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Adipose tissue distribution in relation to insulin sensitivity and inflammation in Pakistani and Norwegian subjects with type 2 diabetes.

https://arctichealth.org/en/permalink/ahliterature267601
Source
Scand J Clin Lab Invest. 2014 Nov;74(8):700-7
Publication Type
Article
Date
Nov-2014
Author
Cecilie Wium
Heidi B Eggesbø
Thor Ueland
Annika E Michelsen
Peter A Torjesen
Pål Aukrust
Kåre Birkeland
Source
Scand J Clin Lab Invest. 2014 Nov;74(8):700-7
Date
Nov-2014
Language
English
Publication Type
Article
Keywords
Abdominal Fat - pathology - radiography
Adipokines - blood
Adult
Body Fat Distribution
Diabetes Mellitus, Type 2 - blood - ethnology - pathology
Female
Humans
Inflammation Mediators - blood
Insulin Resistance
Male
Middle Aged
Muscle, Skeletal - pathology
Norway
Organ Specificity
Pakistan - ethnology
Abstract
Immigrants from South Asia to Western countries have a high prevalence of type 2 diabetes mellitus (T2DM) associated with obesity. We investigated the relationship between diabetes and adipose tissue distribution in a group of younger T2DM subjects from Norway and Pakistan. Eighteen immigrant Pakistani and 21 Norwegian T2DM subjects (age 29-45, 49% men) were included. They underwent anthropometrical measurements including bioelectrical impedance analysis, CT scans measuring fatty infiltration in liver and adipose and muscle tissue compartments in mid-abdomen and thigh, a euglycemic clamp, and blood samples for serum insulin and plasma glucose, adipokines and inflammation markers. Adipose tissue distribution was similar in Norwegians and Pakistanis. Pakistanis, but not Norwegians, showed a negative correlation between insulin sensitivity and visceral adipose tissue (VAT, rs = - 0.704, p = 0.003). Subcutaneous adipose tissue (SAT) correlated to leptin in both Pakistanis and Norwegians (rs = 0.88, p
Notes
Comment In: Scand J Clin Lab Invest. 2015 Sep;75(5):434-525874480
Comment In: Scand J Clin Lab Invest. 2015 Sep;75(5):438-925916836
Comment In: Scand J Clin Lab Invest. 2015 Sep;75(5):44025916835
PubMed ID
25223599 View in PubMed
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Adiposity-related inflammation: effects of pregnancy.

https://arctichealth.org/en/permalink/ahliterature115475
Source
Obesity (Silver Spring). 2013 Jan;21(1):E124-30
Publication Type
Article
Date
Jan-2013
Author
Camilla M Friis
Marie C Paasche Roland
Kristin Godang
Thor Ueland
Tom Tanbo
Jens Bollerslev
Tore Henriksen
Author Affiliation
Division of Obstetrics and Gynaecology, Oslo University Hospital Rikshospitalet, Oslo, Norway. camilla.friis@ous-hf.no
Source
Obesity (Silver Spring). 2013 Jan;21(1):E124-30
Date
Jan-2013
Language
English
Publication Type
Article
Keywords
Adipose Tissue
Adiposity
Adult
Body Composition
Body mass index
European Continental Ancestry Group
Female
Humans
Inflammation - blood - etiology
Inflammation Mediators - blood
Longitudinal Studies
Norway
Obesity - blood - complications
Overweight - blood
Pregnancy
Pregnancy Complications - blood
Reference Values
Statistics, nonparametric
Up-Regulation
Abstract
In the nonpregnant population, there is extensive evidence of a systemic low-grade inflammatory status in relation to excess adipose tissue. Less is known about the relation during pregnancy.
Our main objective was therefore to explore the effect of pregnancy on adiposity-related systemic inflammation.
This study is a longitudinal cohort study of 240 pregnant women of Scandinavian heritage at Oslo University hospital-Rikshospitalet, Norway from 2002 to 2005. The inflammatory markers (C-reactive protein [CRP], Interleukin-6 [IL-6], monocyte chemoattractant protein 1 [MCP-1], IL1-Ra, tumor necrosis factor receptor II, and IL-10) were measured at four timepoints during pregnancy and analyzed by enzyme immuno-assay. The women were categorized based on BMI at inclusion (BMI 30 kg/m(2)). Data were analyzed by Friedman-test, Wilcoxon signed rank test, or Kruskal-Wallis test as appropriate.
