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Dominguez‐Muñoz JE, Vujasinovic M, de la Iglesia D, Cahen D, Capurso G, Gubergrits N, Hegyi P, Hungin P, Ockenga J, Paiella S, Perkhofer L, Rebours V, Rosendahl J, Salvia R, Scheers I, Szentesi A, Bonovas S, Piovani D, Löhr JM. European guidelines for the diagnosis and treatment of pancreatic exocrine insufficiency: UEG, EPC, EDS, ESPEN, ESPGHAN, ESDO, and ESPCG evidence-based recommendations. United European Gastroenterol J 2025; 13:125-172. [PMID: 39639485 PMCID: PMC11866322 DOI: 10.1002/ueg2.12674] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/23/2024] [Accepted: 08/12/2024] [Indexed: 12/07/2024] Open
Abstract
Pancreatic exocrine insufficiency (PEI) is defined as a reduction in pancreatic exocrine secretion below the level that allows the normal digestion of nutrients. Pancreatic disease and surgery are the main causes of PEI. However, other conditions and upper gastrointestinal surgery can also affect the digestive function of the pancreas. PEI can cause symptoms of nutritional malabsorption and deficiencies, which affect the quality of life and increase morbidity and mortality. These guidelines were developed following the United European Gastroenterology framework for the development of high-quality clinical guidelines. After a systematic literature review, the evidence was evaluated according to the Oxford Center for Evidence-Based Medicine and the Grading of Recommendations Assessment, Development, and Evaluation methodology, as appropriate. Statements and comments were developed by the working groups and voted on using the Delphi method. The diagnosis of PEI should be based on a global assessment of symptoms, nutritional status, and a pancreatic secretion test. Pancreatic enzyme replacement therapy (PERT), together with dietary advice and support, are the cornerstones of PEI therapy. PERT is indicated in patients with PEI that is secondary to pancreatic disease, pancreatic surgery, or other metabolic or gastroenterological conditions. Specific recommendations concerning the management of PEI under various clinical conditions are provided based on evidence and expert opinions. This evidence-based guideline summarizes the prevalence, clinical impact, and general diagnostic and therapeutic approaches for PEI, as well as the specifics of PEI in different clinical conditions. Finally, the unmet needs for future research are discussed.
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Affiliation(s)
- J. Enrique Dominguez‐Muñoz
- Department of Gastroenterology and HepatologyUniversity Hospital of Santiago de CompostelaSantiago de CompostelaSpain
| | - Miroslav Vujasinovic
- Department of MedicineKarolinska Institutet and Department of Upper Abdominal DiseasesKarolinska University HospitalStockholmSweden
| | | | - Djuna Cahen
- Department of Gastroenterology and HepatologyErasmus MC University Medical CenterRotterdamThe Netherlands
| | - Gabriele Capurso
- Department of GastroenterologySan Raffaele University HospitalMilanItaly
| | | | - Peter Hegyi
- Centre for Translational MedicineSemmelweis UniversityBudapestHungary
- Institute for Translational MedicineMedical SchoolUniversity of PécsPécsHungary
- Institute of Pancreatic DiseasesSemmelweis UniversityBudapestHungary
- Translational Pancreatology Research GroupInterdisciplinary Center of Excellence for Research and Development and InnovationUniversity of SzegedSzegedHungary
| | - Pali Hungin
- Faculty of Medical SciencesNewcastle UniversityNewcastle‐upon‐TyneUK
| | - Johann Ockenga
- Department of GastroenterologyEndocrinology and Clinical NutritionKlinikum Bremen MitteBremenGermany
| | - Salvatore Paiella
- Unit of Pancreatic SurgeryUniversity of Verona Hospital TrustVeronaItaly
| | - Lukas Perkhofer
- Department of Internal Medicine ISection of Interdisciplinary PancreatologyUlm University HospitalUlmGermany
| | - Vinciane Rebours
- Department of PancreatologyBeaujon HospitalDMU DigestAP‐HPClichyFrance
| | - Jonas Rosendahl
- Department of Internal Medicine IMartin Luther UniversityHalleGermany
| | - Roberto Salvia
- Unit of Pancreatic SurgeryUniversity of Verona Hospital TrustVeronaItaly
| | - Isabelle Scheers
- Pediatric GastroenterologyHepatology and Nutrition UnitCliniques Universitaires Saint‐LucUniversité Catholique de LouvainBrusselsBelgium
| | - Andrea Szentesi
- Institute for Translational MedicineMedical SchoolUniversity of PécsPécsHungary
| | - Stefanos Bonovas
- Department of Biomedical SciencesHumanitas UniversityMilanItaly
- IRCCS Humanitas Research HospitalMilanItaly
| | - Daniele Piovani
- Department of Biomedical SciencesHumanitas UniversityMilanItaly
- IRCCS Humanitas Research HospitalMilanItaly
| | - J. Matthias Löhr
- Department of Clinical SciencesKarolinska Institutet and Department of Upper Abdominal DiseasesKarolinska University HospitalStockholmSweden
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Bejjani J, Ramsey ML, Lee PJ, Phillips AE, Singh VK, Yadav D, Papachristou GI, Hart PA. Alterations in exocrine pancreatic function after acute pancreatitis. Pancreatology 2024; 24:505-510. [PMID: 38485543 PMCID: PMC11215795 DOI: 10.1016/j.pan.2024.03.003] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/03/2024] [Revised: 02/22/2024] [Accepted: 03/06/2024] [Indexed: 04/04/2024]
Abstract
Exocrine pancreatic dysfunction (EPD) is a malabsorptive complication of pancreatic disorders that can lead to a host of symptoms ranging from flatulence to diarrhea and contribute to weight loss and metabolic bone disease. It is increasingly recognized to occur after acute pancreatitis (AP), including episodes with mild severity. The risk of developing EPD after AP is influenced by a range of factors, including the degree of acinar cell destruction and inflammation during AP, and persistent structural derangements following AP. In this article, we discuss the epidemiology, pathophysiology, and clinical management of EPD after AP while highlighting key knowledge gaps.
