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Pergolini I, Schorn S, Friess H, Demir IE. The Role of Magnesium in Acute Pancreatitis and Pancreatic Injury: A Systematic Review. Visc Med 2024; 40:264-275. [PMID: 39398394 PMCID: PMC11466448 DOI: 10.1159/000540507] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/03/2024] [Accepted: 07/22/2024] [Indexed: 10/15/2024] Open
Abstract
Introduction As natural calcium (Ca) antagonist, magnesium (Mg) seems to counteract Ca-signaling pathways involved in the intracellular protease activation leading to acute pancreatitis. We systematically reviewed the current literature to investigate the role of Mg in the pathogenesis of acute pancreatitis and its possible use in detecting, predicting, and preventing acute pancreatitis. Methods A systematic search was performed in PubMed/Scopus/Web of Science to identify in vivo and in vitro studies reporting data on Mg in acute pancreatitis. Results Twelve studies were included. Due to their heterogeneity, we conducted a review without the intent of inference. Mg deficiency in pancreatic acinar cells seems to be frequently associated with serum hypocalcemia and acute pancreatitis. Mg seems to contrast intracellular Ca accumulation which induces premature enzyme activation and acute pancreatitis. Several in vivo and in vitro experiments showed beneficial effects of Mg supplementation in counteracting Ca-signaling pathways and subsequent pathological events. Moreover, a recent randomized trial demonstrated the efficacy of Mg supplementation in reducing the incidence of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis in high-risk patients. Conclusion Mg is a natural antagonist of Ca-signaling pathways and, when deficient, predisposes to acute pancreatitis. Mg supplementation may be useful to prevent acute pancreatitis in many contexts, such as post-ERCP or after pancreatic surgery. The heterogeneity of the included studies represents an important limitation that may hinder robust conclusions.
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Affiliation(s)
- Ilaria Pergolini
- Department of Surgery, Technical University of Munich, Munich, Germany
| | - Stephan Schorn
- Department of Surgery, Technical University of Munich, Munich, Germany
| | - Helmut Friess
- Department of Surgery, Technical University of Munich, Munich, Germany
- German Cancer Consortium (DKTK), Partner Site Munich, Munich, Germany
- CRC 1321 Modelling and Targeting Pancreatic Cancer, Munich, Germany
| | - Ihsan Ekin Demir
- Department of Surgery, Technical University of Munich, Munich, Germany
- German Cancer Consortium (DKTK), Partner Site Munich, Munich, Germany
- CRC 1321 Modelling and Targeting Pancreatic Cancer, Munich, Germany
- Department of General Surgery, HPB-Unit, School of Medicine, Acibadem Mehmet Ali Aydinlar University, Istanbul, Turkey
- Else Kröner Clinician Scientist Professor for Translational Pancreatic Surgery, Munich, Germany
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2
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The Pancreas and Known Factors of Acute Pancreatitis. J Clin Med 2022; 11:jcm11195565. [PMID: 36233433 PMCID: PMC9571992 DOI: 10.3390/jcm11195565] [Citation(s) in RCA: 12] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/08/2022] [Revised: 08/11/2022] [Accepted: 08/30/2022] [Indexed: 11/16/2022] Open
Abstract
Pancreatitis is regarded by clinicians as one of the most complicated and clinically challenging of all disorders affecting the abdomen. It is classified on the basis of clinical, morphological, and histological criteria. Causes of acute pancreatitis can easily be identified in 75–85% of patients. The main causes of acute, recurrent acute, and chronic pancreatitis are gallstone migration and alcohol abuse. Other causes are uncommon, controversial, or unexplained. For instance, cofactors of all forms of pancreatitis are pancreas divisum and hypertriglyceridemia. Another factor that should be considered is a complication of endoscopic retrograde cholangiopancreatography: post-endoscopic retrograde cholangiopancreatography acute pancreatitis. The aim of this study is to present the known risk factors for acute pancreatitis, beginning with an account of the morphology, physiology, and development of the pancreas.
