Prevalence of Metabolic Syndrome and Its Relationship with Clinically Prevalent Cardiovascular Disease in the Veneto Region, Northeastern Italy

Novelletto, Bruno Franco; Guzzinati, Stefano; Avogaro, Angelo

doi:10.1089/met.2011.0065

Cited by 12 publications

(10 citation statements)

References 47 publications

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“…age, BMI, total cholesterol or LDL-cholesterol or presence of dyslipidemia, blood pressure values or presence of hypertension, smoke, glucose values or presence of diabetes) and lack of nutritional information; (d) we estimated the prevalence of metabolic syndrome in single-trial samples using an Italian epidemiological research as reference sample [4]; (e) we investigated the quality of included trials and their risk of bias through the ACROBAT Cochrane checklist [5]; and (f) we used a generalized least-squares regression model to inspect some dose-response effect [6] both at trial level and with a doseresponse meta-analysis; the goodness of fit was explored with a χ 2 -test [7]. We restricted all our described analyses to the end point 'CHD incidence'; their methodological details are available in the online Supplementary material.…”

mentioning

confidence: 99%

Hyperuricemia does not seem to be an independent risk factor for coronary heart disease

Battaggia

Scalisi²,

Puccetti

2017

Clinical Chemistry and Laboratory Medicine (CCLM)

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Federica Braga and coworkers [1] stated recently that hyperuricemia shows to be an independent predictor of coronary heart disease (CHD) risk (RR CHD = 1.206 [1.066-1.364]; RR CHD death = 1.209 [1.003-1.457]), mainly for the results found in women. That message seems to be of great importance: if it is true, the treatment of hyperuricemia should be included in the landscape of the therapeutic strategies to reduce the coronary risk. To ascertain the methodologic validity and robustness of that work, we considered it as a critical appraisal of some methodological aspects.In our approach, (a) we evaluated the overall quality of that systematic review through the AMSTAR checklist [2]; (b) we recovered the nine studies selected by Braga and colleagues [1] in order to repeat the meta-analysis and quantified the heterogeneity through I 2 statistic [3]; (c) we launched new subgroup and sensitivity and metaregression analyses in order to better explore the heterogeneity, considering the following as potential effect modifiers: gender, number of CHD covariates used in the adjustment models (i.e. age, BMI, total cholesterol or LDL-cholesterol or presence of dyslipidemia, blood pressure values or presence of hypertension, smoke, glucose values or presence of diabetes) and lack of nutritional information; (d) we estimated the prevalence of metabolic syndrome in single-trial samples using an Italian epidemiological research as reference sample [4]; (e) we investigated the quality of included trials and their risk of bias through the ACROBAT Cochrane checklist [5]; and (f) we used a generalized least-squares regression model to inspect some dose-response effect [6] both at trial level and with a doseresponse meta-analysis; the goodness of fit was explored with a χ 2 -test [7]. We restricted all our described analyses to the end point 'CHD incidence'; their methodological details are available in the online Supplementary material. What were our results?1. The quality of the meta-analysis assessed with the AMSTAR checklist [2] appears to be medium/low: only 4/11 items were fully satisfied, 3/11 not satisfied and 4/11 uncertain. 2. The metaregression (Figure 1) demonstrates that the number of confounders could be an important cause of heterogeneity, with the risk ratio of CHD associated to hyperuricemia decreasing by 13% for each covariate added to the model (p = 0.056). The subgroup analysis using the number of covariates as effect modifier coherently indicates that the role of hyperuricemia tends to disappear in the best adjusted models (test of interaction, p = 0.056). Notably, the trials that were not adjusted for nutritional status [8][9][10]

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confidence: 99%

Hyperuricemia does not seem to be an independent risk factor for coronary heart disease

Battaggia

Scalisi²,

Puccetti

2017

Clinical Chemistry and Laboratory Medicine (CCLM)

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“…A number of studies have reported that MS, a group metabolic risk factors, increase the risk for cardiovascular disease [75][76][77][78][79].…”

