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's version/PDF cannot be used
    • On author's server, institutional server 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'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: While the randomized clinical trial is considered to provide the highest level of evidence in clinical medicine, its superiority to other study designs in the context of prevention studies is debated. The purpose of this review was (i) to gather evidence about challenges facing both randomized controlled trials and observational designs for the conduct of population-based chronic disease prevention interventions and (ii) to consider the suitability of recently proposed hybrid designs for population-based prevention intervention studies.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Background During the progression of the metabolic syndrome (MetS), cardiovascular diseases (CVD) appear clinically in many individuals and cause death. As a result, it is essential to set-up an optimal animal model to study the mechanism of MetS leading to CVD. SIRT1 and AMPK are the master regulators of lipid and carbohydrate metabolism. The objective of this study was to establish a miniature pig model of Western diet-induced MetS and investigate the role of SIRT1/AMPK during MetS development.Methods Five-month-old Lee-Sung (LS) and Lanyu (LY) minipigs were each randomly assigned to 2 groups: control diet (C) and Western diet (W), in a 6-month experimental period.ResultsWestern diet caused obesity in both minipig models. Compared with the CLS pigs, WLS pigs exhibited hypercholesterolemia. However, WLY pigs maintained a similar plasma lipid profile to the CLY pigs. Western diet caused a lower antioxidant capacity in the liver of both pig models. WLS pigs had higher triglyceride accumulation in the liver than CLS pigs, whereas WLY and CLY pigs had similar hepatic triglyceride accumulation. Compared with CLS pigs, WLS pigs had a lower hepatic SIRT1 expression, whereas WLY pigs had a higher expression of AMPK, FOXO1 and SIRT1 than CLY pigs.Conclusion Long-term feeding of the Western diet to Lee-Sung miniature pigs not only caused obesity but also induced MetS and fatty liver, whereas, Western diet induced obesity in Lanyu pigs without metabolic dysfunctions. SIRT1/AMPK and their downstream pathways might be one of the possible regulators for pathological obesity in Lee-Sung pigs.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Background Although there is no direct evidence, it is generally believed that bed rest shifts the hemostatic system towards hypercoagulability; thus, immobilized patients are commonly treated with anticoagulants. We, therefore, aimed to investigate whether long-term bed rest actually leads to an elevated risk for thromboembolic events.Materials and methodsEleven healthy men were enrolled in our study (bed rest campaign in MEDES Clinique d'Investigation, Toulouse, France). Besides various standard laboratory methods, we used calibrated automated thrombography (CAT) and thrombelastometry (TEM). Activation of samples with minute amounts of relipidated tissue factor allowed sensitive detection of hyper- or hypocoagulable states.ResultsCAT and TEM values were not indicative of bed rest-induced hypercoagulability. On the contrary, several parameters were indicative of a tendency towards a hypocoagulable state. Peak and thrombin formation velocity (VELINDEX) were significantly decreased during bed rest compared to baseline. CTs were significantly increased and alpha angles were significantly decreased, indicating attenuated clot formation. Moreover, F1+2 and TAT values were significantly decreased during bed rest, indicating suppressed coagulation activation. FVII plasma levels were also significantly decreased during the first week of bed rest.Conclusions Our data indicate that the re-ambulation period is associated with a tendency towards hypercoagulability: ttPeak and StartTail were significantly shorter, Peak and VELINDEX were significantly higher compared to baseline. Moreover, plasma levels of F1+2, TAT, FVII, and FVIII were significantly higher compared to baseline. The results from our study suggest that bed rest by itself is not associated with hypercoagulable states in healthy subjects.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: The concept of leukemic stem cells (LSCs) has been developed to explain the complex cellular hierarchy and biology of leukemias, and to screen for pivotal targets that can be employed to improve drug therapies through LSC-eradication in these patients. Some of the newly discovered LSC-markers seem to be expressed in a disease-specific manner and may thus serve as major research-tools and diagnostic parameters. A useful LSC-marker in chronic myeloid leukemia (CML) appears to be CD26, also known as dipeptidyl-peptidase IV (DPPIV). Expression of CD26 is largely restricted to CD34+/CD38─ LSCs in BCR/ABL1+ CML, but is not found on LSCs in other myeloid or lymphoid neoplasms, with the exception of lymphoid blast crisis of CML, BCR/ABL1p210+ acute lymphoblastic leukemia, and a very few cases of acute myeloid leukemia. Moreover, CD26 is usually not expressed on normal bone marrow stem cells. Functionally, CD26 is a cytokine-targeting surface enzyme that may facilitate the mobilization of LSCs from the bone marrow niche. In the current article we review our current knowledge about the biology and function of CD26 on CML LSCs and discuss the diagnostic potential of this new LSC marker in clinical hematology.