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3
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Obeidat AE, Mahfouz R, Monti G, Kozai L, Darweesh M, Mansour MM, Alqam A, Hernandez D. Post-Endoscopic Retrograde Cholangiopancreatography Pancreatitis: What We Already Know. Cureus 2022; 14:e21773. [PMID: 35251843 PMCID: PMC8890589 DOI: 10.7759/cureus.21773] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 01/31/2022] [Indexed: 11/05/2022] Open
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4
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Bouchard D, Brochard C, Vinson-Bonnet B, Staumont G, Abramowitz L, Benfredj P, Fathallah N, Faucheron JL, Higuero T, Panis Y, de Parades V, Siproudhis L, Laharie D, Pigot F. How to manage anal ulcerations and anorectal stenosis in Crohn's disease: algorithm-based decision making : French National Working Group Consensus 2018. Tech Coloproctol 2019; 23:353-360. [PMID: 30937646 DOI: 10.1007/s10151-019-01971-6] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/17/2019] [Accepted: 03/14/2019] [Indexed: 12/24/2022]
Abstract
The French National Society of Coloproctology established national recommendations for the treatment of anoperineal lesions associated with Crohn's disease. Treatment strategies for anal ulcerations and anorectal stenosis are suggested. Recommendations have been graded following international recommendations, and when absent professional agreement was established. For each situation, practical algorithms have been drawn.
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Affiliation(s)
- D Bouchard
- Bagatelle Hospital, 203 route de Toulouse, 33401, Talence Cedex, France.
| | - C Brochard
- University Hospital Center, Rennes Cedex 9, France
| | | | - G Staumont
- La Croix du Sud Clinic, Quint-Fonsegrives, France
| | - L Abramowitz
- Ramsay Générale de Santé, Blomet Clinic, Paris, France
| | | | | | - J-L Faucheron
- University Hospital Center Grenoble-Alpes, La Tronche, France
| | | | - Y Panis
- Beaujon Hospital, Clichy, France
| | | | - L Siproudhis
- University Hospital Center, Rennes Cedex 9, France
| | - D Laharie
- Umniversity Hospital Center Haut Lévêque, Pessac Cedex, France
| | - F Pigot
- Bagatelle Hospital, 203 route de Toulouse, 33401, Talence Cedex, France
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5
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Weiss FU, Laemmerhirt F, Lerch MM. Etiology and Risk Factors of Acute and Chronic Pancreatitis. Visc Med 2019; 35:73-81. [PMID: 31192240 DOI: 10.1159/000499138] [Citation(s) in RCA: 55] [Impact Index Per Article: 9.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/03/2019] [Accepted: 02/25/2019] [Indexed: 12/24/2022] Open
Abstract
Based on the recognition of common etiological and genetic risk factors, acute and chronic pancreatitis are increasingly regarded as a continuum of the same disease, with a significant overlap of clinical manifestations and phenotypes but distinct morphological and imaging appearances. Recent population-based and cohort studies have found that tobacco smoke conveys a greater risk than immoderate alcohol consumption for the development of chronic pancreatitis, and hypertriglyceridemia has been identified as a risk factor for acute pancreatitis - even when plasma levels are only mildly elevated. Hereditary pancreatitis, in its autosomal dominant form, is associated with mutations in the cationic trypsinogen gene (PRSS1), whereas a number of germline variations in other genes have been found to represent risk factors for chronic as well as acute pancreatitis. For now, most of these involve the pancreatic digestive protease/antiprotease system. Oftentimes, affected patients are burdened with multiple or accumulating risk factors, and genetic traits when combined with environmental toxins compound the chance of developing the disease. Determining the underlying etiology of pancreatitis is worth the effort since formerly intractable varieties such as autoimmune pancreatitis are now becoming increasingly treatable, and subtype-specific therapeutic modalities may become available.
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Affiliation(s)
- Frank Ulrich Weiss
- Department of Medicine A, Greifswald Medical School, Greifswald, Germany
| | - Felix Laemmerhirt
- Department of Medicine A, Greifswald Medical School, Greifswald, Germany
| | - Markus M Lerch
- Department of Medicine A, Greifswald Medical School, Greifswald, Germany
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6
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Gorelick FS, Lerch MM. Do Animal Models of Acute Pancreatitis Reproduce Human Disease? Cell Mol Gastroenterol Hepatol 2017; 4:251-262. [PMID: 28752114 PMCID: PMC5518169 DOI: 10.1016/j.jcmgh.2017.05.007] [Citation(s) in RCA: 49] [Impact Index Per Article: 6.1] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/25/2016] [Accepted: 05/26/2017] [Indexed: 12/10/2022]
Abstract
Acute pancreatitis is currently the most common cause of hospital admission among all nonmalignant gastrointestinal diseases. To understand the pathophysiology of the disease and as a potential step toward developing targeted therapies, attempts to induce the disease experimentally began more than 100 years ago. Recent decades have seen progress in developing new experimental pancreatitis models as well as elucidating many underlying cell biological and pathophysiological disease mechanisms. Some models have been developed to reflect specific causes of acute pancreatitis in human beings. However, the paucity of data relating to the molecular mechanisms of human disease, the likelihood that multiple genetic and environmental factors affect the risk of disease development and its severity, and the limited information regarding the natural history of disease in human beings make it difficult to evaluate the value of disease models. Here, we provide an overview of key models and discuss our views on their strengths for characterizing cell biological disease mechanisms or for identifying potential therapeutic targets. We also acknowledge their limitations.