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Affiliation(s)
- Joseph Bejjani
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, OH, USA
| | - Mitchell L Ramsey
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, OH, USA
| | - Peter J Lee
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, OH, USA
| | - Anna Evans Phillips
- Division of Gastroenterology, University of Pittsburgh Medical Center, Pittsburgh, PA, USA
| | - Vikesh K Singh
- Division of Gastroenterology, Johns Hopkins Medical Institutions, Baltimore, MD, USA
| | - Dhiraj Yadav
- Division of Gastroenterology, University of Pittsburgh Medical Center, Pittsburgh, PA, USA
| | - Georgios I Papachristou
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, OH, USA
| | - Phil A Hart
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
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Hsieh PH, Yang TC, Kang EYN, Lee PC, Luo JC, Huang YH, Hou MC, Huang SP. Impact of nutritional support routes on mortality in acute pancreatitis: A network meta-analysis of randomized controlled trials. J Intern Med 2024; 295:759-773. [PMID: 38561603 DOI: 10.1111/joim.13782] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 04/04/2024]
Abstract
BACKGROUND Nutritional administration in acute pancreatitis (AP) management has sparked widespread discussion, yet contradictory mortality results across meta-analyses necessitate clarification. The optimal nutritional route in AP remains uncertain. Therefore, this study aimed to compare mortality among nutritional administration routes in patients with AP using consistency model. METHODS This study searched four major databases for relevant randomized controlled trials (RCTs). Two authors independently extracted and checked data and quality. Network meta-analysis was conducted for estimating risk ratios (RRs) with 95% confidence interval (CI) based on random-effects model. Subgroup analyses accounted for AP severity and nutrition support initiation. RESULTS A meticulous search yielded 1185 references, with 30 records meeting inclusion criteria from 27 RCTs (n = 1594). Pooled analyses showed the mortality risk reduction associated with nasogastric (NG) (RR = 0.34; 95%CI: 0.16-0.73) and nasojejunal (NJ) feeding (RR = 0.46; 95%CI: 0.25-0.84) in comparison to nil per os. Similarly, NG (RR = 0.45; 95%CI: 0.24-0.83) and NJ (RR = 0.60; 95%CI: 0.40-0.90) feeding also showed lower mortality risk than total parenteral nutrition. Subgroup analyses, stratified by severity, supported these findings. Notably, the timing of nutritional support initiation emerged as a significant factor, with NJ feeding demonstrating notable mortality reduction within 24 and 48 h, particularly in severe cases. CONCLUSION For severe AP, both NG and NJ feeding appear optimal, with variations in initiation timings. NG feeding does not appear to merit recommendation within the initial 24 h, whereas NJ feeding is advisable within the corresponding timeframe following admission. These findings offer valuable insights for optimizing nutritional interventions in AP.
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Affiliation(s)
- Ping-Han Hsieh
- Division of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
| | - Tsung-Chieh Yang
- Division of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
- School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
| | - Enoch Yi-No Kang
- Evidence-Based Medicine Center, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
- Institute of Health Policy and Management, College of Public Health, National Taiwan University, Taipei, Taiwan
- Cochrane Taiwan, Taipei Medical University, Taipei, Taiwan
| | - Pei-Chang Lee
- Division of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
- School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
| | - Jiing-Chyuan Luo
- Division of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
- School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
| | - Yi-Hsiang Huang
- Division of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
- School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
- Institute of Clinical Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
- Healthcare and Services Center, Taipei Veterans General Hospital, Taipei, Taiwan
| | - Ming-Chih Hou
- Division of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
- School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan
| | - Shih-Ping Huang
- Division of Gastroenterology, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
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Zahariev OJ, Bunduc S, Kovács A, Demeter D, Havelda L, Budai BC, Veres DS, Hosszúfalusi N, Erőss BM, Teutsch B, Juhász MF, Hegyi P. Risk factors for diabetes mellitus after acute pancreatitis: a systematic review and meta-analysis. Front Med (Lausanne) 2024; 10:1257222. [PMID: 38264039 PMCID: PMC10803425 DOI: 10.3389/fmed.2023.1257222] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/12/2023] [Accepted: 12/12/2023] [Indexed: 01/25/2024] Open
Abstract
Introduction Within 5 years of having acute pancreatitis (AP), approximately 20% of patients develop diabetes mellitus (DM), which later increases to approximately 40%. Some studies suggest that the prevalence of prediabetes (PD) and/or DM can grow as high as 59% over time. However, information on risk factors is limited. We aimed to identify risk factors for developing PD or DM following AP. Methods We systematically searched three databases up to 4 September 2023 extracting direct, within-study comparisons of risk factors on the rate of new-onset PD and DM in AP patients. When PD and DM event rates could not be separated, we reported results for this composite outcome as PD/DM. Meta-analysis was performed using the random-effects model to calculate pooled odds ratios (OR) with 95% confidence intervals (CI). Results Of the 61 studies identified, 50 were included in the meta-analysis, covering 76,797 participants. The studies reported on 79 risk factors, and meta-analysis was feasible for 34 risk factor and outcome pairs. The odds of developing PD/DM was significantly higher after severe and moderately severe AP (OR: 4.32; CI: 1.76-10.60) than mild AP. Hypertriglyceridemic AP etiology (OR: 3.27; CI: 0.17-63.91) and pancreatic necrosis (OR: 5.53; CI: 1.59-19.21) were associated with a higher risk of developing PD/DM. Alcoholic AP etiology (OR: 1.82; CI: 1.09-3.04), organ failure (OR: 3.19; CI: 0.55-18.64), recurrent AP (OR: 1.89; CI: 0.95-3.77), obesity (OR: 1.85; CI: 1.43-2.38), chronic kidney disease (OR: 2.10; CI: 1.85-2.38), liver cirrhosis (OR: 2.48; CI: 0.18-34.25), and dyslipidemia (OR: 1.82; CI: 0.68-4.84) were associated with a higher risk of developing DM. Discussion Severe and moderately severe AP, alcoholic and hypertriglyceridemic etiologies, pancreatic necrosis, organ failure, recurrent acute pancreatitis and comorbidities of obesity, chronic kidney disease liver disease, and dyslipidemia are associated with a higher risk of developing PD or DM. Systematic review registration https://www.crd.york.ac.uk/prospero/, identifier CRD42021281983.
