Database : MEDLINE
Search on : Sepsis [Words]
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[PMID]: 25596607
[Au] Autor:Rech MA; Day SA; Kast JM; Donahey EE; Pajoumand M; Kram SJ; Erdman MJ; Peitz GJ; Allen JM; Palmer A; Kram B; Harris SA; Turck CJ; Critical Care Pharmacotherapy Literature Update Group
[Ad] Address:Megan A. Rech, Pharm.D., BCPS, is Emergency Medicine Clinical Pharmacist, Loyola University Medical Center, Maywood, IL. Sarah A. Day, Pharm.D., BCPS, is Clinical Pharmacist, Critical Care, Doctors Hospital, Columbus, OH. Jenna M. Kast, Pharm.D., BCPS, is Clinical Pharmacy Specialist, Critical Care,...
[Ti] Title:Major publications in the critical care pharmacotherapy literature: January-December 2013.
[So] Source:Am J Health Syst Pharm;72(3):224-36, 2015 Feb 1.
[Is] ISSN:1535-2900
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: Ten recently published articles with important implications for critical care pharmacotherapy are summarized. SUMMARY: The Critical Care Pharmacotherapy Literature Update (CCPLU) group is a national assembly of experienced intensive care unit (ICU) pharmacists across the United States. Group members monitor 25 peer-reviewed journals on an ongoing basis to identify literature relevant to pharmacy practice in the critical care setting. After evaluation by CCPLU group members, selected articles are chosen for summarization and distribution to group members nationwide based on (1) applicability to critical care practice, (2) relevance to pharmacy practitioners, and (3) quality of evidence or research methodology. Hundreds of relevant articles were evaluated by the group during the period January-December 2013, of which 98 were summarized and disseminated nationally to CCPLU group members. Among those 98 publications, 10 deemed to be of particularly high utility to critical care practitioners were included in this review. The 10 articles address topics such as rapid lowering of blood pressure in patients with intracranial hemorrhage, adjunctive therapy to prevent renal injury due to acute heart failure, triple-drug therapy to improve neurologic outcomes after cardiac arrest, and continuous versus intermittent infusion of ß-lactam antibiotics in severe sepsis. CONCLUSION: There were many important additions to the critical care pharmacotherapy literature in 2013, including an updated guideline on the management of myocardial infarction and reports on advances in research focused on improving outcomes in patients with stroke or cardiac arrest and preventing the spread of drug-resistant pathogens in the ICU.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.2146/ajhp140241

  2 / 89413 MEDLINE  
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[PMID]: 25548220
[Au] Autor:Cuenca AG; Joiner DN; Gentile LF; Cuenca AL; Wynn JL; Kelly-Scumpia KM; Scumpia PO; Behrns KE; Efron PA; Nacionales D; Lui C; Wallet SM; Reeves WH; Mathews CE; Moldawer LL
[Ad] Address:Department of Surgery, University of Florida College of Medicine and Dentistry, Gainesville, FL 32610;...
[Ti] Title:TRIF-Dependent Innate Immune Activation Is Critical for Survival to Neonatal Gram-Negative Sepsis.
[So] Source:J Immunol;194(3):1169-77, 2015 Feb 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Current evidence suggests that neonatal immunity is functionally distinct from adults. Although TLR signaling through the adaptor protein, MyD88, has been shown to be critical for survival to sepsis in adults, little is known about the role of MyD88 or TRIF in neonatal sepsis. We demonstrate that TRIF(-/-) but not MyD88(-/-) neonates are highly susceptible to Escherichia coli peritonitis and bacteremia. This was associated with decreased innate immune recruitment and function. Importantly, we found that the reverse was true in adults that MyD88(-/-) but not TRIF(-/-) or wild-type adults are susceptible to E. coli peritonitis and bacteremia. In addition, we demonstrate that TRIF but not MyD88 signaling is critical for the TLR4 protective adjuvant effect we have previously demonstrated. These data suggest a differential requirement for the survival of neonates versus adults to Gram-negative infection, and that modulation of TRIF in neonates can be used to augment survival to neonatal sepsis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1302676