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Affiliation(s)
- Fred S. Gorelick
- Yale University Medical School and Veterans Affairs Medical Center, West Haven, Connecticut
- Correspondence Address correspondence to: Fred S. Gorelick, MD, VA Connecticut Healthcare System/Yale University Medical School, 950 Campbell Avenue, West Haven, Connecticut 06516. fax: (203) 937-3852.VA Connecticut Healthcare System/Yale University Medical School950 Campbell AvenueWest HavenConnecticut 06516
| | - Markus M. Lerch
- Department of Medicine A, University Medicine Greifswald, Greifswald, Germany
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Szentesi A, Tóth E, Bálint E, Fanczal J, Madácsy T, Laczkó D, Ignáth I, Balázs A, Pallagi P, Maléth J, Rakonczay Z, Kui B, Illés D, Márta K, Blaskó Á, Demcsák A, Párniczky A, Pár G, Gódi S, Mosztbacher D, Szücs Á, Halász A, Izbéki F, Farkas N, Hegyi P. Analysis of Research Activity in Gastroenterology: Pancreatitis Is in Real Danger. PLoS One 2016; 11:e0165244. [PMID: 27776171 PMCID: PMC5077088 DOI: 10.1371/journal.pone.0165244] [Citation(s) in RCA: 27] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/02/2016] [Accepted: 10/07/2016] [Indexed: 12/27/2022] Open
Abstract
OBJECTIVE Biomedical investment trends in 2015 show a huge decrease of investment in gastroenterology. Since academic research usually provides the basis for industrial research and development (R&D), our aim was to understand research trends in the field of gastroenterology over the last 50 years and identify the most endangered areas. METHODS We searched for PubMed hits for gastrointestinal (GI) diseases for the 1965-2015 period. Overall, 1,554,325 articles were analyzed. Since pancreatology was identified as the most endangered field of research within gastroenterology, we carried out a detailed evaluation of research activity in pancreatology. RESULTS In 1965, among the major benign GI disorders, 51.9% of the research was performed on hepatitis, 25.7% on pancreatitis, 21.7% on upper GI diseases and only 0.7% on the lower GI disorders. Half a century later, in 2015, research on hepatitis and upper GI diseases had not changed significantly; however, studies on pancreatitis had dropped to 10.7%, while work on the lower GI disorders had risen to 23.4%. With regard to the malignant disorders (including liver, gastric, colon, pancreatic and oesophageal cancer), no such large-scale changes were observed in the last 50 years. Detailed analyses revealed that besides the drop in research activity in pancreatitis, there are serious problems with the quality of the studies as well. Only 6.8% of clinical trials on pancreatitis were registered and only 5.5% of these registered trials were multicentre and multinational (more than five centres and nations), i.e., the kind that provides the highest level of impact and evidence level. CONCLUSIONS There has been a clear drop in research activity in pancreatitis. New international networks and far more academic R&D activities should be established in order to find the first therapy specifically for acute pancreatitis.