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Affiliation(s)
- Olga Julia Zahariev
- Centre for Translational Medicine, Semmelweis University, Budapest, Hungary
- Institute of Pancreatic Diseases, Semmelweis University, Budapest, Hungary
- Institute for Translational Medicine, Medical School, University of Pécs, Pécs, Hungary
| | - Stefania Bunduc
- Centre for Translational Medicine, Semmelweis University, Budapest, Hungary
- Carol Davila University of Medicine and Pharmacy, Bucharest, Romania
| | - Adrienn Kovács
- Centre for Translational Medicine, Semmelweis University, Budapest, Hungary
- Department of Internal Medicine and Hematology, Semmelweis University, Budapest, Hungary
| | - Dóra Demeter
- Centre for Translational Medicine, Semmelweis University, Budapest, Hungary
- Dietetic Services, Central Hospital of Northern Pest - Military Hospital, Budapest, Hungary
| | - Luca Havelda
- Centre for Translational Medicine, Semmelweis University, Budapest, Hungary
- Institute of Pancreatic Diseases, Semmelweis University, Budapest, Hungary
| | - Bettina Csilla Budai
- Centre for Translational Medicine, Semmelweis University, Budapest, Hungary
- Institute of Pancreatic Diseases, Semmelweis University, Budapest, Hungary
| | - Dániel Sándor Veres
- Centre for Translational Medicine, Semmelweis University, Budapest, Hungary
- Department of Biophysics and Radiation Biology, Semmelweis University, Budapest, Hungary
| | - Nóra Hosszúfalusi
- Centre for Translational Medicine, Semmelweis University, Budapest, Hungary
- Department of Internal Medicine and Hematology, Semmelweis University, Budapest, Hungary
| | - Bálint Mihály Erőss
- Centre for Translational Medicine, Semmelweis University, Budapest, Hungary
- Institute of Pancreatic Diseases, Semmelweis University, Budapest, Hungary
- Institute for Translational Medicine, Medical School, University of Pécs, Pécs, Hungary
| | - Brigitta Teutsch
- Centre for Translational Medicine, Semmelweis University, Budapest, Hungary
- Institute for Translational Medicine, Medical School, University of Pécs, Pécs, Hungary
| | - Márk Félix Juhász
- Institute for Translational Medicine, Medical School, University of Pécs, Pécs, Hungary
- Heim Pál National Pediatric Institute, Budapest, Hungary
| | - Péter Hegyi
- Centre for Translational Medicine, Semmelweis University, Budapest, Hungary
- Institute of Pancreatic Diseases, Semmelweis University, Budapest, Hungary
- Institute for Translational Medicine, Medical School, University of Pécs, Pécs, Hungary
- Translational Pancreatology Research Group, Interdisciplinary Center of Excellence for Research Development and Innovation University of Szeged, Szeged, Hungary
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Romero-Herrera I, Nogales F, Gallego-López MDC, Díaz-Castro J, Moreno-Fernandez J, Ochoa JJ, Carreras O, Ojeda ML. Adipose tissue homeostasis orchestrates the oxidative, energetic, metabolic and endocrine disruption induced by binge drinking in adolescent rats. J Physiol 2023; 601:5617-5633. [PMID: 37994192 DOI: 10.1113/jp285362] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/25/2023] [Accepted: 10/31/2023] [Indexed: 11/24/2023] Open
Abstract
Binge drinking (BD) is the most common alcohol consumption model for adolescents, and has recently been related to the generation of high oxidation and insulin resistance (IR). White adipose tissue (WAT) is a target organ for insulin action that regulates whole-body metabolism by secreting adipokines. The present study aimed to analyse the oxidative, inflammatory, energetic and endocrine profile in the WAT of BD-exposed adolescent rats, to obtain an integrative view of insulin secretion and WAT in IR progression. Two groups of male adolescent rats were used: control (n = 8) and BD (n = 8). An intermittent i.p. BD model (20% v/v) was used during 3 consecutive weeks. BD exposure led to a pancreatic oxidative imbalance, which was joint to high insulin secretion by augmenting deacetylase sirtuin-1 (SIRT-1) pancreatic expression and serum adipsin levels. However, BD rats had hyperglycaemia and high homeostasis model assessment of insulin resistance value (HOMA-IR). BD exposure in WAT increased lipid oxidation, as well as decreased insulin receptor substrate 1 (IRS-1) and AKT expression, sterol regulatory element-binding protein 1 (SREBP1), forkhead box O3A (FOXO3a) and peroxisome proliferator-activated receptor γ (PPARγ), and adipocyte size. BD also affected the expression of proteins related to energy balance, such as SIRT-1 and AMP activated protein kinase (AMPK), affecting the adipokine secretion profile (increasing resistin/adiponectin ratio). BD altered the entire serum lipid profile, increasing the concentration of free fatty acids. In conclusion, BD led to an oxidative imbalance and IR process in WAT, which modified the energy balance in this tissue, decreasing the WAT lipogenic/lipolytic ratio, affecting adipokine secretion and the systemic lipid profile, and contributing to the progression of IR. Therefore, WAT is key in the generation of metabolic and endocrine disruption after BD exposure during adolescence in rats. KEY POINTS: Adolescent rat binge drinking (BD) exposure leads to hepatic and systemic oxidative stress (OS) via reactive oxygen species generation, causing hepatic insulin resistance (IR) and altered energy metabolism. In the present study, BD exposure in adolescent rats induces OS in the pancreas, with increased insulin secretion despite hyperglycaemia, indicating a role for IR in white adipose tissue (WAT) homeostasis. In WAT, BD produces IR and an oxidative and energetic imbalance, triggering an intense lipolysis where the serum lipid profile is altered and free fatty acids are increased, consistent with liver lipid accumulation and steatosis. BD exposure heightens inflammation in WAT, elevating pro-inflammatory and reducing anti-inflammatory adipokines, favouring cardiovascular damage. This research provides a comprehensive view of how adolescent BD in rats impacts liver, WAT and pancreas homeostasis, posing a risk for future cardiometabolic complications in adulthood.
