European Journal of Clinical Investigation (Eur J Clin Investig )

Publisher: European Society for Clinical Investigation, Blackwell Publishing

Description

The Journal of the European Society for Clinical Investigation. The European Journal of Clinical Investigation publishes papers in the field of clinical investigation, provided they contribute to the advancement of knowledge in this field. The term 'clinical investigation' is interpreted widely and includes studies relevant to humans in health or disease, including such studies that may have taken place with animals.

  • Impact factor
    3.37
  • 5-year impact
    3.05
  • Cited half-life
    8.00
  • Immediacy index
    0.70
  • Eigenfactor
    0.01
  • Article influence
    0.90
  • Website
    European Journal of Clinical Investigation website
  • Other titles
    European journal of clinical investigation (Online)
  • ISSN
    1365-2362
  • OCLC
    46653881
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Blackwell Publishing

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • Some journals impose embargoes typically of 6 or 12 months, occasionally of 24 months
    • no listing of affected journals available as yet
  • Conditions
    • See Wiley-Blackwell entry for articles after February 2007
    • Publisher version cannot be used
    • On author or institutional or subject-based server
    • Server must be non-commercial
    • Publisher copyright and source must be acknowledged with set statement ("The definitive version is available at www.blackwell-synergy.com ")
    • Articles in some journals can be made Open Access on payment of additional charge
    • 'Blackwell Publishing' is an imprint of 'Wiley-Blackwell'
  • Classification
    ​ yellow

Publications in this journal

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    ABSTRACT: Coupled arterial and left ventricular properties are poorly documented in acute heart failure. The aim of this prospective non invasive study was to document early changes in ventricular-arterial coupling in patients with acutely decompensated HF (ADHF).
    European Journal of Clinical Investigation 09/2014;
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    ABSTRACT: Both hyperuricaemia and left ventricular (LV) hypertrophy are associated with the metabolic syndrome and increased cardiovascular risk. The relationship between uric acid levels and left ventricular mass in hypertension, however, is unclear. In this study, we have investigated this relationship in hypertensive patients without the metabolic syndrome.
    European Journal of Clinical Investigation 09/2014;
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    ABSTRACT: Objectives The post cardiac arrest syndrome occurs after global hypoxia leading to microcirculatory impairment. Nitric oxide (NO) is a key molecule regulating microvascular function. The enzyme arginase has been suggested to modulate microvascular function by regulating NO metabolism. Therefore we investigated whether arginase increase following global hypoxia and resuscitation and tested whether arginase inhibition influences altered microcirculation in resuscitated patients.Methods To determine the effect of global hypoxia on circulating arginase levels, fourteen healthy subjects were exposed to hypoxia in a normobaric hypoxia chamber (FiO²=9.9%). In addition, 31 resuscitated patients were characterized clinically and arginase 1 was measured on day 1 and day 3. In eight resuscitated patients, a microcirculatory analysis was performed using a sidestream darkfield microcirculation camera. Perfused capillary density (PCD) was recorded before and after sublingual incubation of N-omega-hydroxy-nor-L-arginine (nor-NOHA) alone or together with the NOS inhibitor NG-monomethyl-L-arginine (L-NMMA).ResultsCirculating arginase 1 levels increased in healthy volunteers following global hypoxia in the hypoxic chamber (p<0.01). In addition, arginase 1 levels were higher on day 1 (69.1 ± 83.3 ng/ml) and on day 3 (44.2 ± 65.6 ng/ml) after resuscitation than in control subjects (p<0.001). Incubation of the sublingual mucosa with nor-NOHA increased microcirculatory perfusion (p<0.001). This effect was inhibited by co-incubation with L-NMMA.Conclusions Circulating arginase 1 levels are increased following exposure to global hypoxia and in patients that have been successfully resuscitated after cardiac arrest. Topical arginase inhibition improves microcirculatory perfusion following resuscitation. This is of potential therapeutic importance for the post-cardiac arrest syndrome.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 09/2014;
