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Michael Praktiknjo

Other affiliations: University of Bonn
Bio: Michael Praktiknjo is an academic researcher from University Hospital Bonn. The author has contributed to research in topics: Cirrhosis & Portal hypertension. The author has an hindex of 19, co-authored 87 publications receiving 1143 citations. Previous affiliations of Michael Praktiknjo include University of Bonn.


Papers
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Journal ArticleDOI
Jonel Trebicka1, Javier J.M. Fernández, Mária Papp2, Paolo Caraceni3, Wim Laleman4, Carmine Gambino5, Ilaria Giovo6, Frank Erhard Uschner1, Cesar Jimenez7, Rajeshwar P. Mookerjee8, Thierry Gustot9, Agustín Albillos10, Rafael Bañares11, Martin Janicko12, Christian J. Steib13, Thomas Reiberger14, Juan Acevedo, Pietro Gatti, William Bernal15, Stefan Zeuzem1, Alexander Zipprich16, Salvatore Piano5, Thomas Berg17, Tony Bruns18, Flemming Bendtsen, Minneke J. Coenraad19, Manuela Merli, Rudolf E. Stauber20, Heinz Zoller21, Jose Presa Ramos, Cristina Solé, Germán Soriano, Andrea De Gottardi22, Henning Grønbæk23, Faouzi Saliba24, Christian Trautwein18, Osman Ozdogan25, Sven Francque, Stephen D. Ryder26, Pierre Nahon27, Manuel Romero-Gómez, Hans Van Vlierberghe28, Claire Francoz27, Michael Manns29, Elisabet Garcia, Manuel Tufoni3, Alex Amoros, Marco Pavesi, Cristina Sanchez, Anna Curto, Carla Pitarch, Antonella Putignano9, Esau Moreno, Debbie L. Shawcross15, Ferran Aguilar, Joan Clària, Paola Ponzo6, Christian Jansen30, Zsuzsanna Vitális2, Giacomo Zaccherini3, Boglarka Balogh2, Victor Vargas7, Sara Montagnese5, Carlo Alessandria6, Mauro Bernardi3, Pere Ginès, Rajiv Jalan8, Richard Moreau27, Paolo Angeli5, Vicente Arroyo, Miriam Maschmeier31, David Semela32, Laure Elkrief, Ahmed Elsharkawy33, Tamas Tornai2, István Tornai2, István Altorjay2, Agnese Antognoli3, Maurizio Baldassarre3, Martina Gagliardi3, Eleonora Bertoli5, Sara Mareso5, Alessandra Brocca5, Daniela Campion, Giorgio Maria Saracco, Martina Rizzo, Jennifer Lehmann30, Alessandra Pohlmann30, Michael Praktiknjo30, Robert Schierwagen34, Robert Schierwagen30, Elsa Solà, Nesrine Amari, Miguel Á. Rodríguez10, Frederik Nevens4, Ana Clemente11, Peter Jarcuska12, Alexander L. Gerbes13, Mattias Mandorfer14, Christoph Welsch34, Emanuela Ciraci, Vish Patel15, Cristina Ripoll16, Adam Herber, Paul Horn, Karen Vagner Danielsen35, Lise Lotte Gluud35, Jelte J Schaapman19, Oliviero Riggio, Florian Rainer20, Jörg Tobiasch Moritz21, Monica Mesquita, Edilmar Alvarado-Tapias, Osagie Akpata8, Peter Lykke Eriksen23, Didier Samuel24, Sylvie Tresson24, Pavel Strnad18, Roland Amathieu27, Macarena Simón-Talero, Francois Smits, Natalie Van den Ende4, Javier Martínez10, Rita Garcia11, Daniel Markwardt13, Harald Rupprechter14, Cornelius Engelmann 
TL;DR: Acute decompensation without ACLF is a heterogeneous condition with three different clinical courses and two major pathophysiological mechanisms: systemic inflammation and portal hypertension.

228 citations

Journal ArticleDOI
TL;DR: The main outcomes were the incidence of complications of cirrhosis and mortality according to the presence of SPSS, and quality of life and transplantation-free survival were lower in patients with S PSS vs without.