Section: Cardiovascular Diseasesmentioning

confidence: 99%

Metabolic Syndrome: From Human Organ Disease to Fetal Programming

Neto-Ferreira¹

2014

J Metabolic Synd

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Metabolic syndrome is defined as a constellation of metabolic disturbances that coexist in a subject. Due to its complex multi factorial etiology, metabolic syndrome causes damage to different organs, representing an increasing and significant global burden. Insulin resistance plays a central role in metabolic syndrome pathogenesis and underpins the majority of metabolic impairments, including the organ diseases that originate from metabolic syndrome. Regarding white adipose tissue, an altered adipokines profile in obesity characterizes a proinflammatory state, which is implicated in the pathogenesis of liver and cardiac disorders. Regarding the liver, nonalcoholic fatty liver disease is a benign disease that can progress towards liver fibrosis in the presence of persistent inflammation and increased oxidative stress. Concerning cardiovascular diseases, adipokines, reactive oxygen species and over activity of the renin angiotensin system play central roles. Another target organ of metabolic syndrome is the ovary, where polycystic ovary syndrome is also related to insulin resistance and can originate from adverse intrauterine conditions. The notion that maternal obesity can trigger metabolic syndrome in the fetus is alarming, given that it can be passed to other generations even if adequate nutrition is provided after birth. This review aimed to assess the main outcomes of metabolic syndrome in white adipose tissue focusing on insulin resistance and adipokines, the cardiovascular system, the liver and ovaries as well as fetal origins; this review also discusses some proposed pharmacological treatments to provide a better understanding of the related pathways in these secondary findings.

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“…The prevalence of MetS has been increasing over the past two decades (1), and recent studies (3)(4)(5) suggest that it has reached 25 % among the adults worldwide. Reports vary from 21.9 % in men and 16.8 % in women in north-eastern Italy, and 24.6 % in alcohol-dependent male patients in north India to 31.25 % in rural women from Bangladesh.…”

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confidence: 99%

“…Organisations such as the World Health Organization (WHO) and the American Heart Association and the National Heart, Lung, and Blood Institute (AHA/NHLBI) differ in diagnostic criteria for MetS (Table 1) (9)(10)(11)(12). It is also evident that the prevalence of MetS increases with age; Novalletto et al (3) reported the prevalence of 29.8 % in a group aged 60 to 69 years vs. 8.0 % in a group aged 30 to 39. The aetiopathology of MetS is still unclear but is believed to be a combination of modern lifestyle, environmental factors, and heredity in some populations (2,13).…”

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Endocrine, Lifestyle, and Genetic Factors in the Development of Metabolic Syndrome

Slanovic-Kuzmanović

Kos

Domijan

2013

Archives of Industrial Hygiene and Toxicology

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Metabolic syndrome (MetS) is a chronic, multi-component disease characterised by central obesity, hyperglycaemia, dyslipidaemia, and hypertension. Since MetS leads to type 2 diabetes, cardiovascular disease, development of certain cancers, and eventually to premature death, it is not surprising that it draws the attention of scientists around the world. The aetiopathology of MetS is complex and still not fully understood. This review focuses on the role of endocrine factors such as cortisol and insulin in the development of MetS. It also takes a look at some of the contributing lifestyle and genetic factors as well as at the current knowledge about its treatment. Slanovic-Kuzmanović Z, et al. ENDOCRINE, LIFESTYLE, AND GENETIC RISK FACTORS FOR METS Arh Hig Rada Toksikol 2013;64:581-591 Metabolic syndrome (MetS) is a modern disease characterised by the clustering of abnormalities such as central obesity, high levels of fasting glucose and triglyceride, low levels of high-density lipoprotein (HDL), and hypertension (1, 2). The prevalence of MetS has been increasing over the past two decades (1), and recent studies (3-5) suggest that it has reached 25 % among the adults worldwide. Reports vary from 21.9 % in men and 16.8 % in women in north-eastern Italy, and 24.6 % in alcohol-dependent male patients in north India to 31.25 % in rural women from Bangladesh. A small study on salt intake with 92 participants in Croatia reports the prevalence of 31.5 % (6). Among obese adolescents and pubertal children, the prevalence of MetS could be around 15 %, judging by the reports of 14 % in Danish obese adolescents (7) and of 9.7 % to 41.2 % in obese pubertal children and 8.3 % to 34.2 % in obese prepubertal children in Spain (8). KEY WORDS: cardiovascular diseases, circadian rhythm, cortisol, hyperglycaemia, hypertension, insulin, MetS, type 2 diabetes

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Prevalence of Metabolic Syndrome and Its Relationship with Clinically Prevalent Cardiovascular Disease in the Veneto Region, Northeastern Italy

Abstract: The prevalence of metabolic syndrome in the Veneto region among subjects ages 30-69 is high. There is a significant association between prevalent CVD and metabolic syndrome, but the biological basis of association is strongly influenced by gender.

Cited by 12 publications

References 47 publications

Hyperuricemia does not seem to be an independent risk factor for coronary heart disease

Hyperuricemia does not seem to be an independent risk factor for coronary heart disease

Metabolic Syndrome: From Human Organ Disease to Fetal Programming

Endocrine, Lifestyle, and Genetic Factors in the Development of Metabolic Syndrome

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