34
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Evaluation of Prognostic Factors of Severity in Acute Biliary Pancreatitis

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Acute pancreatitis (AP) is an inflammatory disorder of the pancreas that, when classified as severe, is associated with high morbidity and mortality. Promptly identifying the severity of AP is of extreme importance for improving clinical outcomes. The aim of this study was to compare the prognostic value of serological biomarkers, ratios, and multifactorial scores in patients with acute biliary pancreatitis and to identify the best predictors. In this observational and prospective study, the biomarkers, ratios and multifactorial scores were evaluated on admission and at 48 h of the symptom onset. On admission, regarding the AP severity, the white blood count (WBC) and neutrophil–lymphocyte ratio (NLR), and regarding the mortality, the WBC and the modified Marshall score (MMS) showed the best predictive values. At 48 h, regarding the AP severity, the hepcidin, NLR, systemic inflammatory response index (SIRI) and MMS and regarding the mortality, the NLR, hepcidin and the bedside index for severity in AP (BISAP) score, showed the best predictive values. The present study enabled the identification, for the first time, of SIRI as a new prognostic tool for AP severity, and validated hepcidin and the NLR as better prognostic markers than C-reactive protein (CRP) at 48 h of symptom onset.

          Related collections

          Most cited references49

          • Record: found
          • Abstract: found
          • Article: not found

          Interleukin-6 induces hepcidin expression through STAT3.

          Iron homeostasis is maintained through meticulous regulation of circulating hepcidin levels. Hepcidin levels that are inappropriately low or high result in iron overload or iron deficiency, respectively. Although hypoxia, erythroid demand, iron, and inflammation are all known to influence hepcidin expression, the mechanisms responsible are not well defined. In this report we show that the inflammatory cytokine interleukin-6 (IL-6) directly regulates hepcidin through induction and subsequent promoter binding of signal transducer and activator of transcription 3 (STAT3). STAT3 is necessary and sufficient for the IL-6 responsiveness of the hepcidin promoter. Our findings provide a mechanism by which hepcidin can be regulated by inflammation or, in the absence of inflammatory stimuli, by alternative mechanisms leading to STAT3 activation.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            LEAP-1, a novel highly disulfide-bonded human peptide, exhibits antimicrobial activity.

            We report the isolation and characterization of a novel human peptide with antimicrobial activity, termed LEAP-1 (liver-expressed antimicrobial peptide). Using a mass spectrometric assay detecting cysteine-rich peptides, a 25-residue peptide containing four disulfide bonds was identified in human blood ultrafiltrate. LEAP-1 expression was predominantly detected in the liver, and, to a much lower extent, in the heart. In radial diffusion assays, Gram-positive Bacillus megaterium, Bacillus subtilis, Micrococcus luteus, Staphylococcus carnosus, and Gram-negative Neisseria cinerea as well as the yeast Saccharomyces cerevisiae dose-dependently exhibited sensitivity upon treatment with synthetic LEAP-1. The discovery of LEAP-1 extends the known families of mammalian peptides with antimicrobial activity by its novel disulfide motif and distinct expression pattern.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The early prediction of mortality in acute pancreatitis: a large population-based study.

              Identification of patients at risk for mortality early in the course of acute pancreatitis (AP) is an important step in improving outcome. Using Classification and Regression Tree (CART) analysis, a clinical scoring system was developed for prediction of in-hospital mortality in AP. The scoring system was derived on data collected from 17,992 cases of AP from 212 hospitals in 2000-2001. The new scoring system was validated on data collected from 18,256 AP cases from 177 hospitals in 2004-2005. The accuracy of the scoring system for prediction of mortality was measured by the area under the receiver operating characteristic curve (AUC). The performance of the new scoring system was further validated by comparing its predictive accuracy with that of Acute Physiology and Chronic Health Examination (APACHE) II. CART analysis identified five variables for prediction of in-hospital mortality. One point is assigned for the presence of each of the following during the first 24 h: blood urea nitrogen (BUN) >25 mg/dl; impaired mental status; systemic inflammatory response syndrome (SIRS); age >60 years; or the presence of a pleural effusion (BISAP). Mortality ranged from >20% in the highest risk group to <1% in the lowest risk group. In the validation cohort, the BISAP AUC was 0.82 (95% CI 0.79 to 0.84) versus APACHE II AUC of 0.83 (95% CI 0.80 to 0.85). A new mortality-based prognostic scoring system for use in AP has been derived and validated. The BISAP is a simple and accurate method for the early identification of patients at increased risk for in-hospital mortality.
                Bookmark

                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                16 June 2020
                June 2020
                : 21
                : 12
                : 4300
                Affiliations
                [1 ]Health Sciences Research Centre, University of Beira Interior (CICS-UBI), 6200-506 Covilhã, Portugal; mcbranco@ 123456fcsaude.ubi.pt
                [2 ]General Surgery Department, Hospital Amato Lusitano, Unidade Local de Saúde de Castelo Branco, 6000-085 Castelo Branco, Portugal; agouveia@ 123456ulscb.min-saude.pt
                [3 ]Faculty of Health Sciences, University of Beira Interior, 6200-506 Covilhã, Portugal
                [4 ]Clinical Academic Centre of Beiras, CACB, 6200-506 Covilhã, Portugal; sara@ 123456ipcb.pt
                [5 ]Biophysics Institute, Faculty of Medicine, University of Coimbra, 3000-548 Coimbra, Portugal; mabrantes@ 123456fmed.uc.pt (A.M.A.); mfbotelho@ 123456fmed.uc.pt (M.F.B.); jglrt@ 123456hotmail.com (J.G.T.)
                [6 ]Coimbra Institute for Clinical and Biomedical Research (iCBR) Area of Environment Genetics and Oncobiology (CIMAGO), Faculty of Medicine, University of Coimbra, 3000-548 Coimbra, Portugal
                [7 ]CNC.IBILI Consortium/Center for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, 3000-548 Coimbra, Portugal
                [8 ]Clinical Academic Center of Coimbra, CACC, 3004-561 Coimbra, Portugal
                [9 ]Polytechnic Institute of Castelo Branco, Escola Superior de Gestão, 6000-084 Castelo Branco, Portugal
                [10 ]Surgery Department, Centro Hospitalar e Universitário de Coimbra (CHUC), University Hospital, Faculty of Medicine, 3000-075 Coimbra, Portugal
                Author notes
                [* ]Correspondence: pedro.silvavaz@ 123456gmail.com ; Tel.: +351-966-498-337
                Author information
                https://orcid.org/0000-0002-2979-1024
                https://orcid.org/0000-0003-2944-306X
                https://orcid.org/0000-0001-7202-1650
                Article
                ijms-21-04300
                10.3390/ijms21124300
                7352282
                32560276
                e9edcf34-ba12-4413-8a0f-56ee5a6df293
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 15 May 2020
                : 15 June 2020
                Categories
                Article

                Molecular biology
                acute biliary pancreatitis,inflammation,prognostic,severity,hepcidin,systemic inflammatory response index

                Comments

                Comment on this article