Bremer, Sebastian Christopher Benjamin

[["dc.bibliographiccitation.firstpage","2561"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Gut"],["dc.bibliographiccitation.lastpage","2573"],["dc.bibliographiccitation.volume","71"],["dc.contributor.affiliation","Latif, Muhammad Umair; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Schmidt, Geske Elisabeth; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Mercan, Sercan; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Rahman, Raza; \r\n2\r\nGastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA"],["dc.contributor.affiliation","Gibhardt, Christine Silvia; \r\n3\r\nMolecular Physiology, Institute of Cardiovascular Physiology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Stejerean-Todoran, Ioana; \r\n3\r\nMolecular Physiology, Institute of Cardiovascular Physiology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Reutlinger, Kristina; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Hessmann, Elisabeth; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Singh, Shiv K; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Moeed, Abdul; \r\n4\r\nInstitute for Microbiology and Hygiene, Medical Center-University of Freiburg, Freiburg, Baden-Württemberg, Germany"],["dc.contributor.affiliation","Rehman, Abdul; \r\n5\r\nInstitute of Pharmacology and Toxicology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Butt, Umer Javed; \r\n6\r\nClinical Neuroscience, Max-Planck-Institute for Experimental Medicine, Goettingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Bohnenberger, Hanibal; \r\n7\r\nInstitute of Pathology, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Stroebel, Philipp; \r\n7\r\nInstitute of Pathology, University Medical Center Göttingen, Gottingen, Germany"],["dc.contributor.affiliation","Bremer, Sebastian Christopher; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Neesse, Albrecht; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Bogeski, Ivan; \r\n3\r\nMolecular Physiology, Institute of Cardiovascular Physiology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.affiliation","Ellenrieder, Volker; \r\n1\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Gottingen, Niedersachsen, Germany"],["dc.contributor.author","Latif, Muhammad Umair"],["dc.contributor.author","Schmidt, Geske Elisabeth"],["dc.contributor.author","Mercan, Sercan"],["dc.contributor.author","Rahman, Raza"],["dc.contributor.author","Gibhardt, Christine Silvia"],["dc.contributor.author","Stejerean-Todoran, Ioana"],["dc.contributor.author","Reutlinger, Kristina"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Singh, Shiv K."],["dc.contributor.author","Moeed, Abdul"],["dc.contributor.author","Rehman, Abdul"],["dc.contributor.author","Butt, Umer Javed"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Bremer, Sebastian Christopher"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.author","Bogeski, Ivan"],["dc.contributor.author","Ellenrieder, Volker"],["dc.date.accessioned","2022-12-07T08:25:00Z"],["dc.date.available","2022-12-07T08:25:00Z"],["dc.date.issued","2022-04-01"],["dc.date.updated","2022-12-07T00:46:04Z"],["dc.description.abstract","ObjectivesNon-alcoholic fatty liver disease (NAFLD) can persist in the stage of simple hepatic steatosis or progress to steatohepatitis (NASH) with an increased risk for cirrhosis and cancer. We examined the mechanisms controlling the progression to severe NASH in order to develop future treatment strategies for this disease.DesignNFATc1 activation and regulation was examined in livers from patients with NAFLD, cultured and primary hepatocytes and in transgenic mice with differential hepatocyte-specific expression of the transcription factor (Alb-cre, NFATc1c.a\r\n. and NFATc1Δ/Δ\r\n). Animals were fed with high-fat western diet (WD) alone or in combination with tauroursodeoxycholic acid (TUDCA), a candidate drug for NAFLD treatment. NFATc1-dependent ER stress-responses, NLRP3 inflammasome activation and disease progression were assessed both in vitro and in vivo.ResultsNFATc1 expression was weak in healthy livers but strongly induced in advanced NAFLD stages, where it correlates with liver