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Affiliation(s)
- Inés Romero-Herrera
- Department of Physiology, Faculty of Pharmacy, Seville University, Seville, Spain
| | - Fátima Nogales
- Department of Physiology, Faculty of Pharmacy, Seville University, Seville, Spain
| | | | - Javier Díaz-Castro
- Institute of Nutrition and Food Technology 'José Mataix Verdú', University of Granada, Granada, Spain
- Department of Physiology, University of Granada, Granada, Spain
| | - Jorge Moreno-Fernandez
- Institute of Nutrition and Food Technology 'José Mataix Verdú', University of Granada, Granada, Spain
- Department of Physiology, University of Granada, Granada, Spain
| | - Julio José Ochoa
- Institute of Nutrition and Food Technology 'José Mataix Verdú', University of Granada, Granada, Spain
- Department of Physiology, University of Granada, Granada, Spain
| | - Olimpia Carreras
- Department of Physiology, Faculty of Pharmacy, Seville University, Seville, Spain
| | - Mª Luisa Ojeda
- Department of Physiology, Faculty of Pharmacy, Seville University, Seville, Spain
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6
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Manrai M, Singh AK, Birda CL, Shah J, Dutta A, Bhadada SK, Kochhar R. Diabetes mellitus as a consequence of acute severe pancreatitis: Unraveling the mystery. World J Diabetes 2023; 14:1212-1225. [PMID: 37664472 PMCID: PMC10473947 DOI: 10.4239/wjd.v14.i8.1212] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/28/2023] [Revised: 05/19/2023] [Accepted: 07/06/2023] [Indexed: 08/11/2023] Open
Abstract
The occurrence of diabetes mellitus (DM) in pancreatitis is being increasingly recognized lately. Diabetes can develop not only with chronic pancreatitis but even after the first episode of acute pancreatitis (AP). The incidence of diabetes after AP varies from 18% to 23% in 3 years and reaches up to 40% over 5 years. The exact pathogenesis of diabetes after AP is poorly understood and various mechanisms proposed include loss of islet cell mass, AP-induced autoimmunity, and alterations in the insulin incretin axis. Risk factors associated with increased risk of diabetes includes male sex, recurrent attacks of pancreatitis, presence of pancreatic exocrine insufficiency and level of pancreatitic necrosis. Diagnosis of post-pancreatitis DM (PPDM) is often excluded. Treatment includes a trial of oral antidiabetic drugs in mild diabetes. Often, insulin is required in uncontrolled diabetes. Given the lack of awareness of this metabolic disorder after AP, this review will evaluate current information on epidemiology, risk factors, diagnosis and management of PPDM and identify the knowledge gaps.
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Affiliation(s)
- Manish Manrai
- Department of Internal Medicine, Armed Forces Medical College, Pune 411040, Maharashtra, India
| | - Anupam K Singh
- Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India
| | - Chhagan Lal Birda
- Department of Gastroenterology, All India Institutes of Medical Sciences, Jodhpur 342001, India
| | - Jimil Shah
- Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India
| | - Aditya Dutta
- Department of Endocrinology, Max Hospital, New Delhi 110017, India
| | - Sanjay Kumar Bhadada
- Department of Endocrinology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India
| | - Rakesh Kochhar
- Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India
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Cabrera LF, Hernández L, Urrutia A, Marroquin L, Pedraza CM, Padilla-Pinzón LT, Pulido-Segura JA, Sanchez-Ussa S, Salcedo D, Suarez J. [Socioeconomic impact of the current management of severe biliary acute pancreatitis: comparative study]. Rev Salud Publica (Bogota) 2023; 21:513-518. [PMID: 36753202 DOI: 10.15446/rsap.v21n5.80470] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/17/2019] [Accepted: 07/28/2019] [Indexed: 11/09/2022] Open
Abstract
OBJETIVE Acute pancreatitis of biliary origin is a common gastrointestinal pathology, in which timely management still is the most important. The aims of this research is establish the socioeconomic impact in the current management of severe acute pancreatitis of biliary origin comparing two centers of the third level, one of high socioeconomic population and another of low in Bogotá, Colombia. MATERIALS AND METHODS A retrospective, cross-sectional comparative study was conducted between January 2012 and December 2017, in two hospitals of Bogotá DC. We evaluated their socioeconomic characteristics, gender, time of evolution at the time of consultation, Marshall score, ICU stay, hospital stay, complications, surgical management and mortality. RESULTS 101 patients from two different socioeconomic strata (high and low) were analyzed, where a 10 times higher risk of requiring a surgical procedure in the group of patients with low stratum was found, as well as a higher mortality compared with those of high stratum. (11.3% Vs 4.2%). There were also more complications in the low socioeconomic group with respect to the high, as in the exocrine failure (81.1% vs 31.3%) and the compartment syndrome (35.8% vs 4.2%). CONCLUSION There is greater morbidity and mortality in patients of low socioeconomic status in the context of this pathology. This study can guide new research that increases the clarity of the socioeconomic impact on the outcomes of severe acute pancreatitis.