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Recent trends in health care financing and delivery is increasingly generating situations where interests of physicians and patients may not necessarily align. As a result, each party is incentivized to act strategically according to their best interest. This situation can be best approached using game theory precepts. When both doctor and patient act according to their individual strategic interests, which are not aligned, both “players” are worse off. We argue that everyone would be better off if the current health “game” structure is changed to better align doctors’ and patients’ interests while rebuilding trust in the medical profession. Instead of competition, society should incentivize alignment of interests of doctors and patients. When the payoffs of different players are similar, the game theory conflict does not apply. Moreover, selection of rational strategies would be facilitated by improvements in the evidence base of medicine (unbiased knowledge of the probabilities of outcomes with different treatment options) and more accurate knowledge of the patient's and physician's values including those of regret, guilt, and frustration that dominate health care decision-making but are rarely explicitly acknowledged.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Chronic inflammatory diseases and systemic autoimmune conditions can result in the development of inflammatory vascular disease (IVD). The inflammatory response in the vascular bed involves several partners including pro-inflammatory cells (macrophages, lymphocytes, monocytes and neutrophils), as well as vascular smooth muscle cells, extracellular matrix components, and endothelial cells [1]. The latter play an important role since vascular injury can be initiated by their increased activation, increased expression of adhesion molecules and recruitment of pro-inflammatory cells [2-4].This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: The concept of axial Spondyloarthritis (axSpA) includes patients with non-radiographic axSpA and ankylosing spondylitis (AS). Inflammatory and chronic/structural changes of the sacroiliac joints and the spine are pathognomonic in patients who are diagnosed with axSpA. In the last years, the evaluation of the natural course of axSpA has been in the focus of research, especially with respect to the relationship between inflammation or postinflammatory changes (detected by magnetic resonance imaging (MRI)) and bone formation (detected by conventional radiographs).Based on the analysis of spinal MRI data, development of new syndesmophytes is directly associated with the parallel occurrence of inflammatory and postinflammatory (fatty) changes in the edges of the vertebral bodies. In contrast, vertebral edges that show only inflammation but no transformation into fatty lesions show a decreased relative risk for development of new bone formation over time.These data are crucial in the understanding of the long-term clinical course of patients with axSpA in daily practice. According to these results, it becomes obvious that anti-inflammatory treatment, especially by using tumor-necrosis-factor alpha (TNFa)-blockers, has the best effect on the radiographic outcomes when it is started in an early disease stage, where only inflammation is driving the disease activity and where structural, postinflammatory changes have not yet occurred.An inhibitory effect on radiographic progression had not been demonstrated during the first 2 years of continuous anti-TNFa treatment, however, very recently first studies reported a decreased rate of radiographic progression when patients were continuously treated with TNFa-blockers for a time period of ≥4 years.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: BackgroundA highly polymorphic Cytosine-Adenosine (CA) repeat sequence microsatellite has been identified in the promoter region of IGF1 gene. Several studies investigated the relationship between IGF1-(CA)n polymorphism and IGF1 levels, with conflicting results. Aim of this study was to investigate the influence of this polymorphism on clinical and biochemical characteristics of acromegalic patients.Methods Eighty-eight acromegalic patients and 104 normal subjects were included in the study. Blood DNA was extracted and analyzed by microsatellite technique using capillary electrophoresis. Patients and controls were subdivided in 19/19 (homozygous for the (CA)19 allele), 19/X (heterozygous for the (CA)19 allele) and X/X (any other genotype).ResultsThe genotype