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    ABSTRACT: Objective We conducted a nationwide population-based cohort study to investigate the effects of asthma on the risk of stroke development in an Asian population.Methods Newly diagnosed asthmatic patients aged ≧ 18 years were identified, and asthma-free controls were randomly selected from the general population and frequency matched according to age, sex, and index year by using records obtained from the National Health Insurance Research Database between 2000 and 2010. Both cohorts were followed up until the end of 2011 to measure the incidence of stroke. The risk of stroke was analyzed using Cox proportional hazard regression models, including factors such as sex, age, and comorbidities.ResultsWe followed the asthmatic patients for 104 697 person-years and followed the nonasthmatic people for 426 729 person-years. The incidence density rate of stroke increased in all of the groups of asthmatic patients compared with that of the controls when stratified according to sex, age, and comorbidities. The hazard ratio (HR) of stroke was 1.37-fold greater for the asthmatic cohort, compared with that for the nonasthmatic cohort, after adjusting for sex, age, and comorbidities. The adjusted HR of developing stroke substantially increased with older age and the increased frequency of asthmatic exacerbation and hospitalization. The patients receiving beta-2 agonists as a treatment exhibited a significantly greater risk of stroke compared with the patients receiving only inhaled corticosteroids, after adjusting for covariates.Conclusion Asthma may be an independent risk factor for stroke, and its severity exhibits a dose response of stroke development.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 09/2014;
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    ABSTRACT: We would like to thank Dr Kim's and Park's for the points raised in their letter which focus on the statistical analyses of our study concerning the prevalence of primary aldosteronism in hypertensive patients [1]. We would like to address their points one by one.The first point raised by the authors of the letter concerns the correlation coefficient that we used in Figure 2. Indeed they are right; it is the Spearman's correlation coefficient. In addition, we fully agree with them that most of the distributions in Figure 2 are skewed.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 09/2014;
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    ABSTRACT: Background Cardiovascular patients suffer from reduced blood flow leading to ischemia and impaired tissue metabolism. Unfortunately, an increasing group of elderly patients cannot be treated with current revascularization methods. Thus, new treatment strategies are urgently needed. Hypoxia inducible factors (HIFs) upregulate the expression of angiogenic mediators together with genes involved in energy metabolism and recovery of ischemic tissues. Especially, HIF-2α is a novel factor and only limited information is available about its therapeutic potential.Methods Gene transfers with adenoviral HIF-1α and HIF-2α were done into the mouse heart and rabbit ischemic hindlimbs. Angiogenesis was evaluated by histology. Left ventricle function was analysed with echocardiography. Perfusion in rabbit skeletal muscles and energy recovery after electrical stimulation-induced exercise were measured with ultrasound and 31P-magnetic resonance spectroscopy (31P-MRS), respectively.ResultsHIF-1α and HIF-2α gene transfers increased capillary size up to 5-fold in myocardium and ischemic skeletal muscles. Perfusion in skeletal muscles was increased by 4-fold without edema. Especially AdHIF-1α enhanced the recovery of ischemic muscles from electrical stimulation-induced energy depletion. Special characteristic of HIF-2α gene transfer was a strong capillary growth in muscle connective tissue and that HIF-2α gene transfer maintained left ventricle function.Conclusions We conclude that both AdHIF-1α and AdHIF-2α gene transfers induced beneficial angiogenesis in vivo. Transient moderate increases in angiogesis improved energy recovery after exercise in ischemic muscles. This study shows for the first time that a moderate increase in angiogenesis is enough to improve tissue energy metabolism which is potentially a very useful feature for cardiovascular gene therapy.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 09/2014;
