Koziolek, Michael Johann

[["dc.bibliographiccitation.artnumber","R94"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Critical Care"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Johanna, Temme"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Wessels, Johannes Theodor"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T09:01:04Z"],["dc.date.available","2018-11-07T09:01:04Z"],["dc.date.issued","2011"],["dc.description.abstract","Introduction: Sepsis is characterized by systemic microvascular dysfunction. Endothelial progenitor cells (EPCs) are critically involved in maintaining vascular homeostasis under both physiological and pathological conditions. The aim of the present study was to analyze the endothelial progenitor cell system in patients suffering from sepsis with acute renal dysfunction. Methods: Patients with newly diagnosed sepsis were recruited from the ICU in a nonrandomized prospective manner. Blood samples were obtained within the first 12 hours after the diagnosis of sepsis. For quantifying endothelial progenitor cells (EPCs), CD133(+)/Flk-1(+) cells were enumerated by cytometric analysis. Analysis of EPC proliferation was performed by a colony-forming units (CFU) assay. Blood concentrations of proangiogenic mediators were measured by ELISA. Acute renal dysfunction was diagnosed according to the Acute Kidney Injury Network (AKIN) criteria. Depending on the overall mean creatinine concentration during the stay at the ICU, patients were either assigned to a 'normal creatinine group' or to a 'high creatinine group'. Survival rates, frequency of dialysis, the simplified acute physiology score (SAPS) II scores, and different laboratory parameters were collected/used for further clinical characterization Results: Circulating EPCs were significantly higher in all sepsis patients included in the study as opposed to healthy controls. Patients within the 'high creatinine group' showed an even more pronounced EPC increase. In contrast, EPC proliferation was severely affected in sepsis. Neither total circulating EPCs nor EPC proliferation differed between patients requiring dialysis and patients without renal replacement therapy. Cell numbers and cell proliferation also did not differ between surviving patients and patients with sepsis-related death. Serum levels of vascular endothelial growth factor (VEGF), stromal derived factor-1 (SDF-1), and Angiopoietin-2 were higher in sepsis than in healthy controls. Sepsis patients within the 'high creatinine group' showed significantly higher mean serum levels of uric acid. Conclusions: Sepsis significantly affects the endothelial progenitor cell system, as reflected by increased EPC numbers, increased concentrations of proangiogenic mediators, and reduced proliferative capacity of the cells. This occurs independently from the frequency of dialysis and from patient survival. Increased serum levels of uric acid are possibly responsible for stronger EPC mobilization in sepsis patients with higher average creatinine levels."],["dc.identifier.doi","10.1186/cc10100"],["dc.identifier.isi","000292506000018"],["dc.identifier.pmid","21396100"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24323"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/15283 but duplicate"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1466-609X"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.holder","Patschan et al.; licensee BioMed Central Ltd."],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Endothelial progenitor cells (EPC) in sepsis with acute renal dysfunction (ARD)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","598"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Medical Case Reports"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Behlau, Arne"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Heeg, Malte H. J."],["dc.contributor.author","Sweiss, Nadera J."],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Koziolek, Michael Johann"],["dc.date.accessioned","2019-07-09T11:53:25Z"],["dc.date.available","2019-07-09T11:53:25Z"],["dc.date.issued","2011"],["dc.description.abstract","Introduction Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome is a life-threatening condition with various etiopathogeneses. Without therapy approximately 90% of all patients die from the disease. Case presentation We report the case of a 17-year-old Caucasian woman with widespread hematomas and headache. Due to hemolytic anemia, thrombocytopenia, and schistocytosis, thrombotic thrombocytopenic purpura-hemolytic uremic syndrome was suspected and plasma exchange therapy was initiated immediately. Since her thrombocyte level did not increase during the first week of therapy, plasma treatment had to be intensified to a twice-daily schedule. Further diagnostics showed markedly reduced activities of both ADAMTS-13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 - also known as von Willebrand factor-cleaving protease) and factor H. Test results for antibodies against both proteins were positive. While plasma exchange therapy was continued, rituximab was given once weekly for four consecutive weeks. After the last dose, thrombocytes and activities of ADAMTS-13 and factor H increased into the normal range. Our patient improved and was discharged from the hospital. Conclusions Since no clinical symptoms/laboratory findings indicated a malignant or specific autoimmune-mediated disorder, the diagnosis made was thrombotic thrombocytopenic purpura-hemolytic uremic syndrome due to idiopathic combined, autoantibody-mediated ADAMTS-13/factor H deficiency."],["dc.identifier.doi","10.1186/1752-1947-5-598"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7456"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60419"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/15282 but duplicate"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.holder","Patschan et al.; licensee BioMed Central Ltd."],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Idiopathic combined, autoantibody-mediated ADAMTS-13/factor H deficiency in thrombotic thrombocytopenic purpura-hemolytic uremic syndrome in a 17-year-old woman: a case report"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]