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Affiliation(s)
| | | | - Andres Urrutia
- AU: MD. Universidad Pedagógica y Tecnológica de Colombia. Tunja, Boyacá.
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8
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Nøjgaard C, Werge M, Naver A, Wilkens Knudsen A, Wewer Albrechtsen NJ, Møller S, Gluud LL, Novovic S. Long-term changes of pancreatic function in patients with complicated walled-off necrosis. Scand J Gastroenterol 2022; 57:1257-1263. [PMID: 35546222 DOI: 10.1080/00365521.2022.2072176] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
OBJECTIVES Walled-off necrosis (WON) is a serious complication to necrotizing acute pancreatitis with a high morbidity and mortality. The aim of this study was to investigate the long-term changes in pancreatic function, metabolic function and body composition in patients with WON. MATERIAL AND METHODS Observational study including patients with WON who underwent endoscopic transmural drainage and necrosectomy. Patients were prospectively evaluated at baseline, 3-6 months after discharge, and 12 months after discharge. Patients were characterized with fecal elastase, blood samples, computer tomography, dual energy X-ray absorptiometry and Lundh's test. RESULTS The study includes 17 patients (11 men) with WON. The etiologies were gallstones (53%) alcohol intake (35%) and 12% had an unknown etiology. The body mass index (BMI) dropped during baseline and 3 months after discharge (p = .03) and increased 12 months after discharge (p = .002). Twelve months after discharge, 29% had mild exocrine insufficiency, 7% moderate insufficiency and 50% severe insufficiency based on the Lundh's test. Fecal elastase was <100 μg/g in 35% and <200 μg/g in 59% 12 months after discharge. Only, 24% required pancreatic enzyme substitution. Endocrine insufficiency developed in 24%. These patients also had exocrine insufficiency. CONCLUSIONS A considerable proportion of patients with WON experience both endocrine and exocrine pancreatic insufficiency suggesting that long-term follow-up is needed in order to ensure adequate treatment.
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Affiliation(s)
- Camilla Nøjgaard
- Pancreatitis Centre East (PACE), Copenhagen University Hospital, Hvidovre, Denmark
| | - Mikkel Werge
- Pancreatitis Centre East (PACE), Copenhagen University Hospital, Hvidovre, Denmark
| | - Astrid Naver
- Medical Department, Zealand University Hospital, Køge, Denmark
| | - Anne Wilkens Knudsen
- The Dietitians and Nutritional Research Unit, EATEN, Herlev Gentofte University Hospital, Herlev, Denmark
| | - Nicolai J Wewer Albrechtsen
- Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.,NNF Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
| | - Søren Møller
- Department of Clinical Physiology and Nuclear Medicine, Center for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital, Hvidovre, Denmark.,Department of Clinical Medicine, Faculty of Health Sciences University of Copenhagen, Copenhagen, Denmark
| | - Lise Lotte Gluud
- Pancreatitis Centre East (PACE), Copenhagen University Hospital, Hvidovre, Denmark.,Department of Clinical Medicine, Faculty of Health Sciences University of Copenhagen, Copenhagen, Denmark
| | - Srdan Novovic
- Pancreatitis Centre East (PACE), Copenhagen University Hospital, Hvidovre, Denmark.,Department of Clinical Medicine, Faculty of Health Sciences University of Copenhagen, Copenhagen, Denmark
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9
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Dams OC, Vijver MAT, van Veldhuisen CL, Verdonk RC, Besselink MG, van Veldhuisen DJ. Heart Failure and Pancreas Exocrine Insufficiency: Pathophysiological Mechanisms and Clinical Point of View. J Clin Med 2022; 11:4128. [PMID: 35887892 PMCID: PMC9324511 DOI: 10.3390/jcm11144128] [Citation(s) in RCA: 6] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/22/2022] [Revised: 06/28/2022] [Accepted: 07/14/2022] [Indexed: 01/27/2023] Open
Abstract
Heart failure is associated with decreased tissue perfusion and increased venous congestion that may result in organ dysfunction. This dysfunction has been investigated extensively for many organs, but data regarding pancreatic (exocrine) dysfunction are scarce. In the present review we will discuss the available data on the mechanisms of pancreatic damage, how heart failure can lead to exocrine dysfunction, and its clinical consequences. We will show that heart failure causes significant impairment of pancreatic exocrine function, particularly in the elderly, which may exacerbate the clinical syndrome of heart failure. In addition, pancreatic exocrine insufficiency may lead to further deterioration of cardiovascular disease and heart failure, thus constituting a true vicious circle. We aim to provide insight into the pathophysiological mechanisms that constitute this reciprocal relation. Finally, novel treatment options for pancreatic dysfunction in heart failure are discussed.
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Affiliation(s)
- Olivier C. Dams
- Department of Cardiology, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands; (M.A.T.V.); (D.J.v.V.)
| | - Marlene A. T. Vijver
- Department of Cardiology, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands; (M.A.T.V.); (D.J.v.V.)
| | - Charlotte L. van Veldhuisen
- Department of Surgery, Amsterdam UMC, University of Amsterdam, 1100 DD Amsterdam, The Netherlands; (C.L.v.V.); (M.G.B.)
- Amsterdam Gastroenterology Endocrinology Metabolism, 1100 DD Amsterdam, The Netherlands
| | - Robert C. Verdonk
- Department of Gastroenterology and Hepatology, St. Antonius Hospital, 3435 CM Nieuwegein, The Netherlands;
| | - Marc G. Besselink
- Department of Surgery, Amsterdam UMC, University of Amsterdam, 1100 DD Amsterdam, The Netherlands; (C.L.v.V.); (M.G.B.)