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    ABSTRACT: Background Exact associations of gender and age with occurrence of ST-elevation myocardial infarction are inadequately known.DesignGender- and age-differences in frequency and incidence of STEMI were studied using a nationwide, population based (26,723,956 person-years) registry of hospital admissions in patients aged ≥30 during 2001-2008 in Finland. Data was collected from all 22 hospitals with a coronary angiolaboratory nationwide.ResultsThe study period included 27,993 STEMI admissions. Of these patients 65.9% were men and 34.1% women, RR 2.37 (95%CI 2.05-2.74, p<0.0001). Women were significantly older than men (74.3±11.7 vs. 64.7±12.4 years, p<0.0001). Standardized incidence rate of STEMI was 113.0 /100,000 person-years overall, 170.9 /100,000 in men and 66.6 / 100,000 in women. Men had a 3.03 (95%CI 2.86-3.21; p<0.0001) fold age-adjusted relative risk of STEMI compared to women with highest risk difference in population under 55 years of age (RR 5.94; 95%CI 5.36-6.58, p<0.0001). Incidence increased with age up to 90 years-old, with estimated gender-adjusted increase rate of 41% (95%CI 40%-42%; p<0.0001) per 5-year increase in age. Incidence rate had a slowly declining trend (-2.2%; 95%CI -3.4 - -1.0% per year, p<0.001) during the study period.Conclusions Men have a tripled overall risk for STEMI compared to women with highest relative risk in younger adults. Incidence rate of ST-elevation myocardial infarction increases by estimated 41% per 5-year increase in age.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 09/2014;
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    ABSTRACT: First of all, we would like to thank the authors for an interesting and novel research on primary aldosteronism in hypertensive patients, which unexpectedly is a common problem in resistant hypertension, but is often overlooked. However, there are a few confusing points in statistical descriptions, while surely not intentional, that we would like to bring to attention.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 09/2014;
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    ABSTRACT: Objective We had the impression that randomized clinical trials (RCT) frequently over enrolled patients. Thus, we surveyed power calculations in publications of RCTs of biologics in rheumatoid arthritis (RA) to assess over enrollment.MethodsA PubMed search identified 40 reports of original RCTs testing the efficacy of infliximab, etanercept, adalimumab, abatacept, rituximab and tocilizumab in RA patients. As a first analysis, based on a two equal arms study with an alpha error of 0.05 and a power of 80% and of 90%, recalculation of the sample size was done by using the primary outcome results. In the second analysis, only those studies with equal number of patients in both arms and also in which all elements of a power calculation were given, were considered. New sample sizes were calculated based on the presented power elements in the related publications.ResultsIn the first analysis when we assigned a power of 80% and of 90%, 32/40 (80%) studies enrolled more than required number of patients, with a mean 131 ± 147 (SD) and 31/40 (78%) studies having had enrolled extra patients, with a mean 121 ± 147 (SD) in their treatment arms, respectively. Eleven studies qualified for the second analysis. There were still more patients with a mean of 48 ± 30 (SD) extra patients enrolled in the treatment arms.Conclusion Most RCTs in RA enroll more patients than needed. This is costly and has the immediate consequence of exposing needless number of patients to potential harm.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 09/2014;
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    ABSTRACT: Background Serum cholesterol has been demonstrated to correlate with blood pressure values, therefore abnormal levels of serum cholesterol might contribute to the development of hypertension. The aim of the present study was to assess the new-onset of hypertension over a period of 8 years in a pharmacologically untreated population sample in normo- and hypercholesterolemic individuals.Design1864 Caucasian subjects with baseline blood pressure values <140/90 mmHg were subdivided into two different groups, according to LDL-Cholesterol changes observed over a period of 8 years. Group 1 included subjects whose LDL-Cholesterol levels remained or decreased within the normal range, while Group 2 included those whose LDL-Cholesterol levels were persistently increased above the normal range. The 8-year incidence of new-onset hypertension was 7.1% in group 1 and 13.8% in group 2 (p=0.02), after adjustment for the main confounding risk factors. The difference between group 1 and 2 was confirmed in men (8.2 vs. 13.1%, p=0.04) and women (6.1. vs. 14.5%, p=006), as well as in subjects younger than 65 years (5.7 vs. 10.9%; p=0.011), but not in older ones.Conclusions Baseline serum LDL-Cholesterol levels are related to the rate of new-onset hypertension in patients with normal or marginally elevated blood pressure values.