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Heparin-binding protein is significantly increased in acute pancreatitis

BACKGROUND: Most patients with acute pancreatitis (AP) experience mild, self-limiting disease with little or no need for hospital care. However, 20–25% of patients develop a more severe and potentially life-threatening condition with progressive systemic inflammatory response syndrome (SIRS) and mul...

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Autores principales: Sjöbeck, Martina, Sternby, Hanna, Herwald, Heiko, Thorlacius, Henrik, Regnér, Sara
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8403433/
https://www.ncbi.nlm.nih.gov/pubmed/34454419
http://dx.doi.org/10.1186/s12876-021-01910-6
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author Sjöbeck, Martina
Sternby, Hanna
Herwald, Heiko
Thorlacius, Henrik
Regnér, Sara
author_facet Sjöbeck, Martina
Sternby, Hanna
Herwald, Heiko
Thorlacius, Henrik
Regnér, Sara
author_sort Sjöbeck, Martina
collection PubMed
description BACKGROUND: Most patients with acute pancreatitis (AP) experience mild, self-limiting disease with little or no need for hospital care. However, 20–25% of patients develop a more severe and potentially life-threatening condition with progressive systemic inflammatory response syndrome (SIRS) and multiorgan failure, resulting in high morbidity and mortality rates. Predicting disease severity at an early stage is important, as immediate supportive care has been demonstrated to reduce the incidence of SIRS and organ failure, improving patient outcome. Several studies have demonstrated elevated levels of heparin-binding protein (HBP) in patients with sepsis and septic shock, and HBP is believed to play a part in endothelial dysfunction leading to vascular leakage. As HBP levels increase prior to other known biomarkers, HBP has emerged as a promising early predictor of severe sepsis with organ dysfunction. METHODS: Patients admitted to Skåne University Hospital in Malmö between 2010 and 2013 fulfilling the criteria for AP were identified in the emergency department and prospectively enrolled in this study. The primary outcome was measured levels of HBP upon hospital admission in patients with confirmed AP. Correlations among HBP concentrations, disease severity and fluid balance were considered secondary endpoints. The correlation between HBP levels and fluid balance were analysed using Pearson correlation, and the ability of HBP to predict moderately severe/severe AP was assessed using a receiver operating characteristic (ROC) curve. RESULTS: The overall median HBP level in this study was 529 (307–898) ng/ml. There were no significant group differences in HBP levels based on AP severity. Fluid balance differed significantly between patients with mild versus moderately severe and severe pancreatitis, but we found no correlation between HBP concentration and fluid balance. CONCLUSIONS: HBP levels are dramatically increased in patients with AP, and these levels far exceed those previously reported in other conditions. In this study, we did not observe any significant correlation between HBP levels and disease severity or the need for intravenous fluid. Additional studies on HBP are needed to further explore the role of HBP in the pathogenesis of AP and its possible clinical implications. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12876-021-01910-6.
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spelling pubmed-84034332021-08-30 Heparin-binding protein is significantly increased in acute pancreatitis Sjöbeck, Martina Sternby, Hanna Herwald, Heiko Thorlacius, Henrik Regnér, Sara BMC Gastroenterol Research BACKGROUND: Most patients with acute pancreatitis (AP) experience mild, self-limiting disease with little or no need for hospital care. However, 20–25% of patients develop a more severe and potentially life-threatening condition with progressive systemic inflammatory response syndrome (SIRS) and multiorgan failure, resulting in high morbidity and mortality rates. Predicting disease severity at an early stage is important, as immediate supportive care has been demonstrated to reduce the incidence of SIRS and organ failure, improving patient outcome. Several studies have demonstrated elevated levels of heparin-binding protein (HBP) in patients with sepsis and septic shock, and HBP is believed to play a part in endothelial dysfunction leading to vascular leakage. As HBP levels increase prior to other known biomarkers, HBP has emerged as a promising early predictor of severe sepsis with organ dysfunction. METHODS: Patients admitted to Skåne University Hospital in Malmö between 2010 and 2013 fulfilling the criteria for AP were identified in the emergency department and prospectively enrolled in this study. The primary outcome was measured levels of HBP upon hospital admission in patients with confirmed AP. Correlations among HBP concentrations, disease severity and fluid balance were considered secondary endpoints. The correlation between HBP levels and fluid balance were analysed using Pearson correlation, and the ability of HBP to predict moderately severe/severe AP was assessed using a receiver operating characteristic (ROC) curve. RESULTS: The overall median HBP level in this study was 529 (307–898) ng/ml. There were no significant group differences in HBP levels based on AP severity. Fluid balance differed significantly between patients with mild versus moderately severe and severe pancreatitis, but we found no correlation between HBP concentration and fluid balance. CONCLUSIONS: HBP levels are dramatically increased in patients with AP, and these levels far exceed those previously reported in other conditions. In this study, we did not observe any significant correlation between HBP levels and disease severity or the need for intravenous fluid. Additional studies on HBP are needed to further explore the role of HBP in the pathogenesis of AP and its possible clinical implications. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12876-021-01910-6. BioMed Central 2021-08-28 /pmc/articles/PMC8403433/ /pubmed/34454419 http://dx.doi.org/10.1186/s12876-021-01910-6 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Sjöbeck, Martina
Sternby, Hanna
Herwald, Heiko
Thorlacius, Henrik
Regnér, Sara
Heparin-binding protein is significantly increased in acute pancreatitis
title Heparin-binding protein is significantly increased in acute pancreatitis
title_full Heparin-binding protein is significantly increased in acute pancreatitis
title_fullStr Heparin-binding protein is significantly increased in acute pancreatitis
title_full_unstemmed Heparin-binding protein is significantly increased in acute pancreatitis
title_short Heparin-binding protein is significantly increased in acute pancreatitis
title_sort heparin-binding protein is significantly increased in acute pancreatitis
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8403433/
https://www.ncbi.nlm.nih.gov/pubmed/34454419
http://dx.doi.org/10.1186/s12876-021-01910-6
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