  3 / 89413 MEDLINE  
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[PMID]: 25539817
[Au] Autor:Grailer JJ; Fattahi F; Dick RS; Zetoune FS; Ward PA
[Ad] Address:Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109....
[Ti] Title:Cutting Edge: Critical Role for C5aRs in the Development of Septic Lymphopenia in Mice.
[So] Source:J Immunol;194(3):868-72, 2015 Feb 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In the early stages of sepsis, lymphocytes undergo apoptosis, resulting in lymphopenia and immunosuppression. The trigger for septic lymphopenia is unknown. Using the polymicrobial model of murine sepsis, we investigated the role of C5a receptors in septic lymphopenia. In wild-type mice, cecal ligation and puncture resulted in splenocyte apoptosis and significant lymphopenia after 3 d, which was not observed in C5aR1(-/-) or C5aR2(-/-) mice. Our data show that mouse neutrophils exposed to recombinant mouse C5a cause release of histones in a dose-dependent and time-dependent manner. Histone levels in spleen were significantly elevated following cecal ligation and puncture but were reduced by the absence of C5aR1. Histones induced significant lymphocyte apoptosis in vitro. Ab-mediated neutralization of histones prevented the development of lymphopenia in sepsis. Together, these results describe a new pathway of septic lymphopenia involving complement and extracellular histones. Targeting of this pathway may have therapeutic benefit for patients with sepsis or other serious illness.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1401193

  4 / 89413 MEDLINE  
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[PMID]: 25271380
[Au] Autor:Hoover DB; Ozment TR; Wondergem R; Li C; Williams DL
[Ad] Address:*Department of Biomedical Sciences, †Department of Surgery, and ‡Center for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee.
[Ti] Title:Impaired heart rate regulation and depression of cardiac chronotropic and dromotropic function in polymicrobial sepsis.
[So] Source:Shock;43(2):185-91, 2015 Feb.
[Is] ISSN:1540-0514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The scope of cardiac pathophysiology in sepsis has not been fully defined. Accordingly, we evaluated the effects of sepsis on heart rate (HR), HR variability, and conduction parameters in a murine model of sepsis. Electrocardiograms were recorded noninvasively from conscious mice before and after cecal ligation and puncture (CLP) or sham surgery. Responses of isolated atria to tyramine and isoproterenol were quantified to assess the functional state of sympathetic nerves and postjunctional sensitivity to adrenergic stimulation. Cecal ligation and puncture mice had lower HR compared with sham at 16 to 18 h postsurgery (sham, 741 ± 7 beats/min; CLP, 557 ± 31 beats/min; n = 6/group; P < 0.001), and there was significant prolongation of the PR, QRS, and QTc intervals. Slowing of HR and conduction developed within 4 to 6 h after CLP and were preceded by a decrease in HR variability. Treatment of CLP mice with isoproterenol (5 mg/kg, intraperitoneally) at 25 h after surgery failed to increase HR or decrease conduction intervals. The lack of in vivo response to isoproterenol cannot be attributed to hypothermia because robust chronotropic and inotropic responses to isoproterenol were evoked from isolated atria at 25°C and 30°C. These findings demonstrate that impaired regulation of HR (i.e., reduced HR variability) develops before the onset of overt cardiac rate and conduction changes in septic mice. Subsequent time-dependent decreases in HR and cardiac conduction can be attributed to hypothermia and would contribute to decreased cardiac output and organ perfusion. Because isolated atria from septic mice showed normal responsiveness to adrenergic stimulation, we conclude that impaired effectiveness of isoproterenol in vivo can be attributed to reversible effects of systemic factors on adrenergic receptors and/or postreceptor signaling.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/SHK.0000000000000272