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 08/2014;
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    ABSTRACT: Background Although generic and earlier brand-name counterparts are bioequivalent, their equivalence in preventing relevant clinical outcomes is of concern.Objective To compare effectiveness of generic and brand-name antihypertensive drugs for preventing the onset of cardiovascular (CV) outcomes.Design and subjectsA population-based, nested case-control study was carried out by including the cohort of 78,520 patients from Lombardy (Italy) aged 18 years or older who were newly treated with antihypertensive drugs during 2005. Cases were the 2,206 patients who experienced a hospitalization for CV disease from initial prescription until 2011. One control for each case was randomly selected from the same cohort that generated cases. Logistic regression was used to model the CV risk associated with starting on and/or continuing with generic or brand-name agents.ResultsThere was no evidence that patients who started on generics experienced different CV risk than those on brand-name product (OR 0.86; 95% CI 0.63 to 1.17). Patients at whom generics were main dispensed had not significantly difference in CV outcomes than those mainly on brand-name agents (OR 1.19; 95% CI 0.86 to 1.63). Compared with patients who kept initial brand-name therapy, those who experienced brand-to-generic or generic-to-brand switches, and those always on generics, did not show differential CV risks, being the corresponding ORs (and 95% CIs), 1.18 (0.96 to 1.47), 0.87 (0.63 to 1.21), and 1.08 (0.80 to 1.46).Conclusions Our findings do not support the notion that brand-name antihypertensive agents are superior to generics for preventing CV outcomes in the real world clinical practice.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 08/2014;
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    ABSTRACT: Background Acute pancreatitis is characterized by inflammatory processes affecting not only the pancreas, but also the lung. Here, we investigated timing of leukocyte infiltration and chemokine expression within lung and pancreas during pancreatitis and whether treatments selectively inhibiting chemokines (using Evasins) could improve organ injury.Material and methodsC57Bl/6 mice were submitted in vivo to 10-hourly intraperitoneal injections of cerulein and followed for up to 168 hours. Five minutes after the first cerulein injection, a single intraperitoneal injection of 10 μg Evasin-3, 1 μg Evasin-4 or an equal volume of vehicle (PBS) was performed. Leukocytes, reactive oxygen species (ROS), necrosis and chemokine/cytokine mRNA expression were assessed in different organs by immunohistology and Real time RT-PCR, respectively.ResultsIn the lung, neutrophil and macrophage infiltration peaked at 12 hours and was accompanied by increased CXCL2 mRNA expression. CCL2, CXCL1 and TNF-alpha significantly increased after 24 hours as compared to baseline. No increase in CCL3 and CCL5 was observed. In the pancreas, neutrophil infiltration peaked at 6 hours, while macrophages increased only after 72 hours. Treatment with Evasin-3 decreased neutrophil infiltration, ROS production and apoptosis in the lung and reduced neutrophils, macrophages apoptosis and necrosis in the pancreas. Evasin-4 only reduced macrophage content in the lung and did not provide any benefit at the pancreas level.Conclusion Chemokine production and leukocyte infiltration are timely regulated in lung and pancreas during pancreatitis. CXC chemokine inhibition with Evasin-3 improved neutrophil inflammation and injury, potentially interfering with damages in acute pancreatitis and related pulmonary complications.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 08/2014;