Maternal adiposity was associated with significantly higher circulatory levels of several inflammatory markers (CRP, MCP-1, IL-6, and IL-1Ra). However, this proinflammatory upregulation was not evident toward the end of pregnancy, as levels of CRP, MCP-1, and IL-6 were not any longer significantly different between the BMI categories.
Although normal pregnancy exhibits proinflammatory features, this does not seem to have additive or synergistic effects on the inflammation associated with adiposity. On the contrary, we found that the BMI-dependent increase in proinflammatory markers was not evident at the end of pregnancy.
PubMed ID
23505192 View in PubMed
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ALCAM predicts future cardiovascular death in acute coronary syndromes: Insights from the PLATO trial.

https://arctichealth.org/en/permalink/ahliterature307717
Source
Atherosclerosis. 2020 01; 293:35-41
Publication Type
Journal Article
Multicenter Study
Randomized Controlled Trial
Research Support, Non-U.S. Gov't
Date
01-2020
Author
Thor Ueland
Axel Åkerblom
Tatevik Ghukasyan
Annika E Michelsen
Richard C Becker
Maria Bertilsson
Andrzej Budaj
Jan H Cornel
Anders Himmelmann
Stefan K James
Agneta Siegbahn
Robert F Storey
Frederic Kontny
Pål Aukrust
Lars Wallentin
Author Affiliation
Research Institute of Internal Medicine, The National Hospital, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammatory Research Center, University of Oslo, Norway; K.G. Jebsen - Thrombosis Research and Expertise Center (TREC), University of Tromsø, Tromsø, Norway. Electronic address: thor.ueland@medisin.uio.no.
Source
Atherosclerosis. 2020 01; 293:35-41
Date
01-2020
Language
English
Publication Type
Journal Article
Multicenter Study
Randomized Controlled Trial
Research Support, Non-U.S. Gov't
Keywords
Acute Coronary Syndrome - blood - mortality
Aged
Antigens, CD - blood
Biomarkers - blood
Cell Adhesion Molecules, Neuronal - blood
Female
Fetal Proteins - blood
Follow-Up Studies
Humans
Male
Middle Aged
Norway - epidemiology
Prognosis
Risk factors
Survival Rate - trends
Sweden - epidemiology
Abstract
Activated leukocyte cell adhesion molecule (ALCAM) is upregulated during inflammation and involved in transmigration of leukocytes and T-cell activation. We hypothesized that ALCAM might be associated with recurrent events in patients with acute coronary syndromes (ACS).
ALCAM was measured in serum obtained on admission, at discharge, 1 month and 6 months in a subgroup of 5165 patients admitted with ACS and included in the PLATelet inhibition and patient Outcomes (PLATO) trial (NCT00391872). The association between ALCAM and the composite endpoint and its components, including cardiovascular (CV) death, non-procedural spontaneous myocardial infarction (MI) or stroke during 1-year follow-up, was assessed by Cox proportional hazards models with incremental addition of clinical risk factors and biomarkers (including high-sensitivity troponin T, N-terminal pro-B-type natriuretic peptide and growth differentiation factor-15).
The median (Q1-Q3) concentration of ALCAM at admission was 97 (80-116) ng/mL. A 50% higher level of ALCAM on admission was associated with a hazard ratio (HR) of 1.16 (95% confidence interval [1.00-1.34] p = 0.043) for the composite endpoint in fully adjusted analysis, mainly driven by the association with CV death (HR 1.45 [1.16-1.82] p = 0.0012).
In patients with ACS, admission level of ALCAM was independently associated with adverse outcome including CV death even after adjustment for established inflammatory and cardiac biomarkers.
PubMed ID
31835039 View in PubMed
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CCL21 is associated with fatal outcomes in chronic heart failure: data from CORONA and GISSI-HF trials.