frequency was significantly different between patients and controls, the proportion of 19/19 being lower (28.4% vs 50.0%) and 19/X and X/X higher in acromegalic patients than in controls (P = 0.004). There were no significant differences in age, gender, basal and nadir GH, IGF1-SDS, tumor size, metabolic parameters, outcome, and treatment among the three groups. The different frequency of genotypes in acromegalic patients vs controls, as well as the lack of relationship between IGF1-(CA)n polymorphism and clinical and biochemical data in acromegalic patients, was confirmed by using an additional alternative genotyping considering (CA)19 and (CA)20 homozygotes and heterozygotes vs alleles with more than 19/20 repeats or less.Conclusions Our results do not support the hypothesis that IGF-(CA)n alleles may have a significant role in determining clinical, biochemical and outcome of patients with acromegaly. The possible role of IGF1 polymorphism on susceptibility to acromegaly remains to be investigated.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Background Angiopoietin-1 (Ang-1) is an essential mediator of angiogenesis by establishing vascular integrity, whereas angiopoietin-2 (Ang-2) acts as its natural inhibitor.Objective We aimed to determine the levels of angiopoietins in sputum supernatants of patients with optimally treated asthma and to investigate whether smoking represents a significant covariate on the above possible processes.Methods Eighty-seven patients with asthma (42 smokers) and 28 healthy subjects (14 smokers) were studied. All subjects underwent lung function tests, bronchial hyperresponsiveness assessment and sputum induction for cell count identification and measurement of Ang-1, Ang-2, VEGF, TGF-β1, MMP-2, IL-13, ECP, and IL-8 in supernatants. Airway vascular permeability (AVP) index was also assessed.ResultsAng-1 (ng/ml) levels were significantly higher in patients with asthma compared to normal subjects. Smoking significantly increased Ang-1 levels [median, interquartile ranges 24(13-37) in smoking asthmatics vs. 10 (7-14) in non smoking asthmatics vs. 5.3(3.7-6.5) and 4.6 (3.8-5.7) in healthy smokers and non smokers respectively, p<0.001]. Similar results were observed for Ang-2 (pg/ml) [168 (132-203) vs 124 (82-152) vs 94(78-113) vs 100 (96-108) respectively, p<0.001]. Regression analysis in the whole study population showed a significant negative association for Ang-1 with AVP index, and MMP-2. Smoking was a significant covariate for both Ang-1& Ang-2 in asthmatic patients.Conclusions Ang-1 & Ang-2 levels are up regulated in patients with optimally treated asthma. Our data support a possible role for smoking in the angiogenetic process in asthma.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Background Acotiamide is a first-in-class drug that is used to treat functional dyspepsia. It is considered that acotiamide acts as an antagonist on muscarinic autoreceptors in the enteric nervous system and inhibits acetylcholinesterase activity. We examined the effect of acotiamide on gastric emptying in healthy adult humans.Materials and methodsTwelve healthy adult males were enrolled in this double-blind crossover study. Acotiamide or placebo was administered orally in the 12 subjects 30 minutes before ingestion of a nutritional liquid meal (400Kcal/400mL). Six of the 12 participants took 100mg of acotiamide or placebo, and 6 of the 12 participants took 300 mg of acotiamide or placebo in a double-blind crossover fashion. All subjects underwent measurement of gastric emptying by the 13C breath test.ResultsAfter the meal with placebo was ingested, the %dose/h curve ascended. The %dose/h curve after a meal with 100mg or 300 mg of acotiamide ascended in an identical manner compared with the results with placebo. No significant differences were observed at any studied time point, and there were no significant changes in gastric emptying parameters (gastric emptying coefficient, t 1/2 ex and t lag ex).ConclusionsA single administration of 100mg or 300mg of acotiamide did not affect gastric emptying after a liquid meal in healthy adult humans. Acotiamide has profound effects on restoring delayed gastric emptying and impaired accommodation in patients with FD but may have no effect on gastric emptying in healthy subjects. Such pharmacological actions have not been observed in previous gastroprokinetic studies.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 11/2014;
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    ABSTRACT: Estrogen is an important risk factor for cholesterol cholelithiasis not only in women of childbearing age taking oral contraceptives and postmenopausal women undergoing hormone replacement therapy, but also in male patients receiving estrogen therapy for prostatic cancer. In women, hormonal changes occurring during pregnancy markedly increase the risk of developing gallstones. We investigated whether the potent cholesterol absorption inhibitor ezetimibe could prevent the formation of estrogen-induced cholesterol gallstones in mice.