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Affiliation(s)
- Andrea Szentesi
- Institute for Translational Medicine, University of Pécs, Pécs, Hungary
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Emese Tóth
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Emese Bálint
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Júlia Fanczal
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Tamara Madácsy
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Dorottya Laczkó
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Imre Ignáth
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Anita Balázs
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Petra Pallagi
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - József Maléth
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Zoltán Rakonczay
- First Department of Medicine, University of Szeged, Szeged, Hungary
- Department of Pathophysiology, University of Szeged, Szeged, Hungary
| | - Balázs Kui
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Dóra Illés
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Katalin Márta
- Institute for Translational Medicine, University of Pécs, Pécs, Hungary
| | - Ágnes Blaskó
- Institute for Translational Medicine, University of Pécs, Pécs, Hungary
| | - Alexandra Demcsák
- Department of Pediatrics and Pediatric Health Center, University of Szeged, Szeged, Hungary
| | | | - Gabriella Pár
- Department of Gastroenterology, First Department of Medicine, University of Pécs, Pécs, Hungary
| | - Szilárd Gódi
- Department of Translational Medicine, First Department of Medicine, University of Pécs, Pécs, Hungary
| | - Dóra Mosztbacher
- Department of Pediatrics, János Balassa Hospital of County Tolna, Szekszárd, Hungary
| | - Ákos Szücs
- First Department of Surgery, Semmelweis University, Budapest, Hungary
| | - Adrienn Halász
- First Department of Medicine, St. George University Teaching Hospital of County Fejér, Székesfehérvár, Hungary
| | - Ferenc Izbéki
- First Department of Medicine, St. George University Teaching Hospital of County Fejér, Székesfehérvár, Hungary
| | - Nelli Farkas
- Institute of Bioanalysis, University of Pécs, Pécs, Hungary
| | - Péter Hegyi
- Institute for Translational Medicine, University of Pécs, Pécs, Hungary
- First Department of Medicine, University of Szeged, Szeged, Hungary
- Department of Translational Medicine, First Department of Medicine, University of Pécs, Pécs, Hungary
- Hungarian Academy of Sciences—University of Szeged, Momentum Gastroenterology Multidisciplinary Research Group, Szeged, Hungary
- * E-mail:
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8
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Pallagi P, Hegyi P, Rakonczay Z. The Physiology and Pathophysiology of Pancreatic Ductal Secretion: The Background for Clinicians. Pancreas 2015; 44:1211-1233. [PMID: 26465950 DOI: 10.1097/mpa.0000000000000421] [Citation(s) in RCA: 36] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
The human exocrine pancreas consists of 2 main cell types: acinar and ductal cells. These exocrine cells interact closely to contribute to the secretion of pancreatic juice. The most important ion in terms of the pancreatic ductal secretion is HCO3. In fact, duct cells produce an alkaline fluid that may contain up to 140 mM NaHCO3, which is essential for normal digestion. This article provides an overview of the basics of pancreatic ductal physiology and pathophysiology. In the first part of the article, we discuss the ductal electrolyte and fluid transporters and their regulation. The central role of cystic fibrosis transmembrane conductance regulator (CFTR) is highlighted, which is much more than just a Cl channel. We also review the role of pancreatic ducts in severe debilitating diseases such as cystic fibrosis (caused by various genetic defects of cftr), pancreatitis, and diabetes mellitus. Stimulation of ductal secretion in cystic fibrosis and pancreatitis may have beneficial effects in their treatment.
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Affiliation(s)
- Petra Pallagi
- From the *First Department of Medicine, University of Szeged; and †Hungarian Academy of Sciences-University of Szeged Translational Gastroenterology Research Group, Szeged, Hungary
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9
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Abstract
An international symposium entitled "Acute pancreatitis: progress and challenges" was held on November 5, 2014 at the Hapuna Beach Hotel, Big Island, Hawaii, as part of the 45th Anniversary Meeting of the American Pancreatic Association and the Japanese Pancreas Society. The course was organized and directed by Drs. Stephen Pandol, Tooru Shimosegawa, Robert Sutton, Bechien Wu, and Santhi Swaroop Vege. The symposium objectives were to: (1) highlight current issues in management of acute pancreatitis, (2) discuss promising treatments, (3) consider development of quality indicators and improved measures of disease activity, and (4) present a framework for international collaboration for development of new therapies. This article represents a compilation and adaptation of brief summaries prepared by speakers at the symposium with the purpose of broadly disseminating information and initiatives.
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10
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Hauser G, Milosevic M, Stimac D, Zerem E, Jovanović P, Blazevic I. Preventing post-endoscopic retrograde cholangiopancreatography pancreatitis: what can be done? World J Gastroenterol 2015; 21:1069-1080. [PMID: 25632179 PMCID: PMC4306150 DOI: 10.3748/wjg.v21.i4.1069] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/15/2014] [Revised: 09/02/2014] [Accepted: 09/29/2014] [Indexed: 02/06/2023] Open
Abstract
Post-endoscopic retrograde cholangiopancreatography pancreatitis (PEP) is the most common complication of endoscopic retrograde cholangiopancreatography. The incidence of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis varies substantially and is reported around 1%-10%, although there are some reports with an incidence of around 30%. Usually, PEP is a mild or moderate pancreatitis, but in some instances it can be severe and fatal. Generally, it is defined as the onset of new pancreatic-type abdominal pain severe enough to require hospital admission or prolonged hospital stay with levels of serum amylase two to three times greater than normal, occurring 24 h after ERCP. Several methods have been adopted for preventing pancreatitis, such as pharmacological or endoscopic approaches. Regarding medical prevention, only non-steroidal anti-inflammatory drugs, namely diclofenac sodium and indomethacin, are recommended, but there are some other drugs which have some potential benefits in reducing the incidence of post-ERCP pancreatitis. Endoscopic preventive measures include cannulation (wire guided) and pancreatic stenting, while the adoption of the early pre-cut technique is still arguable. This review will attempt to present and discuss different ways of preventing post-ERCP pancreatitis.