https://arctichealth.org/en/permalink/ahliterature115603
Source
Eur J Heart Fail. 2013 Jul;15(7):747-55
Publication Type
Article
Date
Jul-2013
Author
Thor Ueland
Ståle H Nymo
Roberto Latini
John J V McMurray
John Kjekshus
Arne Yndestad
Alessandro Fucili
Aurelia Grosu
Serge Masson
Aldo P Maggioni
Lars Gullestad
Pål Aukrust
Author Affiliation
Research Institute for Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway. r.ueland@medisin.uio.no
Source
Eur J Heart Fail. 2013 Jul;15(7):747-55
Date
Jul-2013
Language
English
Publication Type
Article
Keywords
Aged
Chemokine CCL21 - blood
Disease Progression
Double-Blind Method
Female
Fluorobenzenes - therapeutic use
Heart Failure - blood - drug therapy - mortality
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use
Kaplan-Meier Estimate
Male
Norway - epidemiology
Prognosis
Proportional Hazards Models
Pyrimidines - therapeutic use
Risk factors
Sulfonamides - therapeutic use
Survival Rate - trends
Treatment Outcome
Abstract
Chronic heart failure (HF) is in part characterized by immune activation and inflammation, and factors that regulate lymphocyte trafficking and inflammation may contribute to the progression of this disorder. The homeostatic chemokine CCL21 is a potent regulator of T-cell migration into non-lymphoid tissue and may exert inflammatory properties and influence tissue remodelling. We therefore investigated CCL21 levels and association with fatal outcomes in patients with chronic HF.
Plasma CCL21 was measured at randomization in 1456 patients enrolled in the Controlled Rosuvastatin Multinational Trial in HF (CORONA) and in 1145 from the GISSI-HF trial. Association between CCL21 levels [given below as hazard ratio (HR) with 95% confidence interval (CI) for 1 SD increase] with all-cause (n = 741) or cardiovascular (CV) mortality (n = 576) was evaluated with multivariable Cox proportional hazard models, adjusting for clinical risk factors, C-reactive protein, and NT-proBNP. In multivariable Cox models, CCL21 was associated with higher risk of all-cause mortality (HR 1.16, 95% CI 1.02-1.32; P = 0.020) and CV mortality (HR 1.20, 95% CI 1.08-1.33; P
PubMed ID
23487539 View in PubMed
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Complement Activation Assessed by the Plasma Terminal Complement Complex and Future Risk of Venous Thromboembolism.

https://arctichealth.org/en/permalink/ahliterature298953
Source
J Thromb Haemost. 2019 Mar 28; :
Publication Type
Journal Article
Date
Mar-28-2019
Author
Ina Isabella Høiland
Robin Amanda Liang
Sigrid K Braekkan
Kristin Pettersen
Judith K Ludviksen
Nadezhda Latysheva
Omri Snir
Thor Ueland
Kristian Hindberg
Tom Eirik Mollnes
John-Bjarne Hansen
Author Affiliation
K. G. Jebsen - Thrombosis Research and Expertise Center (TREC), Department of Clinical Medicine, UiT - The Arctic University of Norway, Tromsø.
Source
J Thromb Haemost. 2019 Mar 28; :
Date
Mar-28-2019
Language
English
Publication Type
Journal Article
Abstract
It remains uncertain whether activation of the complement system, assessed by the soluble terminal C5b-9 complement complex (plasma TCC), is associated with future risk of incident venous thromboembolism (VTE).
To investigate the association between plasma levels of TCC and future risk of incident VTE in a nested case-control study, and to explore genetic variants associated with TCC using protein quantitative trait loci (pQTL) analysis of exome sequencing data.
We sampled 415 VTE cases and 848 age- and sex-matched controls from a population-based cohort, the Tromsø study. Logistic regression models were used to calculate odds ratios (ORs) with 95% confidence intervals (CIs) for VTE across quartiles of plasma levels of TCC. Whole exome sequencing was conducted using the Agilent SureSelect 50Mb capture kit.
The risk of VTE increased across increasing quartiles of plasma TCC, particularly for unprovoked VTE. Participants with TCC in the highest quartile (>1.40 CAU/mL) had an OR for unprovoked VTE of 1.74 (95% CI: 1.10-2.78) compared to those with TCC in the lowest quartile (=0.80 CAU/mL) in analyses adjusted for age, sex and body mass index. A substantially higher risk for VTE was observed in samples taken shortly before VTE event. We found no association between genome-wide or complement-related gene variants and plasma levels of TCC.
