in men. (3) Quartiles of concentration of uric acid were computed. Compared with those in the lowest quartile of uric acid, women in the highest quartile had higher CSI score [ 7.0 (2.5-12.0) vs 2. 0( 0.0-6.0), P= 0. 025 ]. Moreover, the uric acid level was higher in women with multivessel lesions than nonCAD patients [ (327.0±81.9 vs 284.9±78.6) μmol/L, P = 0.033 ]. However, no correlation was found between uric acid level and the severity of coronary artery lesion in men. (4) Logistic regression showed that age (β=0.042, P=0. 007) and dyslipidemia(β=0.836, P=0. 037 ) were the independent risk factors of CAD in men, and hypertension(β=1. 127, P=0.039) and dyslipidemia(β=0.901, P=0.009)in women. Conclusions In women with higher uric acid level, the clustering of metabolic abnormalities was increased, and the coronary artery lesion was more severe. High uric acid level might be a marker of CAD for women.     

The implication of hepatokines in metabolic syndrome

Hepatokines are liver–derived proteins with equivocal roles in metabolic syndrome (MetS). These proteins have prominent role in pathogenesis of MetS component such as obesity, insulin resistance, dyslipidemia and hypertension. The identification and functional characterization of hepatokines may provide significant insights that could help in better understanding of MetS pathogenesis. Fetuin-A, Hepatocyte-derived fibrinogen-related protein 1, Fibroblast growth factor 21, Angiopoietin–related growth factor, Selenoprotein-P, Angiopoietin like proteins, Leukocyte cell-derived chemotaxin 2 are regarded as the most significant hepatokines. We describe recent data on these new hormones in progression of MetS. Understanding of the accurate role of these proteins in pathophysiology of MetS can help improving prevention and treatment of this syndrome.     

尿液pH值与代谢综合征的相关性研究

目的:探讨中老年人群尿液pH水平与代谢综合征的相关性。方法:对上海市嘉定社区2 322名40岁以上居民进行问卷调查和体格检查,空腹采血检测肝功能、肾功能、血糖、血脂及胰岛素,收集晨尿检测尿pH值。采用多元线性回归分析代谢综合征与尿液pH值的相关性,Logistic回归分析代谢综合征和低尿液pH水平的相对风险度。代谢综合征采用按亚洲人特点改良的美国国家胆固醇教育计划成人治疗组第3次报告诊断标准。结果:与正常人群相比,代谢综合征患者腰围、体质量指数、血压、空腹血糖、糖化血红蛋白、低密度脂蛋白胆固醇、三酰甘油等指标偏高(P