enzyme values as well as hepatic inflammation and fibrosis. Moreover, high-fat WD increased NFATc1 expression, nuclear localisation and activation to promote NAFLD progression, whereas hepatocyte-specific depletion of the transcription factor can prevent mice from disease acceleration. Mechanistically, NFATc1 drives liver cell damage and inflammation through ER stress sensing and activation of the PERK-CHOP unfolded protein response (UPR). Finally, NFATc1-induced disease progression towards NASH can be blocked by TUDCA administration.ConclusionNFATc1 stimulates NAFLD progression through chronic ER stress sensing and subsequent activation of terminal UPR signalling in hepatocytes. Interfering with ER stress-responses, for example, by TUDCA, protects fatty livers from progression towards manifest NASH."],["dc.description.sponsorship","the Volkswagen-Stiftung"],["dc.description.sponsorship","http://dx.doi.org/10.13039/501100001659Deutsche Forschungsgemeinschaft"],["dc.description.sponsorship","German Cancer Aid"],["dc.identifier","35365570"],["dc.identifier.doi","10.1136/gutjnl-2021-325013"],["dc.identifier.pmid","35365570"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118455"],["dc.identifier.url","https://sfb1190.med.uni-goettingen.de/production/literature/publications/173"],["dc.language.iso","en"],["dc.publisher","BMJ Publishing Group Ltd and British Society of Gastroenterology"],["dc.relation","SFB 1190: Transportmaschinen und Kontaktstellen zellulärer Kompartimente"],["dc.relation","SFB 1190 | P17: Die Rolle mitochondrialer Kontaktstellen im Rahmen tumorrelevanter Calcium- und Redox-Signalwege"],["dc.relation.eissn","1468-3288"],["dc.relation.issn","0017-5749"],["dc.relation.workinggroup","RG Bogeski"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc/4.0/"],["dc.title","NFATc1 signaling drives chronic ER stress responses to promote NAFLD progression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2828"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","14"],["dc.contributor.affiliation","Bremer, Sebastian C. B.; 1Clinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; alexander.koenig@med.uni-goettingen.de (A.O.K.); ahmad.amanzada@med.uni-goettingen.de (A.A.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Bittner, Gabi; 2Institute of Pathology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; bittnergabi@outlook.de (G.B.); omar.elakad@med.uni-goettingen.de (O.E.); dinterhelen@gmail.com (H.D.); philipp.stroebel@med.uni-goettingen.de (P.S.); hanibal.bohnenberger@med.uni-goettingen.de (H.B.)"],["dc.contributor.affiliation","Elakad, Omar; 2Institute of Pathology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; bittnergabi@outlook.de (G.B.); omar.elakad@med.uni-goettingen.de (O.E.); dinterhelen@gmail.com (H.D.); philipp.stroebel@med.uni-goettingen.de (P.S.); hanibal.bohnenberger@med.uni-goettingen.de (H.B.)"],["dc.contributor.affiliation","Dinter, Helen; 2Institute of Pathology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; bittnergabi@outlook.de (G.B.); omar.elakad@med.uni-goettingen.de (O.E.); dinterhelen@gmail.com (H.D.); philipp.stroebel@med.uni-goettingen.de (P.S.); hanibal.bohnenberger@med.uni-goettingen.de (H.B.)"],["dc.contributor.affiliation","Gaedcke, Jochen; 3Clinic for General, Visceral and Pediatric Surgery, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; jochen.gaedcke@med.uni-goettingen.de"],["dc.contributor.affiliation","König, Alexander O.; 1Clinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; alexander.koenig@med.uni-goettingen.de (A.O.K.); ahmad.amanzada@med.uni-goettingen.de (A.A.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Amanzada, Ahmad; 1Clinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; alexander.koenig@med.uni-goettingen.de (A.O.K.); ahmad.amanzada@med.uni-goettingen.de (A.A.