We found that high levels of plasma TCC were associated with VTE risk, and unprovoked events in particular. There was no genome-wide association between gene variants and plasma levels of TCC. This article is protected by copyright. All rights reserved.
PubMed ID
30920726 View in PubMed
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Cytokine responses, microbial aetiology and short-term outcome in community-acquired pneumonia.

https://arctichealth.org/en/permalink/ahliterature294315
Source
Eur J Clin Invest. 2018 Jan; 48(1):
Publication Type
Journal Article
Date
Jan-2018
Author
William W Siljan
Jan C Holter
Ståle H Nymo
Einar Husebye
Thor Ueland
Pål Aukrust
Tom E Mollnes
Lars Heggelund
Author Affiliation
Department of Internal Medicine, Drammen Hospital, Vestre Viken Hospital Trust, Drammen, Norway.
Source
Eur J Clin Invest. 2018 Jan; 48(1):
Date
Jan-2018
Language
English
Publication Type
Journal Article
Keywords
Aged
Biomarkers - metabolism
Community-Acquired Infections - blood - mortality
Complement Activation - physiology
Complement Membrane Attack Complex - metabolism
Cytokines - metabolism
Female
Hospitalization - statistics & numerical data
Humans
Male
Middle Aged
Norway - epidemiology
Pneumonia - blood - mortality
Prognosis
Abstract
The inflammatory response to community-acquired pneumonia (CAP) is orchestrated through activation of cytokine networks and the complement system. We examined the association of multiple cytokines and the terminal complement complex (TCC) with microbial aetiology, disease severity and short-term outcome.
Plasma levels of 27 cytokines and TCC were analysed in blood samples obtained at hospital admission, clinical stabilization and 6-week follow-up from 247 hospitalized adults with CAP. Fourteen mediators were included in final analyses. Adverse short-term outcome was defined as intensive care unit (ICU) admission and 30-day mortality.
Cytokine and TCC levels were dynamic in the clinical course of CAP, with highest levels seen at admission for most mediators. Admission levels of cytokines and TCC did not differ between groups of microbial aetiology. High admission levels of IL-6 (odds ratio [OR] 1.47, 95% confidence interval [CI] 1.18-1.84, P = .001), IL-8 (OR 1.79, 95% CI 1.26-2.55, P = .001) and MIP-1ß (OR 2.28, 95% CI 1.36-3.81, P = .002) were associated with a CURB-65 severity score of =3, while IL-6 (OR 1.37, 95% CI 1.07-1.74, P = .011) and MIP-1ß (OR 1.86, 95% CI 1.03-3.36, P = .040) were associated with a high risk of an adverse short-term outcome.
In this CAP cohort, admission levels of IL-6, IL-8 and MIP-1ß were associated with disease severity and/or adverse short-term outcome. Still, for most mediators, only nonsignificant variations in inflammatory responses were observed for groups of microbial aetiology, disease severity and short-term outcome.
Notes
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PubMed ID
29171871 View in PubMed
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Effect of everolimus introduction on cardiac allograft vasculopathy--results of a randomized, multicenter trial.

https://arctichealth.org/en/permalink/ahliterature133675
Source
Transplantation. 2011 Jul 27;92(2):235-43
Publication Type
Article
Date
Jul-27-2011
Author
Satish Arora
Thor Ueland
Bertil Wennerblom
Vilborg Sigurdadottir
Hans Eiskjær
Hans E Bøtker
Bjorn Ekmehag
Kjell Jansson
Svend-Aage Mortensen
Kari Saunamaki
Svein Simonsen
Einar Gude
Bjørn Bendz
Dag Solbu
Pål Aukrust
Lars Gullestad
Author Affiliation
Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Source
Transplantation. 2011 Jul 27;92(2):235-43
Date
Jul-27-2011
Language
English
Publication Type
Article
Keywords
Aged
Azathioprine - therapeutic use
C-Reactive Protein - metabolism
Calcineurin - antagonists & inhibitors
Disease Progression
Dose-Response Relationship, Drug
Drug Therapy, Combination
Female
Follow-Up Studies
Heart Transplantation - immunology
Humans
Immunosuppressive Agents - therapeutic use
Incidence
Male
Middle Aged
Mycophenolic Acid - analogs & derivatives - therapeutic use
Risk factors
Scandinavia
Sirolimus - analogs & derivatives - therapeutic use
Ultrasonography, Interventional
Vascular Cell Adhesion Molecule-1 - blood
Vascular Diseases - epidemiology - prevention & control - ultrasonography
von Willebrand Factor - metabolism
Abstract
Everolimus reduces the progression of cardiac allograft vasculopathy (CAV) in de novo heart transplant (HTx) recipients, but the influence on established CAV is unknown.