    European Journal of Clinical Investigation 10/2014;
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    ABSTRACT: Background Low bone turnover osteoporosis is common in cholestatic diseases. Ursodeoxycholic acid (UDCA) counteracts the damaging effects of bilirubin or lithocholic acid (LCA) on osteoblast viability, proliferation and mineralization. UDCA is antiapoptotic in various cell lines, but this effect in bone cells is unknown. Therefore, the consequences of bilirubin and LCA on apoptosis, and if UDCA has antiapoptotic effects have been assessed on osteoblasts.Materials and Methods Human osteoblasts (hOB), and osteosarcoma cell line (Saos-2) were treated with camptothecin as a proapoptotic agent, and UDCA, LCA and bilirubin. Apoptosis was determined by DNA fragmentation, flow cytometry, caspase-3 activity, and expression of proapoptotic (Bcl-2–associated X protein BAX), and antiapoptotic (BCL2 and BCL2-like 1 protein, BCL2L) genes.ResultsBoth LCA (10 μM) and bilirubin (50 μM) induced apoptosis as indicated by DNA fragmentation (4.7 and 3.7 fold, respectively, p<0.001), caspase-3 activity and flow cytometry in Saos-2 and hOB. UDCA (10 μM) reduced the apoptotic effects of camptothecin (0.5 μM) by 61%, (p<0.001), and counteracted the apoptotic effects of LCA and bilirubin determined by DNA fragmentation (56% and 60%, respectively, p<0.001), cytometry and caspase-3 activity in Saos-2, with lower effects in hOB. UDCA (10 μM) downregulated BAX (75%), and upregulated BCL2L (10-fold, p<0.01) genes, and neutralized BAX upregulation (p<0.01) and BCL2L downregulation (p<0.01) induced by LCA and bilirubin.Conclusions Bilirubin and LCA induce apoptosis in osteoblastic cells. UDCA counteracts the apoptotic consequences of these two substances and therefore, it may have further beneficial effects on the decreased bone formation in the cholestasis.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 10/2014;
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    ABSTRACT: Background Elevated levels of fibroblast growth factor 23 (FGF23) are associated with incident heart failure in individuals with or without chronic kidney disease. We aimed to investigate the association between serum FGF23 concentrations and disease severity and long-term outcome in patients with stable heart failure.Materials and methodsSerum levels of C-term FGF23 (Ct-FGF23) concentrations, inorganic phosphate (Pi), parathormone (PTH), and 25-hydroxyvitamin D (25(OH)D) were measured in 208 patients with non-ischemic heart failure (age 48±15 years; 70% male; NYHA Class I 27.8%, NYHA Class II 43.4%, NYHA Class III/IV 28.8%; LV-EF 34±15%; eGFR ≥60ml/min/1.73m2 in 86%).ResultsMedian Ct-FGF23 levels were 18.2 RU/ml (7.5-40.8RU/ml). A dose-response relationship was found between median Ct-FGF23 levels and increasing NYHA class (I: 11.9 RU/ml, II: 15.8 RU/ml, III/IV: 38.8 RU/ml; p<0.001). Ct-FGF23 correlated with NTproBNP (r=0.307, p<0.001), central venous pressure, mean pulmonary arterial pressure, pulmonary capillary wedge pressure and inversely correlated with cardiac output after adjustment for renal function (eGFR) and Pi. LnCt-FGF23 was related with the combined endpoint of death or heart transplantation (hazard ratio 1.452 [1.029 to 2.048]; p=0.034) independent of Pi, PTH, 25(OH)D, age and sex.Conclusion The phosphatonin FGF23 is strongly associated with disease severity and long-term outcome in patients with non-ischemic heart failure and preserved renal function. Further studies are needed to evaluate the pathophysiologic role of FGF23 and its potential as a biomarker in heart failure.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 10/2014;
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    ABSTRACT: Background/Objectives The impact of an elevation of cardiac biomarkers occurring after percutaneous coronary intervention (PCI) on long-term outcome remains controversial. Most available data are based on observational registries using multivariable analysis. In the present study, a case control approach was used to assess separately the impact of post-PCI elevation of CK-MB on the short-term in-hospital outcome and on the long-term outcome after hospital discharge.Methods Between 01.01.1996 and 31.12.2008, a post-procedural rise of CKMB was observed in 363 among 8346 consecutive PCI procedures (4.3%). The overall in-hospital mortality for patients with or without CKMB elevation after PCI was 8.5% and 1.5% respectively (p<0.001). For 245 hospital survivors with CKMB elevation, we found 245 control cases matched for 9 relevant clinical parameters in our PCI database during the same period. The long-term survival of these patients was assessed by KM estimates.ResultsDespite an increased in-hospital mortality among patients with peri-procedural elevation of CKMB, the long-term outcome of patients who are discharged alive is independent of CKMB release, curves of overall survival and of survival free of recurrence of myocardial infarction being similar up to 10 years after hospital discharge.Conclusions In our population, the elevation of CKMB after PCI identified a high risk subgroup for in-hospital mortality but had no impact on the long-term prognosis, once the patient is discharged alive from the hospital.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 10/2014;