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Ellenrieder, Volker; 1Clinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; alexander.koenig@med.uni-goettingen.de (A.O.K.); ahmad.amanzada@med.uni-goettingen.de (A.A.); volker.ellenrieder@med.uni-goettingen.de (V.E.)"],["dc.contributor.affiliation","Freiherr von Hammerstein-Equord, Alexander; 4Clinic for Cardiac, Thoracic and Vascular Surgery, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; alexander.hammerstein@med.uni-goettingen.de"],["dc.contributor.affiliation","Ströbel, Philipp; 2Institute of Pathology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; bittnergabi@outlook.de (G.B.); omar.elakad@med.uni-goettingen.de (O.E.); dinterhelen@gmail.com (H.D.); philipp.stroebel@med.uni-goettingen.de (P.S.); hanibal.bohnenberger@med.uni-goettingen.de (H.B.)"],["dc.contributor.affiliation","Bohnenberger, Hanibal; 2Institute of Pathology, University Medical Center Goettingen, Georg-August-University, 37075 Goettingen, Germany; bittnergabi@outlook.de (G.B.); omar.elakad@med.uni-goettingen.de (O.E.); dinterhelen@gmail.com (H.D.); philipp.stroebel@med.uni-goettingen.de (P.S.); hanibal.bohnenberger@med.uni-goettingen.de (H.B.)"],["dc.contributor.author","Bremer, Sebastian C. B."],["dc.contributor.author","Bittner, Gabi"],["dc.contributor.author","Elakad, Omar"],["dc.contributor.author","Dinter, Helen"],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","König, Alexander O."],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Freiherr von Hammerstein-Equord, Alexander"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.date.accessioned","2022-07-01T07:35:31Z"],["dc.date.available","2022-07-01T07:35:31Z"],["dc.date.issued","2022"],["dc.date.updated","2022-07-08T10:03:36Z"],["dc.description.abstract","Tumor grading is a robust prognostic predictor in patients with neuroendocrine neoplasms (NEN) and guides therapy, especially in tumors with high proliferation. NEN can be separated into well-differentiated and poorly differentiated types. The more aggressive NEN have been further separated into neuroendocrine tumors (NET G3) with a better prognosis and neuroendocrine carcinomas (NEC) with a worse prognosis. Despite this distinction’s tremendous clinical and therapeutic relevance, optimal diagnostic biomarkers are still lacking. In this study, we analyzed the protein expression and prognostic impact of Enhancer of Zeste Homolog 2 (EZH2) by immunohistochemistry in 219 tissue samples of gastroenteropancreatic (GEP-NEN) and pulmonary NEN (P-NEN). EZH2 was almost exclusively expressed in NEN with a proliferation rate above 20% (G3), while all low-grade tumors were nearly negative. Among high-grade NEN, 65% showed high and 35% low expression of EZH2. In this group, the high expression of EZH2 was significantly associated with poor overall survival and NEC histology. Interestingly, EZH2 seems to act independently of Polycomb Repressive Complex 2 (PRC2) in NEN. In conclusion, we propose EZH2 as a robust biomarker for distinguishing between NET G3 and NEC among gastroenteropancreatic and pulmonary NEN."],["dc.description.sponsorship","Deutsche Krebshilfe"],["dc.description.sponsorship","University Medical Center Göttingen"],["dc.description.sponsorship","Else-Kröner-Fresenius-Stiftung"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3390/cancers14122828"],["dc.identifier.pii","cancers14122828"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112190"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112412"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","2072-6694"],["dc.rights","CC BY 4.0"],["dc.title","Enhancer of Zeste Homolog 2 (EZH2) Is a Marker of High-Grade Neuroendocrine Neoplasia in Gastroenteropancreatic and Pulmonary Tract and Predicts Poor Prognosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","367"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Clinical Ultrasound"],["dc.bibliographiccitation.lastpage","374"],["dc.bibliographiccitation.volume","50"],["dc.contributor.affiliation","Bremer, Sebastian C. B.; 1\r\nClinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology\r\nUniversity Medical Center Goettingen, Georg‐August‐University\r\nGoettingen Germany"],["dc.contributor.affiliation","Knoop, Richard F.; 1\r\nClinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology\r\nUniversity Medical Center Goettingen, Georg‐August‐University\r\nGoettingen Germany"],["dc.contributor.affiliation","Porsche, Melissa; 