In this Nordic Certican Trial in Heart and lung Transplantation substudy, 111 maintenance HTx recipients (time post-HTx 5.8 ± 4.3 years) randomized to everolimus+reduced calcineurin inhibitor (CNI) or standard CNI had matching (intravascular ultrasound) examinations at baseline and 12 months allowing accurate assessment of CAV progression.
No significant difference in CAV progression was evident between the treatment groups (P = 0.30). When considering patients receiving concomitant azathioprine (AZA) therapy (n = 39), CAV progression was attenuated with everolimus versus standard CNI (?maximal intimal thickness 0.00 ± 0.04 and 0.04 ± 0.04 mm, ?percent atheroma volume 0.2% ± 3.0% and 2.6% ± 2.5%, and ?total atheroma volume 0.25 ± 14.1 and 19.8 ± 20.4 mm(3), respectively [P
Notes
Comment In: Transplantation. 2011 Jul 27;92(2):127-821555972
PubMed ID
21677600 View in PubMed
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Endostatin is higher and associated with pulmonary involvement in primary Sjögren's syndrome.

https://arctichealth.org/en/permalink/ahliterature276099
Source
Clin Exp Rheumatol. 2016 Jul-Aug;34(4):690-3
Publication Type
Article
Author
Øyvind Palm
Thor Ueland
Torhild Garen
Annika E Michelsen
Silje Reiseter
Pål Aukrust
Trond Mogens Aaløkken
Øyvind Molberg
Source
Clin Exp Rheumatol. 2016 Jul-Aug;34(4):690-3
Language
English
Publication Type
Article
Keywords
Adult
Aged
Biomarkers - blood
Case-Control Studies
Endostatins - blood
Enzyme-Linked Immunosorbent Assay
Female
Humans
Lung Diseases, Interstitial - blood - diagnosis - immunology
Male
Middle Aged
Norway
Registries
Sjogren's Syndrome - blood - diagnosis - immunology
Tomography, X-Ray Computed
Up-Regulation
Abstract
To investigate serum levels of endostatin in a well characterised cohort of patients with primary Sjögren's syndrome (pSS) and healthy controls (HC) and assess associations between these mediators and clinical parameters.
All patients (n=144) were recruited from the Norwegian systemic connective tissue disease and vasculitis registry (NOSVAR) and fulfilled American-European classification criteria for pSS. Pulmonary involvement was based on clinical symptoms and abnormal findings on high-resolution computed tomography of the lungs. The controls were 100 healthy blood donors. Serum levels of endostatin was determined by enzyme immunoassay.
We found higher mean levels of serum endostatin in patients with pSS compared with the controls (p
PubMed ID
27214260 View in PubMed
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Enhanced liver fibrosis score predicts transplant-free survival in primary sclerosing cholangitis.