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    ABSTRACT: Background Matrix metalloproteinases (MMPs), especially MMP-2 and MMP-9, have been identified in atherosclerotic plaques and have been directly associated with plaque remodeling and vulnerability. Cardiovascular disease is related to insulin-resistance (IR) and obesity, characterized by changes in plasma levels of inflammatory markers, such as adiponectin and C reactive protein (CRP). Our aim was to evaluate the impact of both proteins on MMP-2 and MMP-9 behavior in individuals with IR.Materials and methodsPlasma MMP-2 and MMP-9 activity, adiponectin and hs-CRP concentration and lipoprotein profile were determined in 52 patients with Metabolic Syndrome (MS) and 27 controls.ResultsPatients with MS presented significantly higher MMP-2 activity than controls: 0.95 ± 0.12 vs 0.77 ± 0.15 relative units (RU) (p<0.001), while MMP-9 activity was no detectable MMP-2 activity decreased across quartiles of adiponectin, being significantly reduced in individuals with the highest levels of adiponectin in compared with the lowest levels (0.75±0.17 vs 0.93±0.09 RU, p<0.005). This difference persisted significant after adjusting by obesity markers. MMP-2 activity was significantly increased in individuals with the highest levels (G3) compared with those with the lowest levels (G1) of hs-CRP (0.94±0.12 vs 0.86±0.12, p=0.041)Conclusion In this study we observed that adiponectin levels predicted MMP-2 plasma activity independently of obesity. This finding suggests that the inflammatory process, associated with the highest CVD risk, would be involved in MMPs vascular production.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 08/2014;
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    ABSTRACT: BackgroundA new 4-classification of left ventricular hypertrophy (LVH) based on LV concentricity and dilation has been proposed, however, the association between the new categorization of LV geometry and outcomes in patients with coronary artery disease (CAD) is still unknown.Methods All the 2297 CAD patients included underwent echocardiographic examination prior to discharge. Left ventricular mass (LVM) was calculated and left ventricular end-diastolic volume (EDV) was indexed by body surface area (BSA). Study cohort were divided into 5 groups according to LV geometry: 1) eccentric non-dilated LVH (normal LVM/EDV(2/3) and EDV/BSA) (n=129); 2) eccentric dilated LVH (normal LVM/EDV(2/3) with increased EDV/BSA) (n=222); 3) concentric non-dilated LVH (increased LVM/EDV(2/3) with normal EDV/BSA) (n=441); 4) concentric dilated LVH (increased LVM/EDV(2/3) and EDV/BSA) (n=118); 5) normal LV mass (n=1387).ResultsDilated LVH was associated with a higher event rates of all-cause death (eccentric 13.1% vs. 3.1%; concentric: 13.6% vs. 8.4%) and composite events (eccentric: 17.6% vs. 5.4%; concentric: 18.6% vs. 12.7%) compared with non-dilated LVH. While eccentric non-dilated LVH had comparable risk for adverse outcomes compared with normal LV mass (all-cause death: relative risk (RR) 0.68, 95% confidential interval (CI) 0.25-1.85; composite events: RR 0.75, 95% CI 0.36-1.58). Cox regression analyses showed that eccentric dilated LVH had the highest propensity to all-cause death (adjusted hazard ratio [aHR] 2.752 [95% CI 1.749-4.328], P<0.001) and composite events (aHR 2.462 [95% CI 1.688-3.592], P<0.001).Conclusion In patients with CAD, dilated and non-dilated LVH provide distinct prognostic information. Eccentric non-dilated LVH does not predict adverse outcomes.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 08/2014;
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    ABSTRACT: IntroductionThere are no data about the efficacy of gemcitabine in combination with oxaliplatin (GEMOX) and erlotinib for the treatment of metastatic pancreatic cancer (mPC). Thus, we performed this retrospective analysis in mPC patients in order to investigate the activity and safety of GEMOX plus erlotinib and correlated the benefit with ERCC1 expression, a potential biomarker for treatment response.Patients and methodsPatients with untreated mPC receiving off-protocol GEMOX plus erlotinib were included. Data collection included baseline demographic, response and toxicity data as well as PFS and OS. Additionally, immunohistochemistry was performed to stain for ERCC1 expression.ResultsA total of 51 patients were included. The median age was 62 years and the median ECOG performance score was 1 (range, 0-1). Objective response or disease stabilization was achieved in 54% of the patients. The median PFS