1\r\nClinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology\r\nUniversity Medical Center Goettingen, Georg‐August‐University\r\nGoettingen Germany"],["dc.contributor.affiliation","Amanzada, Ahmad; 1\r\nClinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology\r\nUniversity Medical Center Goettingen, Georg‐August‐University\r\nGoettingen Germany"],["dc.contributor.affiliation","Ellenrieder, Volker; 1\r\nClinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology\r\nUniversity Medical Center Goettingen, Georg‐August‐University\r\nGoettingen Germany"],["dc.contributor.affiliation","Neesse, Albrecht; 1\r\nClinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology\r\nUniversity Medical Center Goettingen, Georg‐August‐University\r\nGoettingen Germany"],["dc.contributor.affiliation","Kunsch, Steffen; 1\r\nClinic for Gastroenterology, Gastrointestinal Oncology and Endocrinology\r\nUniversity Medical Center Goettingen, Georg‐August‐University\r\nGoettingen Germany"],["dc.contributor.author","Bremer, Sebastian C. B."],["dc.contributor.author","Knoop, Richard F."],["dc.contributor.author","Porsche, Melissa"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.author","Kunsch, Steffen"],["dc.contributor.author","Petzold, Golo"],["dc.date.accessioned","2021-12-01T09:23:12Z"],["dc.date.available","2021-12-01T09:23:12Z"],["dc.date.issued","2021"],["dc.date.updated","2022-06-14T22:49:32Z"],["dc.description.abstract","Abstract Purpose Increased gallbladder wall thickness (GBWT) is a common finding. Reported causes include advanced chronic liver disease (ACLD), ascites and hypalbuminemia. GBWT is a marker for the prediction of esophageal varices. It remains unclear which of these factors is the decisive driver of GBWT. We aim to investigate whether there is a predominant factor associated with the GBWT. Methods We enrolled 258 patients with ascites, hypalbuminemia and/or ACLD and 98 healthy volunteers that underwent abdominal ultrasound. Differences of mean GBWT in subgroups of patients with ACLD, ascites, and/or hypalbuminemia were analyzed. Correlation between various parameters and GBWT were calculated using multiple regression analysis. Results GBWT in patients with ACLD + ascites + hypalbuminemia (n = 59; 5.70 ± 2.05 mm) was pathologically increased compared to patients with hypalbuminemia + ascites without ACLD (n = 36; 2.14 ± 0.66 mm; p < .001) and to patients with only hypalbuminemia (n = 76; 2.02 ± 0.80 mm; p < .001). GBWT of patients with ACLD + hypalbuminemia (n = 30; 3.42 ± 1.52 mm) and with ACLD and normal albumin level were not different (n = 46; 3.10 ± 1.62 mm; p > .999). Significant correlation was seen between GBWT and ACLD (r = .53; p < .001) and ascites (r = .51; p < .001) but not albumin level (r = .04; p = .510). Conclusion We demonstrate that ACLD is predominantly associated with GBWT. In contrast to the current literature, serum albumin level appears not to be associated with pathological GBWT."],["dc.description.abstract","Representative image of a gallbladder of a patient with liver cirrhosis and ascites using a convex transducer (4.0 MHz). The gallbladder wall is pathologically thickened image"],["dc.identifier.doi","10.1002/jcu.23077"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94586"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.publisher","John Wiley & Sons, Inc."],["dc.relation.eissn","1097-0096"],["dc.relation.issn","0091-2751"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.title","Pathological gallbladder wall thickening is associated with advanced chronic liver disease and independent of serum albumin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","320"],["dc.bibliographiccitation.journal","Frontiers in Medicine"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Bremer, Sebastian C. B."],["dc.contributor.author","Reinhardt, Lars"],["dc.contributor.author","Sobotta, Michael"],["dc.contributor.author","Hasselluhn, Marie C."],["dc.contributor.author","Lorf, Thomas"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Schwörer, Harald"],["dc.date.accessioned","2019-07-09T11:49:36Z"],["dc.date.available","2019-07-09T11:49:36Z"],["dc.date.issued","2018"],["dc.description.abstract","Background: Liver transplant recipients are frequently treated with proton pump inhibitors. Drug interactions have been described especially with respect to omeprazole. Due to the lower binding capacity of pantoprazole to CYP2C19 this drug became preferred and became the most used proton pump inhibitor in Germany. The data on the influence of pantoprazole on immunosuppressive drugs in liver transplant recipients a very scarce. Methods: The authors performed a single center analysis in liver transplant recipients on the effect of pantoprazole on the serum trough levels of different immunosuppressants. The trough levels were compared over a period of 1 year before and after start or stop of a continuous oral co-administration of 40 mg pantoprazole once daily. Results: The serum trough levels of tacrolimus (n = 30), everolimus (n = 7), or sirolimus (n = 3) remain constant during an observation period of at least 1 year before and after co-administration of pantoprazole. None of the included patients needed a change of dosage of the observed immunosuppressants during the observation period. Conclusions: The oral co-administration of pantoprazole is safe in immunosuppressed liver transplant recipients according to the serum trough levels of tacrolimus, everolimus, and sirolimus. This analysis provides first data on the influence of pantoprazole on immunosuppressive drugs in liver transplant recipients."],["dc.identifier.doi","10.3389/fmed.2018.00320"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15722"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59589"],["dc.language.iso","en"],["dc.subject.ddc","610"],["dc.title","Pantoprazole Does not Affect Serum Trough Levels of Tacrolimus and Everolimus in Liver Transplant Recipients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e000258"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMJ Open Gastroenterology"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Mavropoulou, Eirini"],["dc.contributor.author","Ternes, Kristin"],["dc.contributor.author","Mechie, Nicolae-Catalin"],["dc.contributor.author","Bremer, Sebastian Christopher Benjamin"],["dc.contributor.author","Kunsch, Steffen"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.author","Amanzada, Ahmad"],["dc.date.accessioned","2019-07-09T11:50:10Z"],["dc.date.available","2019-07-09T11:50:10Z"],["dc.date.issued","2019"],["dc.description.abstract","Background Concurrent cytomegalovirus (CMV) colitis in inflammatory bowel disease (IBD) and after haematopoietic stem cell transplantation (HSCT) is an important clinical entity associated with high rates of morbidity and mortality. Methods A retrospective study of 47 patients with IBD and 61 HSCT patients was performed regarding the evaluation of diagnostic accuracy of applied methods, predictors, risk factors for CMV disease manifestation, the proportion of patients with antiviral treatment and disease outcome. Results The sensitivity of quantitative PCR (qPCR) with a cut-off value of >250 copies/mg for CMV colitis in patients with IBD and HSCT patients was 79% and 92%, respectively. Predictors for CMV colitis in the IBD cohort were anaemia and the presence of endoscopic ulcers. Glucocorticoids, calcineurin inhibitors and >2 concurrent lines of treatment with immunosuppressive drugs could be identified as risk factors for CMV colitis in the IBD cohort with an OR of 7.1 (95% CI 1.7 to 29.9), 21.3 (95% CI 2.4 to 188.7) and 13.4 (95% CI 3.2 to 56.1), respectively. Predictors and risk factors for CMV gastroenteritis in the HSCT cohort was the presence of endoscopic ulcers (OR 18.6, 95% CI 3.3 to 103.7) and >2 concurrent lines of treatment with immunosuppressive drugs. Antiviral therapy was administered in 70% of patients with IBD and 77% of HSCT patients with CMV disease. 