  5 / 89413 MEDLINE  
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[PMID]: 25564146
[Au] Autor:Mansur A; Klee Y; Popov AF; Erlenwein J; Ghadimi M; Beissbarth T; Bauer M; Hinz J
[Ad] Address:Department of Anesthesiology, University Medical Center, Georg August University, Goettingen, Niedersachsen, Germany....
[Ti] Title:Primary bacteraemia is associated with a higher mortality risk compared with pulmonary and intra-abdominal infections in patients with sepsis: a prospective observational cohort study.
[So] Source:BMJ Open;5(1):e006616, 2015.
[Is] ISSN:2044-6055
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To investigate whether common infection foci (pulmonary, intra-abdominal and primary bacteraemia) are associated with variations in mortality risk in patients with sepsis. DESIGN: Prospective, observational cohort study. SETTING: Three surgical intensive care units (ICUs) at a university medical centre. PARTICIPANTS: A total of 327 adult Caucasian patients with sepsis originating from pulmonary, intra-abdominal and primary bacteraemia participated in this study. PRIMARY AND SECONDARY OUTCOME MEASURES: The patients were followed for 90 days and mortality risk was recorded as the primary outcome variable. To monitor organ failure, sepsis-related organ failure assessment (Sequential Organ Failure Assessment, SOFA) scores were evaluated at the onset of sepsis and throughout the observational period as secondary outcome variables. RESULTS: A total of 327 critically ill patients with sepsis were enrolled in this study. Kaplan-Meier survival analysis showed that the 90-day mortality risk was significantly higher among patients with primary bacteraemia than among those with pulmonary and intra-abdominal foci (58%, 35% and 32%, respectively; p=0.0208). To exclude the effects of several baseline variables, we performed multivariate Cox regression analysis. Primary bacteraemia remained a significant covariate for mortality in the multivariate analysis (HR 2.10; 95% CI 1.14 to 3.86; p=0.0166). During their stay in the ICU, the patients with primary bacteraemia presented significantly higher SOFA scores than those of the patients with pulmonary and intra-abdominal infection foci (8.5±4.7, 7.3±3.4 and 5.8±3.5, respectively). Patients with primary bacteraemia presented higher SOFA-renal score compared with the patients with other infection foci (1.6±1.4, 0.8±1.1 and 0.7±1.0, respectively); the patients with primary bacteraemia required significantly more renal replacement therapy than the patients in the other groups (29%, 11% and 12%, respectively). CONCLUSIONS: These results indicate that patients with sepsis with primary bacteraemia present a higher mortality risk compared with patients with sepsis of pulmonary or intra-abdominal origins. These results should be assessed in patients with sepsis in larger, independent cohorts.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1136/bmjopen-2014-006616

  6 / 89413 MEDLINE  
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[PMID]: 25151022
[Au] Autor:Rello J; Lisboa T; Koulenti D
[Ad] Address:Critical Care Department, Hospital Universitari Vall d'Hebron, Barcelona, Spain; Centro de Investigación Biomédica en Red Enfermedades Respiratorias, Barcelona, Spain; Universitat Autonoma de Barcelona, Barcelona, Spain. Electronic address: jrello@crips.es.
[Ti] Title:Respiratory infections in patients undergoing mechanical ventilation.
[So] Source:Lancet Respir Med;2(9):764-74, 2014 Sep.
[Is] ISSN:2213-2619
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Lower respiratory tract infections in mechanically ventilated patients are a frequent cause of antibiotic treatment in intensive-care units. These infections present as severe sepsis or septic shock with respiratory dysfunction in intubated patients. Purulent respiratory secretions are needed for diagnosis, but distinguishing between pneumonia and tracheobronchitis is not easy. Both presentations are associated with longlasting mechanical ventilation and extended intensive-care unit stay, providing a rationale for antibiotic treatment initiation. Differentiation of colonisers from true pathogens is difficult, and microbiological data show Staphylococcus aureus and Pseudomonas aeruginosa to be of great concern because of clinical outcomes and therapeutic challenges. Key management issues include identification of the pathogen, choice of initial empirical antibiotic, and decisions with regard to the resolution pattern.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Process