147 citations

Journal ArticleDOI
Jonel Trebicka1, Javier Romaní Fernández2, Mária Papp3, Paolo Caraceni4, Wim Laleman5, Carmine Gambino6, Ilaria Giovo, Frank Erhard Uschner1, Christian Jansen7, Cesar Jimenez8, Rajeshwar P. Mookerjee9, Thierry Gustot, Agustín Albillos10, Rafael Bañares11, Peter Jarcuska12, Christian J. Steib13, Thomas Reiberger14, Juan Acevedo, Pietro Gatti, Debbie L. Shawcross15, Stefan Zeuzem1, Alexander Zipprich16, Salvatore Piano6, Thomas Berg17, Tony Bruns18, Karen Vagner Danielsen19, Minneke J. Coenraad20, Manuela Merli, Rudolf E. Stauber21, Heinz Zoller22, Jose Presa Ramos, Cristina Solé2, Germán Soriano, Andrea De Gottardi23, Henning Grønbæk24, Faouzi Saliba25, Christian Trautwein18, Haluk Tarik Kani26, Sven Francque, Stephen D. Ryder27, Pierre Nahon28, Pierre Nahon29, Manuel Romero-Gómez, Hans Van Vlierberghe30, Claire Francoz28, Michael Manns31, Elisabet Garcia-Lopez, Manuel Tufoni4, Alex Amoros, Marco Pavesi, Cristina Sanchez, Michael Praktiknjo7, Anna Curto, Carla Pitarch, Antonella Putignano, Esau Moreno, William Bernal15, Ferran Aguilar, Joan Clària2, Paola Ponzo, Zsuzsanna Vitális3, Giacomo Zaccherini4, Boglarka Balogh3, Alexander L. Gerbes13, Victor Vargas8, Carlo Alessandria, Mauro Bernardi4, Pere Ginès2, Richard Moreau28, Paolo Angeli6, Rajiv Jalan9, Vicente Arroyo, Miriam Maschmeier32, David Semela33, Laure Elkrief, Ahmed Elsharkawy34, Tamas Tornai34, István Tornai3, István Altorjay3, Agnese Antognoli4, Maurizio Baldassarre4, Martina Gagliardi4, Eleonora Bertoli6, Sara Mareso6, Alessandra Brocca6, Daniela Campion, Giorgio Maria Saracco, Martina Rizzo, Jennifer Lehmann7, Alessandra Pohlmann7, Maximilian J. Brol7, Johannes Chang7, Robert Schierwagen1, Elsa Solà, Nesrine Amari, Miguel Á. Rodríguez10, Frederik Nevens5, Ana Clemente11, Martin Janicko12, Daniel Markwardt13, Mattias Mandorfer14, Christoph Welsch1, T.M. Welzel1, Emanuela Ciraci, Vish Patel15, Cristina Ripoll16, Adam Herber17, Paul Horn, Flemming Bendtsen19, Lise Lotte Gluud19, Jelte J Schaapman20, Oliviero Riggio, Florian Rainer21, Joerg Tobiasch Moritz22, Monica Mesquita, Edilmar Alvarado-Tapias, Osagie Akpata9, Luise Aamann24, Didier Samuel25, Sylvie Tresson25, Pavel Strnad18, Roland Amathieu28, Roland Amathieu29, Macarena Simón-Talero8, Francois Smits, Natalie Van den Ende5, Javier Martínez10, Rita Garcia11, Harald Rupprechter14, Cornelius Engelmann17, Osman Ozdogan26 
TL;DR: This study identified precipitants that are significantly associated with a distinct clinical course and prognosis of patients with AD and specific preventive and therapeutic strategies targeting these events may improve outcome in decompensated cirrhosis.

125 citations

Journal ArticleDOI
01 Mar 2019-Gut
TL;DR: The circulating microbiome in portal vein is characterised as the link between gut and liver and 65 genera belonging to four phyla (predominantly Proteobacteria) in this cohort are identified.
Abstract: We read with interest the recent review by Tilg et al ,1 which summarised the role of microbiota in liver diseases and pointed out that a causal link with systemic inflammation has still not been established. This letter fills in this gap and provides an analysis of the circulating microbiota in portal vein as the link between gut and liver. The access to portal circulation is possible during the implantation of a transjugular intrahepatic portosystemic shunt (TIPS). Therefore, we characterised the circulating microbiome in portal vein (first venous outflow in gut–liver axis), liver outflow, central venous blood and peripheral venous blood from seven patients with decompensated liver cirrhosis receiving TIPS for either variceal bleeding (n=3) or refractory ascites (n=4) (mean Model for End-stage Liver Disease (MELD) 8.4 (range 6–13), Child-Pugh-Score (CHILD) A: n=4, CHILD B: n=3) (figure 1A). We performed 16S ribosomal RNA (rRNA) gene sequencing of buffy coat samples and identified 65 genera belonging to four phyla (predominantly Proteobacteria) in this cohort (online supplementary figure 1 and figure 1B). Blood microbiome phylum compositions identified in our …

111 citations

Journal ArticleDOI
TL;DR: While TIPS might improve sarc Openia and thereby survival, persistence of sarcopenia after TIPS is associated with a reduced response to TIPS and a higher risk of acute‐on‐chronic liver failure development and mortality.