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    ABSTRACT: Background Higher body mass index (BMI) is associated with incident heart failure (HF), but paradoxically associated with better prognosis, recognized as the obesity paradox in HF. However, the impact of BMI on detailed prognosis on HF and the mechanism of obesity paradox remain still unclearMethods We researched consecutive 648 patients admitted for HF: Underweight (BMI < 18.5 kg/m2, n=86), Normal (18.5 ≤ BMI < 25, n=380), Overweight (25 ≤ BMI <30, n=147), and Obese (30 ≤ BMI, n=35), and compared the results from their laboratory tests and echocardiography. We also followed cardiac and all-cause mortalityResultsObese group had a higher prevalence of obesity-related co-morbidity (hypertension, diabetes, dyslipidemia), however, tumor necrosis factor-α, adiponectin, troponin T, and systolic pulmonary arterial pressure were higher in the Underweight group than in the other groups (P<0.05, respectively). Left and right ventricular systolic function did not differ among the groups. In the Kaplan-Meier analysis, cardiac and all-cause mortality progressively increased from Obese to Overweight, Normal and Underweight group. Importantly, in the Cox proportional hazard analyses after adjusting for known risk factors, BMI was an independent predictor of cardiac and all-cause mortality (P<0.01, respectively) in HF patientsConclusionsBMI was an independent predictor of cardiac death and all-cause mortality in HF patients. Furthermore, lower BMI was associated with higher circulating levels of tumor necrosis factor-α, adiponectin and troponin T, and higher systolic pulmonary arterial pressureThis article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 10/2014;
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    ABSTRACT: Background Erosive esophagitis (EE) may be complicated by esophageal ulcers, peptic stricture, Barrett's esophagus and esophageal adenocarcinoma. There have been few studies examining the influence of nonalcoholic fatty liver disease (NAFLD) on EE, and even fewer exploring the simultaneous effects of NAFLD, general and central obesity on EE. We thus aim to clarify the relationship between NAFLD and EE when general and/or central obesity are considered simultaneously.Materials and methodsIn this cross-sectional study, we enrolled 12,090 subjects who underwent a health checkup at the Health Examination Center of a university hospital between January 2000 and August 2009 for analysis. NAFLD was diagnosed using liver ultrasound and EE was defined according to the Los Angeles classification by esophagogastroduodenoscopy.ResultsSubjects with EE (1,922; 15.9%) had a higher proportion of NAFLD, general and central obesity. With adjustment for age, gender, hypertension, diabetes mellitus, hiatal hernia, hypertriglyceridemia, high-density lipoprotein cholesterol, alcohol consumption, tea drinking, smoking and habitual exercise, the results of the multivariate analyses showed that general obesity, central obesity and NAFLD were all significantly associated with EE in their separate models. When considering general obesity, central obesity and NAFLD simultaneously, NAFLD, but neither general nor central obesity, remained positively correlated to EE. In addition, male gender, hiatal hernia and hypertriglyceridemia were all significantly associated with EE.Conclusion In addition to general and central obesity, NAFLD is independently associated with increased risk of EE, and the detrimental effect of NAFLD on EE might be greater than those of general and central obesity.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 10/2014;
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    ABSTRACT: Background Patients with obstructive sleep apnea (OSA) experience repetitive cessation of breathing during sleep, leading to intermittent hypoxemia, excessive oxidative stress and systemic inflammation. These insults may damage the vasculature and provoke the corresponding repair response, such as stem cell mobilization to peripheral blood. This study aimed to investigate nocturnal mobilization of stem cells in OSA.Methods Thirty-five OSA patients and thirteen healthy controls were enrolled. Polysomnography was performed, and severity of OSA was defined by apnea-hyponea index (AHI). Peripheral venous blood was drawn after and before sleep for measurement of CD34+ cell and SDF-1α level. Stem cell mobilization was gauged by ratios of the CD34+ level in the morning to that at night or their difference. Correlation analysis was done to identify factors related to stem cell mobilizationResultsCompared to controls, the nocturnal ratios and difference of CD34+ cell level were larger in OSA patients (ratios: 1.141 vs. 0.896, p=0.036; difference: 340 vs. -166 /cc blood, p=0.036), suggestive of stem cell mobilization. The mobilization ratios were related to AHI、body mass index (BMI)、SpO2 nadir、oxygen desaturation index and time sustaining hypoxemia. After adjusting age, gender and BMI, AHI (r=0.357, p=0.016) and hypoxemia-related parameter remained significant. Paired nocturnal differences in CD34+ cell count (p=0.009) and SDF-1α (p=0.001) were also significant in OSA patients, but not in controls. After CPAP therapy for 6 months, the elevated mobilization ratios in OSA patients tended to decline (p=0.059).ConclusionCD34+ stem cell mobilization during sleep was observed in OSA.This article is protected by copyright. All rights reserved.
    European Journal of Clinical Investigation 10/2014;