  7 / 89413 MEDLINE  
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[PMID]: 25360828
[Au] Autor:Badurdeen S; Mulongo M; Berkley JA
[Ad] Address:Department of Paediatrics, Oxford University Hospitals NHS Trust, Oxford, UK.
[Ti] Title:Arginine depletion increases susceptibility to serious infections in preterm newborns.
[So] Source:Pediatr Res;77(2):290-7, 2015 Feb.
[Is] ISSN:1530-0447
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Preterm newborns are highly susceptible to bacterial infections. This susceptibility is regarded as being due to immaturity of multiple pathways of the immune system. However, it is unclear whether a mechanism that unifies these different, suppressed pathways exists. Here, we argue that the immune vulnerability of the preterm neonate is critically related to arginine depletion. Arginine, a "conditionally essential" amino acid, is depleted in acute catabolic states, including sepsis. Its metabolism is highly compartmentalized and regulated, including by arginase-mediated hydrolysis. Recent data suggest that arginase II-mediated arginine depletion is essential for the innate immune suppression that occurs in newborn models of bacterial challenge, impairing pathways critical for the immune response. Evidence that arginine depletion mediates protection from immune activation during first gut colonization suggests a regulatory role in controlling gut-derived pathogens. Clinical studies show that plasma arginine is depleted during sepsis. In keeping with animal studies, small clinical trials of L-arginine supplementation have shown benefit in reducing necrotizing enterocolitis in premature neonates. We propose a novel, broader hypothesis that arginine depletion during bacterial challenge is a key factor limiting the neonate's ability to mount an adequate immune response, contributing to the increased susceptibility to infections, particularly with respect to gut-derived sepsis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/pr.2014.177

  8 / 89413 MEDLINE  
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[PMID]: 25548221
[Au] Autor:Park SH; Baek SI; Yun J; Lee S; Yoon da Y; Jung JK; Jung SH; Hwang BY; Hong JT; Han SB; Kim Y
[Ad] Address:College of Pharmacy, Chungbuk National University, Cheongju 362-763, Korea;...
[Ti] Title:IRAK4 as a Molecular Target in the Amelioration of Innate Immunity-Related Endotoxic Shock and Acute Liver Injury by Chlorogenic Acid.
[So] Source:J Immunol;194(3):1122-30, 2015 Feb 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mice lacking the IL-1R-associated kinase 4 (IRAK4) are completely resistant to LPS-induced endotoxic disorder or the TLR9 agonist CpG DNA plus d-galactosamine-induced acute liver injury (ALI), whereas wild-type strains succumb. However, translational drugs against sepsis or ALI remain elusive. Lonicerae flos extract is undergoing the clinical trial phase I in LPS-injected healthy human volunteers for sepsis treatment. In the current study, chlorogenic acid (CGA), a major anti-inflammatory constituent of lonicerae flos extract, rescued endotoxic mortality of LPS-intoxicated C57BL/6 mice, as well as ameliorated ALI of LPS/d-galactosamine-challenged C57BL/6 mice. As a mechanism, CGA inhibited various TLR agonist-, IL-1α-, or high-mobility group box-1-stimulated autophosphorylation (activation) of IRAK4 in peritoneal macrophages from C57BL/6 or C3H/HeJ mice via directly affecting the kinase activity of IRAK4, a proximal signal transducer in the MyD88-mediated innate immunity that enhances transcriptional activity of NF-κB or AP-1. CGA consequently attenuated protein or mRNA levels of NF-κB/AP-1 target genes encoding TNF-α, IL-1α, IL-6, and high-mobility group box-1 in vivo under endotoxemia or ALI. Finally, this study suggests IRAK4 as a molecular target of CGA in the treatment of innate immunity-related shock and organ dysfunction following insult of various TLR pathogens from bacteria and viruses.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1402101

