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Anti-GP2 IgA: a biomarker for disease severity and/or cholangiocarcinoma in primary sclerosing cholangitis?
  1. Sumera Rizvi,
  2. Ju Dong Yang,
  3. Gregory J Gores
  1. Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA
  1. Correspondence to Gregory J Gores, Division of Gastroenterology and Hepatology, Mayo Clinic, 200 First Street SW, Rochester MN 55905, USA; gores.gregory{at}mayo.edu

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Primary sclerosing cholangitis (PSC) is a heterogeneous and complex syndrome with highly variable disease progression and unknown etiopathogenesis, the latter perhaps influenced by the microbiome.1 ,2 Moreover, it is a premalignant disease in that it confers a significant risk for the development of cholangiocarcinoma (CCA) in a subset of patients.3 Detection of CCA in PSC poses a major diagnostic dilemma as inflammation-related dominant strictures in PSC may mimic malignant strictures.3 Contemporary diagnostic modalities for early detection of CCA in patients with PSC remain suboptimal although innovative approaches are emerging.4 Hence, there is a critical need for the development of a biomarker which may identify the subgroup of patients with PSC at risk for CCA. Such a biomarker would enable earlier CCA detection which in turn increases the likelihood of having curative treatment options. Biomarkers, in general, are analytes which can be detected in tissues, cells or body fluids, and signify either the presence of a disease or its outcome.5 The ideal biomarker should be readily detected in a non-invasive manner, and be highly sensitive and specific in its diagnostic, predictive and prognostic capability.5

In this issue, Jendrek et al report a potential biomarker, antiglycoprotein 2 (anti-GP2), in PSC, CCA, as well as secondary sclerosing cholangitis (SSC).6 Autoantibodies against glycoproteins of the pancreatic acini (PABs) are reported to have a high specificity …

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Footnotes

  • Contributors All three authors contributed substantially to the writing and editing of this commentary.

  • Funding This work was supported by National Institutes of Health grant DK59427 (GJG) and the Mayo Foundation.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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