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Pathogenesis and Management of Pancreatitis
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Pathogenesis and Management of Pancreatitis

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Infectious Diseases".

Deadline for manuscript submissions: closed (25 May 2019)

Special Issue Editor

Prof. Dr. Robert Sutton

E-Mail Website
Guest Editor
Professor of Surgery, Liverpool Pancreatitis Research Group, Royal Liverpool University Hospital and Institute of Translational Medicine, University of Liverpool, Liverpool, UK
Interests: molecular and cell biology of pancreatitis; diagnosis and treatment of pancreatitis; multiomics; clinical trials

Special Issue Information

Dear Colleagues,

Advances in basic, translational and clinical research in acute and chronic pancreatitis place us on the cusp of a step change in understanding and patient management. Progress in the identification and characterization of molecular pathways, subcellular organelles, cellular and extracellular interactions, organ dysfunction, disease course and patient experience all contribute.  Yet we have to continue striving for solutions to many challenges that will bring this step change about and make full use of the opportunities this presents. We still lack accurate biomarkers and effective therapies, particularly as we have no licensed specific therapy to protect the pancreas in acute pancreatitis or chronic pancreatitis. How are the mechanisms of acute pancreatitis similar or different from those of chronic pancreatitis? What will enable us to achieve earlier diagnosis of either condition? What can we learn about disease mechanisms that will clarify targets for treatment? What biomarkers can we pinpoint that will increase the accuracy of prognostication or evaluation of therapies? What can we learn from better study designs to map disease course and appreciate as well as improve patient experience? What are the next steps in developing new treatments? The Journal of Clinical Medicine is calling for original papers (the majority) and reviews that address these and other related important issues in pancreatitis, to be published in a special edition in mid-2019. You are invited to submit articles that report basic, translational and clinical studies in pancreatitis, to be evaluated with this special edition. Whether at the bench in the laboratory or office or at the bedside with patients, our focus is the same: greater insight and capability to understand and manage pancreatitis and so improve human health.

Prof. Dr. Robert Sutton
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Acute pancreatitis
  • Chronic pancreatitis
  • Aetiology
  • Acinar cell injury
  • Ductal cell injury
  • Inflammation
  • Systemic injury
  • Biomarkers
  • Diagnosis
  • Pancreatic insufficiency
  • Treatment
  • Quality of life

Published Papers (2 papers)

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Research

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14 pages, 919 KiB  
Article
Serum Urokinase-Type Plasminogen Activator Receptor Does Not Outperform C-Reactive Protein and Procalcitonin as an Early Marker of Severity of Acute Pancreatitis
by Witold Kolber, Beata Kuśnierz-Cabala, Paulina Dumnicka, Małgorzata Maraj, Małgorzata Mazur-Laskowska, Michał Pędziwiatr and Piotr Ceranowicz
J. Clin. Med. 2018, 7(10), 305; https://doi.org/10.3390/jcm7100305 - 27 Sep 2018
Cited by 16 | Viewed by 2442
Abstract
Severe acute pancreatitis (SAP) concerns 10–20% of acute pancreatitis (AP) patients and is associated with a poor prognosis and high mortality. An early prognosis of the unfavorable outcome, transfer to an intensive care unit (ICU) and the introduction of an adequate treatment are [...] Read more.
Severe acute pancreatitis (SAP) concerns 10–20% of acute pancreatitis (AP) patients and is associated with a poor prognosis and high mortality. An early prognosis of the unfavorable outcome, transfer to an intensive care unit (ICU) and the introduction of an adequate treatment are crucial for patients’ survival. Recently, the elevated circulating urokinase-type plasminogen activator receptor (uPAR) has been reported to predict SAP with a high diagnostic accuracy among patients in a tertiary center. The aim of the study was to compare the diagnostic utility of uPAR and other inflammatory markers as the predictors of the unfavorable course of AP in patients admitted to a secondary care hospital within the first 24 h of the onset of AP. The study included 95 patients, eight with a SAP diagnosis. Serum uPAR was measured on admission and in the two subsequent days. On admission, uPAR significantly predicted organ failure, acute cardiovascular failure, acute kidney injury, the need for intensive care, and death. The diagnostic accuracy of the admission uPAR for the prediction of SAP, organ failure, and ICU transfer or death was low to moderate and did not differ significantly from the diagnostic accuracy of interleukin-6, C-reactive protein, procalcitonin, D-dimer and soluble fms-like tyrosine kinase-1. In the secondary care hospital, where most patients with AP are initially admitted, uPAR measurements did not prove better than the currently used markers. Full article
(This article belongs to the Special Issue Pathogenesis and Management of Pancreatitis)
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Review

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16 pages, 268 KiB  
Review
The Etiology of Pancreatic Manifestations in Patients with Inflammatory Bowel Disease
by Tomoya Iida, Kohei Wagatsuma, Daisuke Hirayama, Yoshihiro Yokoyama and Hiroshi Nakase
J. Clin. Med. 2019, 8(7), 916; https://doi.org/10.3390/jcm8070916 - 26 Jun 2019
Cited by 25 | Viewed by 4926
Abstract
Inflammatory bowel disease (IBD) is an idiopathic chronic and recurrent condition that comprises Crohn’s disease and ulcerative colitis. A pancreatic lesion is one of the extraintestinal lesions in patients with IBD. Acute pancreatitis is the representative manifestation, and various causes of pancreatitis have [...] Read more.
Inflammatory bowel disease (IBD) is an idiopathic chronic and recurrent condition that comprises Crohn’s disease and ulcerative colitis. A pancreatic lesion is one of the extraintestinal lesions in patients with IBD. Acute pancreatitis is the representative manifestation, and various causes of pancreatitis have been reported, including those involving adverse effects of drug therapies such as 5-aminosalicylic acid and thiopurines, gall stones, gastrointestinal lesions on the duodenum, iatrogenic harm accompanying endoscopic procedures such as balloon endoscopy, and autoimmunity. Of these potential causes, autoimmune pancreatitis (AIP) is a relatively newly recognized disease and is being increasingly diagnosed in IBD. AIP cases can be divided into type 1 cases involving lymphocytes and IgG4-positive plasma cells, and type 2 cases primarily involving neutrophils; the majority of AIP cases complicating IBD are type 2. The association between IBD and chronic pancreatitis, exocrine pancreatic insufficiency, pancreatic cancer, etc. has also been suggested; however, studies with high-quality level evidence are limited, and much remains unknown. In this review, we provide an overview of the etiology of pancreatic manifestation in patients with IBD. Full article
(This article belongs to the Special Issue Pathogenesis and Management of Pancreatitis)
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