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Abstract
Post-procedure pancreatitis is the most common complication of endoscopic retrograde cholangio pancreatography (ERCP) and carries a high morbidity and mortality occurring in at least 3%-5% of all procedures. We reviewed the available literature searching for "ERCP" and "pancreatitis" and "post-ERCP pancreatitis". in PubMed and Medline. This review looks at the diagnosis, risk factors, causes and methods of preventing post-procedure pancreatitis. These include the evidence for patient selection, endoscopic techniques and pharmacological prophylaxis of ERCP induced pancreatitis. Selecting the right patient for the procedure by a risk benefits assessment is the best way of avoiding unnecessary ERCPs. Risk is particularly high in young women with sphincter of Oddi dysfunction (SOD). Many of the trials reviewed have rather few numbers of subjects and hence difficult to appraise. Meta-analyses have helped screen for promising modalities of prophylaxis. At present, evidence is emerging that pancreatic stenting of patients with SOD and rectally administered nonsteroidal anti-inflammatory drugs in a large unselected trial reduce the risk of post-procedure pancreatitis. A recent meta-analysis have demonstrated that rectally administered indomethecin, just before or after ERCP is associated with significantly lower rate of pancreatitis compared with placebo [OR = 0.49 (0.34-0.71); P = 0.0002]. Number needed to treat was 20. It is likely that one of these prophylactic measures will begin to be increasingly practised in high risk groups.
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Affiliation(s)
- Lin-Lee Wong
- Lin-Lee Wong, Her-Hsin Tsai, Department of Gastroenterology, Castle Hill Hospital, HEY NHS Trust and Hull York Medical School, Cottingham HU165JQ, United Kingdom
| | - Her-Hsin Tsai
- Lin-Lee Wong, Her-Hsin Tsai, Department of Gastroenterology, Castle Hill Hospital, HEY NHS Trust and Hull York Medical School, Cottingham HU165JQ, United Kingdom
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12
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Abstract
Endoscopic retrograde cholangiopancreatography (ERCP) is widely used in the diagnosis and treatment of cholangiopancreatic diseases, and pancreatitis remains the most common and severe complication. It is therefore important to minimize the incidence and severity of pancreatitis. This paper discusses the recent progress in the prevention and treatment of post-ERCP pancreatitis.
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Wong LL, Tsai HH. Prevention of post-ERCP pancreatitis. World J Gastrointest Pathophysiol 2014; 5:1-10. [PMID: 24891970 PMCID: PMC4024515 DOI: 10.4291/wjgp.v5.i1.1] [Citation(s) in RCA: 23] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/05/2013] [Revised: 10/26/2013] [Accepted: 01/14/2014] [Indexed: 02/06/2023] Open
Abstract
Post-procedure pancreatitis is the most common complication of endoscopic retrograde cholangio pancreatography (ERCP) and carries a high morbidity and mortality occurring in at least 3%-5% of all procedures. We reviewed the available literature searching for “ERCP” and “pancreatitis” and “post-ERCP pancreatitis”. in PubMed and Medline. This review looks at the diagnosis, risk factors, causes and methods of preventing post-procedure pancreatitis. These include the evidence for patient selection, endoscopic techniques and pharmacological prophylaxis of ERCP induced pancreatitis. Selecting the right patient for the procedure by a risk benefits assessment is the best way of avoiding unnecessary ERCPs. Risk is particularly high in young women with sphincter of Oddi dysfunction (SOD). Many of the trials reviewed have rather few numbers of subjects and hence difficult to appraise. Meta-analyses have helped screen for promising modalities of prophylaxis. At present, evidence is emerging that pancreatic stenting of patients with SOD and rectally administered nonsteroidal anti-inflammatory drugs in a large unselected trial reduce the risk of post-procedure pancreatitis. A recent meta-analysis have demonstrated that rectally administered indomethecin, just before or after ERCP is associated with significantly lower rate of pancreatitis compared with placebo [OR = 0.49 (0.34-0.71); P = 0.0002]. Number needed to treat was 20. It is likely that one of these prophylactic measures will begin to be increasingly practised in high risk groups.
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