71% of antiviraltreated patients with IBD showed an improvement of their disease activity and 14% underwent colectomy. The mortality rate of HSCT patients was 21% irrespective of their CMV status. Conclusions In addition to the implementation of histological methods, qPCR may be performed in patients with suspected high-risk IBD and HSCT patients for CMV colitis. Independent validations of these results in further prospective studies are needed."],["dc.identifier.doi","10.1136/bmjgast-2018-000258"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15876"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59717"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Cytomegalovirus colitis in inflammatory bowel disease and after haematopoietic stem cell transplantation: diagnostic accuracy, predictors, risk factors and disease outcome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","BioMed Research International"],["dc.bibliographiccitation.lastpage","6"],["dc.bibliographiccitation.volume","2022"],["dc.contributor.author","Knoop, Richard F."],["dc.contributor.author","Gaertner, Pauline C."],["dc.contributor.author","Petzold, Golo"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Neesse, Albrecht"],["dc.contributor.author","Bremer, Sebastian C. B."],["dc.contributor.author","Kunsch, Steffen"],["dc.date.accessioned","2022-06-01T09:39:38Z"],["dc.date.available","2022-06-01T09:39:38Z"],["dc.date.issued","2022"],["dc.description.abstract","Background and Aims. In contrast to guideline recommendations, endoscopic testing for Helicobacter pylori is frequently performed under Helicobacter pylori suppressive conditions, e.g., intake of proton-pump inhibitors (PPI), preceded antibiotic treatment, or recent gastrointestinal bleeding. Our study\\’s aim was to retest patients with—under suppressive conditions—negative test results. This was carried out in order to examine the rate of false negative tests previously gathered under suppressive conditions. Methods. The trial was conducted in a large patient collective in a university hospital. Every elective esophagogastroduodenoscopy from in- and outpatients was included. Prior to endoscopy, suppressive conditions were collected via standardized questionnaire. If Helicobacter pylori testing was indicated, both helicobacter urease test and histology were performed in analogy to the Sydney classification. In case of a negative result under suppressive conditions, the patient was reinvited after, if possible, withdrawal of suppressive condition in order to perform a urea breath test (UBT). Results. 1,216 patients were included (median 59 years, 72.0% inpatients, 28.0% outpatients). Overall, 60.6% (737) were under Helicobacter pylori suppressive conditions. The main suppressive condition was intake of PPIs (54.5%). In 53.7% (653) of all included cases, Helicobacter pylori testing was performed. Of those, 14.1% (92) had a positive test, and 85.9% (561) were negative. Out of the patients with negative result, 50.8% (285) were tested under suppressive conditions and consequently invited for retesting via UBT. In 20.4% (45), suppressive conditions could not be ceased. In 22.8% (65), retesting was conducted. Of those, 98.5% (64) congruently presented a negative result again, and only 1.5% (1) was positive for Helicobacter pylori. Conclusion. Many patients undergoing esophagogastroduodenoscopy in everyday clinical practice are tested for Helicobacter pylori under suppressive conditions leading to a potentially higher risk of false negative results. However, our research shows that this issue might be overestimated."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1155/2022/5380001"],["dc.identifier.pii","5380001"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108523"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","2314-6141"],["dc.relation.issn","2314-6133"],["dc.rights","CC BY 4.0"],["dc.title","Systematic Retesting for Helicobacter pylori: The Potential Overestimation of Suppressive Conditions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2926"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Petzold, Golo"],["dc.contributor.author","Bremer, Sebastian C. B."],["dc.contributor.author","Heuschert, Felix C."],["dc.contributor.author","Treiber, Hannes"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Kunsch, Steffen"],["dc.contributor.author","Neesse, Albrecht"],["dc.date.accessioned","2021-08-12T07:45:52Z"],["dc.date.available","2021-08-12T07:45:52Z"],["dc.date.issued","2021"],["dc.description.abstract","Treatment