was 4.4 months (95% CI 4.4-5.4) and median OS was 8.5 months (95% CI 6.1-10.9). The 27 patients, who benefited from this regimen, had a median PFS of 6.7, a median OS of 11.2 months and an overexpression of ERCC1 (histoscore 10, p≤0.05) compared to non-responders (histoscore 7.2). Myelosuppression was the most frequent side effect. The most common severe nonhematological toxicities were diarrhea and skin toxicity in 6 (12%) patients each.Conclusions These data suggest that the combination of GEMOX plus erlotinib is safe and active in about half of the patients. Patients, who had a higher ERCC1 staining pattern, benefited most from this therapy. Prospective biomarker studies are warranted to confirm these findings.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 08/2014;
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    ABSTRACT: Background Periodontitis is the most common oral infection seen in humans worldwide. It is characterized by gradual destruction of tooth supporting tissues, eventually leading to loss of tooth. The periodontal biofilm associated with periodontitis comprises of gram-positive and gram-negative bacteria, instrumental for the initiation and progression of periodontitis. Evidence based literature has identified the nature of periodontal infection as a possible causative condition in the inducement of “low grade systemic inflammation and infection.” The periodontal pathogens exert systemic effects via the hematogenous route.AimThe present review provides an insight into the pathophysiology of the endothelial dysfunction with reference to periodontal infectionand highlights the association between periodontitis and endothelial dysfunction. Various studies addressing the implication of periodontitis on endothelial dysfunction will be described, with a focus of periodontal treatment on improvement of endothelial function.Materials and methodsStudies examining the effects of periodontitis on vascular endothelial function were segregated. Studies conducted on both animal and human models were identified using MEDLINE data base search with key search terms such as ‘‘Periodontitis’’, ‘‘vascular endothelium’’, “endothelial dysfunction”, “periodontal bacteria”, ‘‘periodontal therapy”. Systematic reviews, meta-analysis were also screened. Only studies published in English language were considered. The review has been prepared by screening MEDLINE database from 1989 to 2012.Results and conclusionsChronic periodontitis results in altered vascular response, increased expression of pro-inflammatory cytokines and adhesion molecules inducing vascular endothelial dysfunction. Periodontal therapy may ameliorate the perturbed vascular endothelial function.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 08/2014;
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    ABSTRACT: PurposeTo evaluate whether diabetes is a risk factor for breast cancer considering confounders and potential detection examinations.Methods National Health Insurance data on 501,747 women without breast cancer were retrieved. Three-year cumulative incidence (2003–2005) and risk ratios (RRs) between diabetic and non-diabetic women were calculated. Potential detection examinations were compared between diabetic and non-diabetic women by Chi square test. Odds ratios (ORs) were estimated by logistic regression for diabetes status/duration with and without adjustment for potential detection examinations and confounders.ResultsThe crude RR (95% confidence interval [CI]) for all ages, and age groups <50, 50–64 and ≥65 years, was 2.62 (2.31–2.91), 2.69 (2.11–3.44), 1.39 (1.15–1.68) and 1.37 (1.03–1.84), respectively. Diabetes patients more frequently received potential detection examinations than non-diabetes (17.5% versus 7.4%, P-value <0.001). The unadjusted OR (95% CI) for breast cancer for diabetes status (yes versus no) was 2.63 (2.31-2.98), and was significant for any diabetes duration. The OR for diabetes status was 1.81 (95% CI: 1.59-2.06) after adjustment for potential detection examinations. In models adjusted for potential detection examinations, age, living region, occupation, comorbidities and used medications, OR for diabetes status attenuated to 1.13 (95% CI 0.96-1.32, P-value=0.14); and none was significant for any diabetes duration. Potential detection examinations were associated with a 5-fold to 7-fold higher risk in various models, indicating a strong impact of detection bias.Conclusions An association between diabetes and breast cancer is observed, but this can be due to potential detection bias and confounders.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 08/2014;