- Amsterdam Gastroenterology Endocrinology Metabolism, 1100 DD Amsterdam, The Netherlands
| | - Dirk J. van Veldhuisen
- Department of Cardiology, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands; (M.A.T.V.); (D.J.v.V.)
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10
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Bhanot A, Majbar AA, Candler T, Hunt LP, Cusick E, Johnson PRV, Shield JP. Acute pancreatitis in children - morbidity and outcomes at 1 year. BMJ Paediatr Open 2022; 6:10.1136/bmjpo-2022-001487. [PMID: 36053577 PMCID: PMC9258515 DOI: 10.1136/bmjpo-2022-001487] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/06/2022] [Accepted: 06/10/2022] [Indexed: 12/18/2022] Open
Abstract
OBJECTIVE To establish short-term and medium-term complications 1-year postdiagnosis, of acute pancreatitis (AP) in children aged 0-14 years. DESIGN One-year follow-up of a prospective monthly surveillance of new cases of AP in children under 15 years through the British Paediatric Surveillance Unit (BPSU) from April 2013 to April 2014. SETTING A monthly surveillance of >3700 consultant paediatricians and paediatric surgeons in the UK and Ireland using the BPSU. PATIENTS Children aged 0-14 years with a new diagnosis of AP. MAIN OUTCOME MEASURES The outcomes following AP, including the incidence of complications and comorbidity at diagnosis and at 1 year. RESULTS Of the 94 new confirmed cases of AP identified in the UK during the study period, 90 cases (96%) were included in the 1-year follow-up. 30 patients (32%) developed further episode(s) of AP. Over one-fifth of patients developed one or more major complication. At initial admission, the most common of these was pancreatic necrosis (n=8, 9%), followed by respiratory failure (n=7, 7%). Reported complications by 1 year were pseudocyst formation (n=9, 10%), diabetes requiring insulin therapy (n=4, 4%) and maldigestion (n=1, 1%). At 1-year postdiagnosis, only 59% of children made a full recovery with no acute or chronic complications or recurrent episodes of AP. Two patients died, indicating a case fatality of ~2.0%. CONCLUSIONS AP in childhood is associated with significant short-term and medium-term complications and comorbidities including risk of recurrence in approximately a third of cases.
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Affiliation(s)
- A Bhanot
- Faculty of Health Sciences, University of Bristol, Bristol, UK
| | - A A Majbar
- Department of Paediatrics, Sabratha Teaching Hospital, Sabratha, Libya
| | - Toby Candler
- Paediatric Diabetes and Endocrinology, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
| | - L P Hunt
- NIHR Bristol Biomedical Research Centre, Nutrition Theme, University of Bristol, Bristol, UK
| | - E Cusick
- Paediatric Surgery, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
| | - Paul R V Johnson
- Nuffield Department of Surgery, University of Oxford, OXFORD, UK.,NIHR Oxford Biomedical Research Centre, University of Oxford, Oxford, UK
| | - Julian Ph Shield
- Paediatric Diabetes and Endocrinology, University Hospitals Bristol NHS Foundation Trust, Bristol, UK.,NIHR Bristol Biomedical Research Centre, Nutrition Theme, University of Bristol, Bristol, UK
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11
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Yi Y, Sun X, Liang B, He N, Gibson-Corley KN, Norris AW, Engelhardt JF, Uc A. Acute pancreatitis-induced islet dysfunction in ferrets. Pancreatology 2021; 21:839-847. [PMID: 33994067 PMCID: PMC8355067 DOI: 10.1016/j.pan.2021.04.008] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/13/2021] [Revised: 04/22/2021] [Accepted: 04/24/2021] [Indexed: 12/11/2022]
Abstract
BACKGROUND /Objectives: The pathogenesis of hyperglycemia during acute pancreatitis (AP) remains unknown due to inaccessibility of human tissues and lack of animal models. We aimed to develop an animal model to study the mechanisms of hyperglycemia and impaired glucose tolerance in AP. METHODS We injected ferrets with intraperitoneal cerulein (50 μg/kg, 9 hourly injections) or saline. Blood samples were collected for glucose (0, 4, 8, 12, 24h); TNF-α, IL-6 (6h); amylase, lipase, insulin, glucagon, pancreatic polypeptide (PP), glucagon-like peptide-1 (GLP-1), and gastric inhibitory polypeptide (GIP) (24h). Animals underwent oral glucose tolerance test (OGTT), mixed meal tolerance test (MMTT) at 24h or 3 months, followed by harvesting pancreas for histopathology and immunostaining. RESULTS Cerulein-injected ferrets exhibited mild pancreatic edema, neutrophil infiltration, and elevations in serum amylase, lipase, TNF-α, IL-6, consistent with AP. Plasma glucose was significantly higher in ferrets with AP at all time points. Plasma glucagon, GLP-1 and PP were significantly higher in cerulein-injected animals, while plasma insulin was significantly lower compared to controls. OGTT and MMTT showed abnormal glycemic responses with higher area under the curve. The hypoglycemic response to insulin injection was completely lost, suggestive of insulin resistance. OGTT showed low plasma insulin; MMTT confirmed low insulin and GIP; abnormal OGTT and MMTT responses returned to normal 3 months after cerulein injection. CONCLUSIONS Acute cerulein injection causes mild acute pancreatitis in ferrets and hyperglycemia related to transient islet cell dysfunction and insulin resistance. The ferret cerulein model may contribute to the understanding of hyperglycemia in acute pancreatitis.
