Characteristics of Participants in the Epidemiologic Survey in Ogliastra, Sardinia, 2002–2008.

<p>Abbreviations: BMI, body mass index; DBP, diastolic blood pressure; SBP, systolic blood pressure; SD, standard deviation.</p>*<p><i>P</i><0.0001.</p>a<p><i>P</i> values refer to Pearson Chi-square test comparing frequencies of categorical variables or to t-test comparing mean values of quantitative variables in men and women.</p>b<p>prior cardiovascular diseases include hypertension, TIA, stroke, myocardial infarction (ischemic heart disease), heart failure, peripheral vasculopathy or evidence of atherosclerosis.</p>c<p>Test on the equality of standard deviations (variances) in men and women.</p

Overall age- and sex-specific prevalence of hypertension, Ogliastra, 2002–2008.

<p>Overall age- and sex-specific prevalence of hypertension, Ogliastra, 2002–2008.</p

Anthropometric and Serological determinants of SBP and DBP in Ogliastra, 2002–2008.

<p>Abbreviations: β, regression coefficient; DBP, diastolic blood pressure; SBP, systolic blood pressure.</p>*<p><i>P</i><0.001;</p>**<p><i>P</i><0.05.</p>a<p>HDL and LDL cholesterol, S-sodium and S-calcium were excluded from the final multiple models because their coefficients were statistically significant only in the simple regression models.</p>b<p>Contribution of single independent variables to the explanation of the dependent variables (partial R²).</p>c<p>Age classes: 18–29, 30–39, 40–49, 50–59, 60–69, 70–79, >80 years.</p

Mean systolic and diastolic blood pressure by age and sex in the overall sample, Ogliastra, 2002–2008.

<p>Men are represented by blue lines.</p

Heritability estimates of BP measures along with proportion of variance explained by covariates.

<p>Ogliastra, 2002–2008.</p><p>Abbreviations: CI, confidence interval; h², heritability.</p>a<p>The proportion of variance explained by covariates refers to the variables included in the model: sex, age, BMI, alcohol consumption, education, smoking and, exercise.</p

Odds ratio to have aminotransferase elevations in <i>MYH9</i>-RD patients as compared with the three control populations.

<p>Data represent ORs (95% CIs).</p><p>N.A. = not available</p><p>Note:</p>1<p> = Calculation of the OR is not possible since none of the 77 analysed ITP patients presented an elevation of AST.</p

Prevalence of liver enzyme alterations in the analyzed patient populations.

<p>Data are presented as n° of patients with altered value/total n° of evaluable patients (%).</p><p>N.A. = not available.</p

Genetic analysis of the 75 <i>MYH9</i>-RD patients described in this study.

<p>Abbreviations: Ref. = references.</p

Demographic characteristics of the study populations.

<p>Demographic characteristics of the study populations.</p

Increased Serum Hepcidin Levels in Subjects with the Metabolic Syndrome: A Population Study

<div><p>The recent discovery of hepcidin, the key iron regulatory hormone, has changed our view of iron metabolism, which in turn is long known to be linked with insulin resistant states, including type 2 diabetes mellitus and the Metabolic Syndrome (MetS). Serum ferritin levels are often elevated in MetS (Dysmetabolic hyperferritinemia - DHF), and are sometimes associated with a true mild-to-moderate hepatic iron overload (dysmetabolic iron overload syndrome - DIOS). However, the pathophysiological link between iron and MetS remains unclear. This study was aimed to investigate, for the first time, the relationship between MetS and hepcidin at population level. We measured serum hepcidin levels by Mass Spectrometry in 1,391 subjects from the Val Borbera population, and evaluated their relationship with classical MetS features. Hepcidin levels increased significantly and linearly with increasing number of MetS features, paralleling the trend of serum ferritin. In multivariate models adjusted for relevant variables including age, C-Reactive Protein, and the HFE C282Y mutation, ferritin was the only significant independent predictor of hepcidin in males, while in females MetS was also independently associated with hepcidin. Overall, these data indicate that the fundamental iron regulatory feedback is preserved in MetS, i.e. that hepcidin tends to progressively increase in response to the increase of iron stores. Due to recently discovered pleiotropic effects of hepcidin, this may worsen insulin resistance and contribute to the cardiovascular complications of MetS.</p> </div