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Faecal microbiota profiles as diagnostic biomarkers in primary sclerosing cholangitis
  1. Malte Christoph Rühlemann1,
  2. Femke-Anouska Heinsen1,
  3. Roman Zenouzi2,
  4. Wolfgang Lieb3,
  5. Andre Franke1,
  6. Christoph Schramm2
  1. 1Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany
  2. 2First Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
  3. 3Institute of Epidemiology, Christian-Albrechts-University of Kiel, Kiel, Germany
  1. Correspondence to Dr. Christoph Schramm, First Department of Medicine, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, Hamburg 20246, Germany; cschramm{at}uke.de

https://doi.org/10.1136/gutjnl-2016-312180

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    Dear Sir,

    Primary sclerosing cholangitis (PSC) is a progressive disease of unknown aetiology. The presumed involvement of the gut–liver axis in disease pathogenesis1 has prompted investigations into mucosal2 and faecal intestinal microbiota composition, as has been reported by Kummen et al3 in this journal. Microbiota as diagnostic biomarkers of disease are of interest from the clinician’s point of view and Kummen et al3 have suggested a panel of taxa and even a single genus (Veillonella) with a reasonable diagnostic accuracy differentiating PSC and healthy controls (HCs).

    We here report on a cohort study from northern Germany, using stool samples of 98 HC subjects, 73 patients with well-characterised PSC and 88 subjects with UC for 16S rDNA sequencing of the V1-V2 variable region. The PSC subgroup included 38 subjects with concomitant UC (PSC-UC). The data were subjected to quality control and operational taxonomic units (OTU) picking according to the methods described.3 Of the 12 taxa proposed to be differentially abundant in …

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    Footnotes

    • MCR and F-AH contributed equally.

    • AF and CS jointly supervised.

    • Contributors AF and CS designed the study. CS, RZ and WL provided patient data and material. MCR, F-AH and AF analysed the data. AF, CS, MCR and F-AH wrote the manuscript. All authors have read and approved the final version.

    • Funding This work was supported by the Deutsche Forschungsgemeinschaft (DFG), KFO306 and Cluster of Excellence ‘Inflammation at Interfaces’, the biobank popgen (the popgen 2.0 network is financed by the German Ministry of Education and Research (grant 01EY1103)) and the German Federal Ministry of Education and Research (BMBF) within the framework of the e:Med research and funding program (SysInflame grant 01ZX1306A).

    • Competing interests None declared.

    • Ethics approval Ethics committees of University of Kiel and University of Hamburg.

    • Provenance and peer review Not commissioned; internally peer reviewed.