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Affiliation(s)
- Yaling Yi
- Department of Anatomy and Cell Biology, Iowa City, IA, USA
| | - Xingshen Sun
- Department of Anatomy and Cell Biology, Iowa City, IA, USA
| | - Bo Liang
- Department of Anatomy and Cell Biology, Iowa City, IA, USA
| | - Nan He
- Department of Anatomy and Cell Biology, Iowa City, IA, USA
| | - Katherine N Gibson-Corley
- Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA
| | - Andrew W Norris
- Fraternal Order of Eagles Diabetes Research Center, Iowa City, IA, USA; Department of Pediatrics, lowa City, IA, USA; Department of Biochemistry, Iowa City, IA, USA
| | - John F Engelhardt
- Department of Anatomy and Cell Biology, Iowa City, IA, USA; Fraternal Order of Eagles Diabetes Research Center, Iowa City, IA, USA
| | - Aliye Uc
- Fraternal Order of Eagles Diabetes Research Center, Iowa City, IA, USA; Department of Pediatrics, lowa City, IA, USA; Department of Radiation Oncology; University of Iowa, Iowa City, IA, USA.
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12
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Richardson A, Park WG. Acute pancreatitis and diabetes mellitus: a review. Korean J Intern Med 2021; 36:15-24. [PMID: 33147904 PMCID: PMC7820652 DOI: 10.3904/kjim.2020.505] [Citation(s) in RCA: 39] [Impact Index Per Article: 9.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/14/2020] [Accepted: 11/02/2020] [Indexed: 02/08/2023] Open
Abstract
Diabetes following acute pancreatitis (AP) is becoming increasingly recognized. It is unclear what subtype of diabetes mellitus (DM) occurs; however, type 3c diabetes mellitus (T3cDM) is gaining increasing recognition. T3cDM has differing pathophysiology than other subtypes of DM and therefore differing disease course and treatment. Current studies have examined the incidence and prevalence of DM following AP, and meta-analyses have shown around 15% develop DM at 1 year with an increasing proportion developing DM at 5 years. It has been observed that some patients have transient hyperglycemia following AP episode with a subset developing persistent impaired glucose metabolism; however, the exact timeline is not well defined. The data on risk factors for developing DM after AP is limited and mixed; however, it is likely that severity of AP may impact the propensity to develop DM. Screening guidelines have not been established following AP; however, screening 1-year post-event will likely capture a sizable proportion of newly developed DM. The endocrine and exocrine pancreas are closely linked, and studies have found significant overlap in dysfunction of both after AP. Finally, there are some data to suggest that diabetes predisposes patients to structural changes in the pancreas and increased risk of developing AP.
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Affiliation(s)
- Allyson Richardson
- Department of Internal Medicine, Stanford University Medical Center, Stanford, CA,
USA
| | - Walter G. Park
- Department of Gastroenterology and Hepatology, Stanford University Medical Center, Stanford, CA,
USA
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13
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Assessment of Weight Loss and Gastrointestinal Symptoms Suggestive of Exocrine Pancreatic Dysfunction After Acute Pancreatitis. Clin Transl Gastroenterol 2020; 11:e00283. [PMID: 33464001 PMCID: PMC7743841 DOI: 10.14309/ctg.0000000000000283] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/22/2020] [Accepted: 11/02/2020] [Indexed: 02/07/2023] Open
Abstract
INTRODUCTION Studies evaluating the natural history of exocrine pancreatic dysfunction (EPD) after acute pancreatitis (AP) are sparse. This study aims to assess incidence and predictors of weight loss and gastrointestinal (GI) symptoms suggestive of EPD 12 months after an AP episode. METHODS Patients enrolled in the Pancreatitis-associated Risk of Organ Failure Study at the time of an AP episode were included. Weight and GI symptom data were prospectively collected by self-report at enrollment and at 3- and 12-month (windows 2-7 and 8-20) telephone follow-ups. Multivariable logistic regression was used to assess factors associated with ≥10% total body weight loss (EPD surrogate) at 12 months. A generalized estimating equation was used to measure each factor's population effect (in pounds) over 12 months after AP. RESULTS Follow-up at 12 months in 186 patients (median age = 54 years, 46% men, 45% biliary, 65% first AP attack) revealed weight loss ≥10% from baseline, occurring in 44 patients (24%). Risk of weight loss increased with higher baseline body mass index, previous diagnosis of diabetes mellitus, and worsening AP severity (all P < 0.010). GI symptoms were reported in 13/31 (42%) patients at 12 months. AP severity was independently associated with ≥10% weight loss at 12 months. Over 12 months, men lost more weight than women (average 9.5 lbs); patients with severe AP lost, on average, 14 lbs. DISCUSSION Weight loss after AP occurs in one-quarter of patients and is associated with AP severity. EPD incidence after AP is likely underappreciated. Further work is needed to assess EPD and potential for pancreatic enzyme supplementation.