https://arctichealth.org/en/permalink/ahliterature266246
Source
Hepatology. 2015 Jul;62(1):188-97
Publication Type
Article
Date
Jul-2015
Author
Mette Vesterhus
Johannes Roksund Hov
Anders Holm
Erik Schrumpf
Ståle Nygård
Kristin Godang
Ina Marie Andersen
Sigrid Naess
Douglas Thorburn
Francesca Saffioti
Morten Vatn
Odd Helge Gilja
Fridtjof Lund-Johansen
Trygve Syversveen
Knut Brabrand
Albert Parés
Cyriel Y Ponsioen
Massimo Pinzani
Martti Färkkilä
Bjørn Moum
Thor Ueland
Helge Røsjø
William Rosenberg
Kirsten Muri Boberg
Tom H Karlsen
Source
Hepatology. 2015 Jul;62(1):188-97
Date
Jul-2015
Language
English
Publication Type
Article
Keywords
Adult
Case-Control Studies
Cholangitis, Sclerosing - mortality - pathology
Female
Fibrosis
Humans
Liver - pathology
Male
Middle Aged
Norway - epidemiology
Severity of Illness Index
Abstract
There is a need to determine biomarkers reflecting disease activity and prognosis in primary sclerosing cholangitis (PSC). We evaluated the prognostic utility of the enhanced liver fibrosis (ELF) score in Norwegian PSC patients. Serum samples were available from 305 well-characterized large-duct PSC patients, 96 ulcerative colitis patients, and 100 healthy controls. The PSC patients constituted a derivation panel (recruited 1992-2006 [n?=?167]; median age 41 years, 74% male) and a validation panel (recruited 2008-2012 [n?=?138]; median age 40 years, 78% male). We used commercial kits to analyze serum levels of hyaluronic acid, tissue inhibitor of metalloproteinases-1, and propeptide of type III procollagen and calculated ELF scores by the previously published algorithm. Results were also validated by analysis of ELF tests using the ADVIA Centaur XP system and its commercially available reagents. We found that PSC patients stratified by ELF score tertiles exhibited significantly different transplant-free survival in both panels (P?
PubMed ID
25833813 View in PubMed
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Etiology of community-acquired pneumonia and diagnostic yields of microbiological methods: a 3-year prospective study in Norway.

https://arctichealth.org/en/permalink/ahliterature268736
Source
BMC Infect Dis. 2015;15:64
Publication Type
Article
Date
2015
Author
Jan C Holter
Fredrik Müller
Ola Bjørang
Helvi H Samdal
Jon B Marthinsen
Pål A Jenum
Thor Ueland
Stig S Frøland
Pål Aukrust
Einar Husebye
Lars Heggelund
Source
BMC Infect Dis. 2015;15:64
Date
2015
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Coinfection
Community-Acquired Infections - diagnosis - epidemiology - microbiology - virology
Female
Humans
Male
Microbiological Techniques - methods
Middle Aged
Mycoplasma pneumoniae - isolation & purification
Norway - epidemiology
Pneumonia, Bacterial - diagnosis - epidemiology - microbiology - virology
Predictive value of tests
Prospective Studies
Real-Time Polymerase Chain Reaction
Young Adult
Abstract
Despite recent advances in microbiological techniques, the etiology of community-acquired pneumonia (CAP) is still not well described. We applied polymerase chain reaction (PCR) and conventional methods to describe etiology of CAP in hospitalized adults and evaluated their respective diagnostic yields.
267 CAP patients were enrolled consecutively over our 3-year prospective study. Conventional methods (i.e., bacterial cultures, urinary antigen assays, serology) were combined with nasopharyngeal (NP) and oropharyngeal (OP) swab samples analyzed by real-time quantitative PCR (qPCR) for Streptococcus pneumoniae, and by real-time PCR for Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bordetella pertussis and 12 types of respiratory viruses.
Etiology was established in 167 (63%) patients with 69 (26%) patients having =1 copathogen. There were 75 (28%) pure bacterial and 41 (15%) pure viral infections, and 51 (19%) viral-bacterial coinfections, resulting in 126 (47%) patients with bacterial and 92 (34%) patients with viral etiology. S. pneumoniae (30%), influenza (15%) and rhinovirus (12%) were most commonly identified, typically with =1 copathogen. During winter and spring, viruses were detected more frequently (45%, P=.01) and usually in combination with bacteria (39%). PCR improved diagnostic yield by 8% in 64 cases with complete sampling (and by 15% in all patients); 5% for detection of bacteria; 19% for viruses (P=.04); and 16% for detection of =1 copathogen. Etiology was established in 79% of 43 antibiotic-naive patients with complete sampling. S. pneumoniae qPCR positive rate was significantly higher for OP swab compared to NP swab (P
Notes
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