  9 / 89413 MEDLINE  
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[PMID]: 25281422
[Au] Autor:O H-Ici D; Jeuthe S; Dietrich T; Berger F; Kuehne T; Kozerke S; Messroghli DR
[Ad] Address:Unit for Cardiovascular Imaging, Department of Congenital Heart Disease and Pediatric Cardiology, Deutsches Herzzentrum Berlin, Augustenburger Platz 1, 13353, Berlin, Germany, darachohici@gmail.com.
[Ti] Title:Closed-chest small animal model to study myocardial infarction in an MRI environment in real time.
[So] Source:Int J Cardiovasc Imaging;31(1):115-21, 2015 Jan.
[Is] ISSN:1875-8312
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Current models for real time study of the effects of myocardial ischemia/reperfusion have major limitations and confounders. Confounders include the surgical stresses of a thoracotomy and abnormal physiology of an open chest. The need to reposition the animal interferes with the study of the early changes associated with ischemia. Direct comparison of pre-ischemia and post-ischemia images is then difficult. We developed a novel "closed chest" model of ischemia/reperfusion to overcome these issues. Following thoracotomy, we sutured a balloon occluder to the left coronary artery of male Sprague-Dawley rats. We used both visual inspection and ECG to assess for successful occlusion and reperfusion of the coronary artery at the time of operation by brief inflation and deflation of the balloon. The tubing was then placed under the skin and the incision closed. Following a recovery period (5-10 days), the animals underwent MRI. We performed baseline assessment of left ventricle function, and repeated LV measurement during a 15-min coronary occlusion and again during a 60-min reperfusion period following reopening of the coronary artery. The occluder was successfully placed in 40 of 44 animals. Four developed intraoperative complications; two large myocardial infarction, two terminal bleeding. Six died in the week following surgery, [four sudden deaths (presumed arrhythmic), one anterior infarction, one sepsis]. Cine-MRI demonstrated localised hypokinesia in 31 of the remaining 34 animals. LV ejection fraction (EF) was reduced from 63 ± 7 % at baseline, to 49 ± 9 % during coronary occlusion. LV EF recovered to 61 ± 2 %. The area at risk on staining of the heart was 41.9 ± 15.8 %. This method allows the effects of ischemia/reperfusion to be studied before, during, and after coronary occlusion. Ischemia can be caused while the animal is in the MRI. This new and clinically relevant small animal model is a valuable tool to study the effects of single or repeated coronary occlusion/reperfusion in real-time.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s10554-014-0539-0

  10 / 89413 MEDLINE  
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[PMID]: 24810631
[Au] Autor:Verbout NG; Yu X; Healy LD; Phillips KG; Tucker EI; Gruber A; McCarty OJ; Offner H
[Ad] Address:Department of Biomedical Engineering, School of Medicine, Oregon Health & Science University, Portland, OR, 97239, USA, verboutn@ohsu.edu.
[Ti] Title:Thrombin mutant W215A/E217A treatment improves neurological outcome and attenuates central nervous system damage in experimental autoimmune encephalomyelitis.
[So] Source:Metab Brain Dis;30(1):57-65, 2015 Feb.
[Is] ISSN:1573-7365
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) is a neuroinflammatory disease characterized by demyelination and axonal damage of the central nervous system. The pathogenesis of MS has also been linked to vascular inflammation and local activation of the coagulation system, resulting in perivascular fibrin deposition. Treatment of experimental autoimmune encephalomyelitis (EAE), a model of human MS, with antithrombotic and antiinflammatory activated protein C (APC) reduces disease severity. Since recombinant APC (Drotecogin alfa), originally approved for the treatment of severe sepsis, is not available for human MS studies, we tested the hypothesis that pharmacologic activation of endogenous protein C could likewise improve the outcome of EAE. Mice were immunized with murine myelin oligodendrocyte glycoprotein (MOG) peptides and at the onset of EAE symptoms, were treated every other day with either WE thrombin (25 µg/kg; i.v.), a selective recombinant protein C activator thrombin analog, or saline control. Mice were monitored for changes in disease score until euthanized for ex vivo analysis of inflammation. Administration of WE thrombin significantly ameliorated clinical severity of EAE, reduced inflammatory cell infiltration and demyelination, suppressed the activation of macrophages comprising the CD11b + population and reduced accumulation of fibrin (ogen) in the spinal cord. These data suggest that symptomatic MS may respond to a treatment strategy that involves temporal pharmacological enhancement of endogenous APC generation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150116
[Lr] Last revision date:150116
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s11011-014-9558-8


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