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Bloos F.,Jena University Hospital | Bloos F.,Jena University Hospital Jena | Thomas-Ruddel D.,Jena University Hospital | Thomas-Ruddel D.,Jena University Hospital Jena | And 62 more authors.
Critical Care | Year: 2014

Introduction: Current sepsis guidelines recommend antimicrobial treatment (AT) within one hour after onset of sepsis-related organ dysfunction (OD) and surgical source control within 12 hours. The objective of this study was to explore the association between initial infection management according to sepsis treatment recommendations and patient outcome.Methods: In a prospective observational multi-center cohort study in 44 German ICUs, we studied 1,011 patients with severe sepsis or septic shock regarding times to AT, source control, and adequacy of AT. Primary outcome was 28-day mortality.Results: Median time to AT was 2.1 (IQR 0.8 - 6.0) hours and 3 hours (-0.1 - 13.7) to surgical source control. Only 370 (36.6%) patients received AT within one hour after OD in compliance with recommendation. Among 422 patients receiving surgical or interventional source control, those who received source control later than 6 hours after onset of OD had a significantly higher 28-day mortality than patients with earlier source control (42.9% versus 26.7%, P <0.001). Time to AT was significantly longer in ICU and hospital non-survivors; no linear relationship was found between time to AT and 28-day mortality. Regardless of timing, 28-day mortality rate was lower in patients with adequate than non-adequate AT (30.3% versus 40.9%, P < 0.001).Conclusions: A delay in source control beyond 6 hours may have a major impact on patient mortality. Adequate AT is associated with improved patient outcome but compliance with guideline recommendation requires improvement. There was only indirect evidence about the impact of timing of AT on sepsis mortality. © 2014 Bloos et al.; licensee BioMed Central Ltd. Source

Roth J.,Jena University Hospital Jena | Muller N.,Jena University Hospital Jena | Lehmann T.,University Hospital Jena | Wolf G.,Jena University Hospital Jena | Muller U.A.,Jena University Hospital Jena
Experimental and Clinical Endocrinology and Diabetes | Year: 2016

Objective: Target HbA1c values given in the most National Therapeutic Guidelines for patients with diabetes and cut-off HbA1c values for diabetes diagnosis are usually not taking the age of the respective patients into account; despite the fact that an increase in HbA1c in subjects without diabetes with age is known for some time. In order to further quantify the association between age and HbA1c in non-diabetic subjects an analysis of one German register was performed. Methods: In this cross-sectional study we analyzed data from 7 699 visits of 2 921 patients without diabetes (age 46.6 y [range 18–93 y]; 69.1% women; BMI 27.6±6.4 kg/m²) who had at least one HbA1c and blood glucose measurement. Data were drawn from an electronic patient record system (EMIL™) in which data were collected between 01/1992 and 01/2014. The patients were divided in 6 age groups (< 30 years [n=1 057];>30–40 years [n=1 160];>40–50 years [n=1 693];>50–60 years [n=1 523];>60–70 years [n=1 310];>70 years [n=956]) and the HbA1c values of these groups were compared. Patients with: gestational diabetes, use of systemic glucocorticoids, malignant neoplasm, age<18 y at time of first visit and IGT were excluded. HbA1c measurements were DCCT adjusted. Results: Patients with age>70 years have a 0.47% [5.14 mmol/mol] higher HbA1c compared to those<30 years. The mean HbA1c of the age groups was:<30 4.98% [30.96 mmol/mol],>30–40 5.07% [31.99 mmol/mol],>40–50 5.17% [33.10 mmol/mol],>50–60 5.33% [34.79 mmol/mol],>60–70 5.42% [35.79 mmol/mol] and>70 years 5.45% [36.10 mmol/mol]. In a multiple linear model the regression coefficient for each year of age increase was β=0.0074 (p<0.001); thus age results in an increase of 0.074% in HbA1c per decade. Conclusion: HbA1c increases significantly with ageing in people without diabetes. The use of different cut-off values for every age range for diagnosis of diabetes should be discussed. Copyright © 2016, Georg Thieme Verlag KG. All rights reserved. Source

Rennert K.,University Hospital Jena | Rennert K.,Jena University Hospital Jena | Heisig K.,University Hospital Jena | Groeger M.,University Hospital Jena | And 8 more authors.
Cytokine | Year: 2016

Fractalkine (FKN, CX3CL1) is a regulator of leukocyte recruitment and adhesion, and controls leukocyte migration on endothelial cells (ECs). We show that FKN triggers different effects in CD16+ and CD16- monocytes, the two major subsets of human monocytes. In the presence of ECs a lipopolysaccharide (LPS)-stimulus led to a significant increase in tumor necrosis factor (TNF)-secretion by CD16+ monocytes, which depends on the interaction of CX3CR1 expressed on CD16+ monocytes with endothelial FKN. Soluble FKN that was efficiently shed from the surface of LPS-activated ECs in response to binding of CD16+ monocytes to ECs, diminished monocyte adhesion in down-regulating CX3CR1 expression on the surface of CD16+ monocytes resulting in decreased TNF-secretion. In this process the TNF-converting enzyme (TACE) acts as a central player regulating FKN-shedding and TNFα-release through CD16+ monocytes interacting with ECs. Thus, the release and local accumulation of sFKN represents a mechanism that limits the inflammatory potential of CD16+ monocytes by impairing their interaction with ECs during the initial phase of an immune response to LPS. This regulatory process represents a potential target for therapeutic approaches to modulate the inflammatory response to bacterial components. © 2016 Elsevier Ltd. Source

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