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    ABSTRACT: IntroductionIrisin activates the thermogenic function in adipose tissues. However, little is known on the association between human irisin and different cardiometabolic risk factors. We analyze the influence of morbid obesity on irisin levels and its relation with leptin and different cardiovascular risk factors.Material and Methods We measured the serum irisin level and the fibronectin type III domain containing 5 (FNDC5) expression in adipose tissue from 33 morbidly obese subjects and 12 non-obese subjects. We also studied the effect of leptin on FNDC5 expression.ResultsSerum irisin was higher in the non-obese subjects than in morbidly obese subjects, both before (p=0.043) and after bariatric surgery (p=0.042). The variable that best explained the serum irisin levels in a multiple linear regression model was the waist-to-hip ratio (WHR) (R2=0.201) (Beta=-0.357, p=0.046). Those morbidly obese subjects with android-type obesity had lower serum irisin levels than those with gynecoid-type obesity, both before (p=0.027) and after bariatric surgery (p=0.006). Only the percentage change in WHR was associated with serum irisin levels after bariatric surgery (r=-0.529, p=0.005). FNDC5 expression levels in subcutaneous adipose tissue (SAT) were higher in the non-obese than in the morbidly obese subjects (p=0.042). In SAT explants from non-obese subjects, leptin (20 and 150 ng/ml) produced a decrease in FNDC5 expression (p=0.009 and p=0.037, respectively).Conclusions We showed decreased serum irisin levels in morbidly obese subjects, related mainly to WHR. FNDC5 expression could be regulated by leptin.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 08/2014;
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    ABSTRACT: Background In animal models and clinical trials, statins are reported as effective in reducing cholesterol levels and lowering the risk of cardiovascular diseases. We have aggregated the findings in animal models - mice, rats and rabbits - using the technique of systematic review and meta-analysis to highlight differences in the efficacy of statins.Materials and Methods We searched Medline and Embase. After examining all eligible articles, we extracted results about total cholesterol and other blood parameters, blood pressure, myocardial infarction and survival. Weighted and standard mean difference random effects meta-analysis was used to measure overall efficacy in pre-specified species, strains and subgroups.ResultsWe included in systematic review 161 animal studies and we analyzed 120 studies, accounting for 2432 animals. Statins lowered the total cholesterol across all species, although with large differences in the effect size: -30% in rabbits, -20% in mice and -10% in rats. The reduction was larger in animals fed on a high-cholesterol diet. Statins reduced infarct volume, but did not consistently reduce the blood pressure or effect the overall survival. Few studies considered strains at high risk of cardiovascular diseases or hard outcomes.Conclusions Although statins showed substantial efficacy in animal models, few preclinical data considered conditions mimicking human pathologies for which the drugs are clinically indicated and utilized. The empirical finding that statins are more effective in lowering cholesterol derived from an external source (i.e. diet) conflicts with statin's supposed primary mechanism of action.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 07/2014;
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    ABSTRACT: Atrial fibrillation is a sustained arrhythmia commonly encountered in clinical practice. It has a high prevalence among the elderly, and contributes significantly to the global social-economic burden. Among many risk factors predisposing to atrial fibrillation is left atrial remodeling and wall fibrosis. Frequently, pathological left atrial wall remodeling and fibrosis results in low atrial compliance and elastance significantly increase the risk of developing permanent atrial fibrillation. Current imaging tools may play a role in the detection of atrial fibrosis hence providing valuable information for risk stratification and management of patients with atrial fibrillation.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 07/2014;

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