109 citations


Cited by
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Journal ArticleDOI
TL;DR: The first update of the 2013 EFSUMB (European Federation of Societies for Ultrasound in Medicine and Biology) Guidelines and Recommendations on the clinical use of elastography is presented, focused on the assessment of diffuse liver disease.
Abstract: We present here the first update of the 2013 EFSUMB (European Federation of Societies for Ultrasound in Medicine and Biology) Guidelines and Recommendations on the clinical use of elastography with a focus on the assessment of diffuse liver disease. The short version provides clinical information about the practical use of elastography equipment and interpretation of results in the assessment of diffuse liver disease and analyzes the main findings based on published studies, stressing the evidence from meta-analyses. The role of elastography in different etiologies of liver disease and in several clinical scenarios is also discussed. All of the recommendations are judged with regard to their evidence-based strength according to the Oxford Centre for Evidence-Based Medicine Levels of Evidence. This updated document is intended to act as a reference and to provide a practical guide for both beginners and advanced clinical users.

740 citations

Journal ArticleDOI
TL;DR: The identification of the elements of the gut-liver axis primarily damaged in each chronic liver disease offers possibilities to intervention.

709 citations

Journal Article
TL;DR: More rapid completion of a 3‐hour bundle of sepsis care and rapid administration of antibiotics, but not rapid completed of an initial bolus of intravenous fluids, were associated with lower risk‐adjusted in‐hospital mortality.
Abstract: BACKGROUND In 2013, New York began requiring hospitals to follow protocols for the early identification and treatment of sepsis. However, there is controversy about whether more rapid treatment of sepsis improves outcomes in patients. METHODS We studied data from patients with sepsis and septic shock that were reported to the New York State Department of Health from April 1, 2014, to June 30, 2016. Patients had a sepsis protocol initiated within 6 hours after arrival in the emergency department and had all items in a 3‐hour bundle of care for patients with sepsis (i.e., blood cultures, broad‐spectrum antibiotic agents, and lactate measurement) completed within 12 hours. Multilevel models were used to assess the associations between the time until completion of the 3‐hour bundle and risk‐adjusted mortality. We also examined the times to the administration of antibiotics and to the completion of an initial bolus of intravenous fluid. RESULTS Among 49,331 patients at 149 hospitals, 40,696 (82.5%) had the 3‐hour bundle completed within 3 hours. The median time to completion of the 3‐hour bundle was 1.30 hours (interquartile range, 0.65 to 2.35), the median time to the administration of antibiotics was 0.95 hours (interquartile range, 0.35 to 1.95), and the median time to completion of the fluid bolus was 2.56 hours (interquartile range, 1.33 to 4.20). Among patients who had the 3‐hour bundle completed within 12 hours, a longer time to the completion of the bundle was associated with higher risk‐adjusted in‐hospital mortality (odds ratio, 1.04 per hour; 95% confidence interval [CI], 1.02 to 1.05; P<0.001), as was a longer time to the administration of antibiotics (odds ratio, 1.04 per hour; 95% CI, 1.03 to 1.06; P<0.001) but not a longer time to the completion of a bolus of intravenous fluids (odds ratio, 1.01 per hour; 95% CI, 0.99 to 1.02; P=0.21). CONCLUSIONS More rapid completion of a 3‐hour bundle of sepsis care and rapid administration of antibiotics, but not rapid completion of an initial bolus of intravenous fluids, were associated with lower risk‐adjusted in‐hospital mortality. (Funded by the National Institutes of Health and others.)

662 citations

Journal ArticleDOI
TL;DR: The authors describe how metabolic disorders, such as type 2 diabetes and nonalcoholic fatty liver disease, are driven by alterations in the composition of the intestinal microbiota and its metabolites, which translocate from the gut across a disrupted intestinal barrier and contribute to metabolic inflammation.
Abstract: Low-grade inflammation is the hallmark of metabolic disorders such as obesity, type 2 diabetes and nonalcoholic fatty liver disease. Emerging evidence indicates that these disorders are characterized by alterations in the intestinal microbiota composition and its metabolites, which translocate from the gut across a disrupted intestinal barrier to affect various metabolic organs, such as the liver and adipose tissue, thereby contributing to metabolic inflammation. Here, we discuss some of the recently identified mechanisms that showcase the role of the intestinal microbiota and barrier dysfunction in metabolic inflammation. We propose a concept by which the gut microbiota fuels metabolic inflammation and dysregulation. Here, the authors describe how metabolic disorders, such as type 2 diabetes and nonalcoholic fatty liver disease, are driven by alterations in the composition of the intestinal microbiota and its metabolites, which translocate from the gut across a disrupted intestinal barrier and contribute to metabolic inflammation.

502 citations