of recurrent malignant ascites in cancer patients is a challenge. Evidence based guidelines regarding the best treatment strategy are lacking. The aim of this prospective study was to investigate the safety and efficacy of a tunnelled peritoneal catheter (PleurX) in cancer patients with symptomatic ascites. Patients with symptomatic, diuretics-refractory ascites and indication for the implantation of a tunnelled peritoneal PleurX catheter were prospectively enrolled between August 2018 and July 2020. The number of catheter days, complications, amount of drained ascites and ascites-associated symptoms and hospitalization rate pre- and post-PleurX insertion were analysed. 51 Patients (64.7% male) were prospectively enrolled. The mean age was 66.6 (±7.9) years. The most common cause of ascites was pancreatic adenocarcinoma (n = 10) followed by cholangiocellular carcinoma (n = 9) and hepatocellular carcinoma (n = 8). The technical success rate of PleurX implantation was 100%. The mean volume of weakly drained ascites was 5.44l (±4.08). Major complications included cellulitis (n = 2), peritonitis and drainage dislocation (each n = 1). The mean catheter days per patient was 59.8 (±107.4) (Min 4, Max 668). Abdominal discomfort, impaired mobility, dyspnoea, fatigue, nausea and vomiting were significantly reduced 30 days after PleurX insertion (p < 0.05). Moreover, hospitalization rate was significantly reduced (p < 0.001; 27.08% of days preimplantation vs. 11.27% postimplantation). We conclude that implantation of a tunnelled ascites catheter is a safe and effective method for the treatment of refractory ascites in cancer patients with advanced disease. Serious complications are rare. Burdensome ascites-associated symptoms and hospitalization rates can be significantly reduced over a longer period of time."],["dc.description.abstract","Treatment of recurrent malignant ascites in cancer patients is a challenge. Evidence based guidelines regarding the best treatment strategy are lacking. The aim of this prospective study was to investigate the safety and efficacy of a tunnelled peritoneal catheter (PleurX) in cancer patients with symptomatic ascites. Patients with symptomatic, diuretics-refractory ascites and indication for the implantation of a tunnelled peritoneal PleurX catheter were prospectively enrolled between August 2018 and July 2020. The number of catheter days, complications, amount of drained ascites and ascites-associated symptoms and hospitalization rate pre- and post-PleurX insertion were analysed. 51 Patients (64.7% male) were prospectively enrolled. The mean age was 66.6 (±7.9) years. The most common cause of ascites was pancreatic adenocarcinoma (n = 10) followed by cholangiocellular carcinoma (n = 9) and hepatocellular carcinoma (n = 8). The technical success rate of PleurX implantation was 100%. The mean volume of weakly drained ascites was 5.44l (±4.08). Major complications included cellulitis (n = 2), peritonitis and drainage dislocation (each n = 1). The mean catheter days per patient was 59.8 (±107.4) (Min 4, Max 668). Abdominal discomfort, impaired mobility, dyspnoea, fatigue, nausea and vomiting were significantly reduced 30 days after PleurX insertion (p < 0.05). Moreover, hospitalization rate was significantly reduced (p < 0.001; 27.08% of days preimplantation vs. 11.27% postimplantation). We conclude that implantation of a tunnelled ascites catheter is a safe and effective method for the treatment of refractory ascites in cancer patients with advanced disease. Serious complications are rare. Burdensome ascites-associated symptoms and hospitalization rates can be significantly reduced over a longer period of time."],["dc.identifier.doi","10.3390/cancers13122926"],["dc.identifier.pii","cancers13122926"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88562"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.publisher","MDPI"],["dc.relation.eissn","2072-6694"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Tunnelled Peritoneal Catheter for Malignant Ascites—An Open-Label, Prospective, Observational Trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]