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14
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Leonel Javeres MN, Raza S, Judith N, Anwar F, Habib R, Batool S, Nurulain SM. Mixture of Organophosphates Chronic Exposure and Pancreatic Dysregulations in Two Different Population Samples. Front Public Health 2020; 8:534902. [PMID: 33194944 PMCID: PMC7655777 DOI: 10.3389/fpubh.2020.534902] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/14/2020] [Accepted: 08/20/2020] [Indexed: 12/13/2022] Open
Abstract
Organophosphates (OP) are a major agrochemical. The application of OP pesticides is expected to increase multifold in the coming decades. The etiology of diabetic diseases is attributed to multiple factors including OP pesticide exposure. The present study investigates pancreatic dysregulation with respect to exocrine enzymes and diabesity in groups of Pakistani and Cameroonian people exposed to a mixture of OP pesticides. Nine hundred and four OP exposed individuals were enrolled for this cross-sectional study after due consent and approval from an ethical review committee. Pesticides' residues were measured by GC-MS spectrometry. Cholinergic enzymes were measured by Elman's method. Serum glucose, insulin, serum amylase, lipase, and triglyceride were measured by spectrophotometry and ELISA; HOMA-IR was determined in OP exposed and non-exposed participants. Stata 15 and R 3.2.0 software were used for statistical analysis of the data. Malathion, chlorpyrifos, and parathion residues were evident in plasma samples. RBC-acetylcholinesterase was significantly depressed in OP exposed groups. In both population samples, investigated pancreatic functions were found to be statistically significantly more dysregulated than non-exposed. OP exposure indicated risk of diabetes and insulin, glycaemia, adiponectin, triglycerides, and TNF-α dysregulations. The study concludes that both OP exposed population groups exhibited a mixture of OP residues and pancreatic dysregulation, although the effect was more pronounced in the Cameroonian population. In addition, serum lipase has a positive correlation with OP exposure and diabetes and may be suggested as an alternate/additional diagnostic marker for diabesity under OP exposure. However, screening of other environmental co-factors with OP for pancreatic dysregulation is suggested.
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Affiliation(s)
| | - Saqlain Raza
- Department of Mathematics, COMSATS University Islamabad, Islamabad, Pakistan
| | - Ngondi Judith
- Department of Biochemistry, Yaoundé I University, Yaoundé, Cameroon
| | - Fozia Anwar
- Department of Health Informatic, COMSATS University Islamabad, Islamabad, Pakistan
| | - Rabia Habib
- Department of Biosciences, COMSATS University Islamabad, Islamabad, Pakistan
| | - Sajida Batool
- Department of Biosciences, COMSATS University Islamabad, Islamabad, Pakistan
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15
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Leonard-Murali S, Lezotte J, Kalu R, Blyden DJ, Patton JH, Johnson JL, Gupta AH. Necrotizing pancreatitis: A review for the acute care surgeon. Am J Surg 2020; 221:927-934. [PMID: 32878690 DOI: 10.1016/j.amjsurg.2020.08.027] [Citation(s) in RCA: 17] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/27/2020] [Revised: 07/30/2020] [Accepted: 08/22/2020] [Indexed: 02/07/2023]
Abstract
BACKGROUND Necrotizing pancreatitis is a common condition with high mortality; the acute care surgeon is frequently consulted for management recommendations. Furthermore, there has been substantial change in the timing, approach, and frequency of surgical intervention for this group of patients. METHODS In this article we summarize key clinical and research developments regarding necrotizing pancreatitis, including current recommendations for treatment of patients requiring intensive care and those with common complications. Articles from all years were considered to provide proper historical context, and most recent management recommendations are identified. RESULTS Epidemiology, diagnosis, treatment in the acute phase, and complications (both short-term and long-term) are discussed. Images of surgical interventions are included from our institutional experience. CONCLUSION Necrotizing pancreatitis management remains heavily based on clinical judgement, although technological advances and clinical trials have made decision making more straightforward.
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Affiliation(s)
- Shravan Leonard-Murali
- Department of Surgery, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI, 48202, USA.
| | - Jonathan Lezotte
- Department of Surgery, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI, 48202, USA.
| | - Richard Kalu
- Department of Surgery, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI, 48202, USA.
| | - Dionne J Blyden
- Department of Surgery, Division of Acute Care Surgery, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI, 48202, USA.
| | - Joe H Patton
- Department of Surgery, Division of Acute Care Surgery, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI, 48202, USA.
| | - Jeffrey L Johnson
- Department of Surgery, Division of Acute Care Surgery, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI, 48202, USA.
| | - Arielle H Gupta
- Department of Surgery, Division of Acute Care Surgery, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI, 48202, USA.
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16
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Yu BJ, Li NS, He WH, He C, Wan JH, Zhu Y, Lu NH. Pancreatic necrosis and severity are independent risk factors for pancreatic endocrine insufficiency after acute pancreatitis: A long-term follow-up study. World J Gastroenterol 2020; 26:3260-3270. [PMID: 32684740 PMCID: PMC7336320 DOI: 10.3748/wjg.v26.i23.3260] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/22/2020] [Revised: 03/29/2020] [Accepted: 05/15/2020] [Indexed: 02/06/2023] Open
Abstract
BACKGROUND Pancreatic endocrine insufficiency after acute pancreatitis (AP) has drawn increasing attention in recent years.
AIM To assess the impact of risk factors on the development of pancreatic endocrine insufficiency after AP.
METHODS This retrospective observational long-term follow-up study was conducted in a tertiary hospital. Endocrine function was evaluated by the oral glucose tolerance test. The data, including age, sex, body mass index, APACHE II score, history of smoking and drinking, organ failure, pancreatic necrosis, debridement of necrosis (minimally invasive and/or open surgery), and time interval, were collected from the record database.
RESULTS A total of 361 patients were included in the study from January 1, 2012 to December 30, 2018. A total of 150 (41.6%) patients were diagnosed with dysglycemia (including diabetes mellitus and impaired glucose tolerance), while 211 (58.4%) patients had normal endocrine function. The time intervals (mo) of the above two groups were 18.73 ± 19.10 mo and 31.53 ± 27.27 mo, respectively (P = 0.001). The morbidity rates of pancreatic endocrine insufficiency were 46.7%, 28.0%, and 25.3%, respectively, in the groups with different follow-up times. The risk factors for pancreatic endocrine insufficiency after AP were severity (odds ratio [OR] = 3.489; 95% confidence interval [CI]: 1.501-8.111; P = 0.004) and pancreatic necrosis (OR = 4.152; 95%CI: 2.580-6.684; P = 0.001).
CONCLUSION Pancreatic necrosis and severity are independent risk factors for pancreatic endocrine insufficiency after AP. The area of pancreatic necrosis can affect pancreatic endocrine function.
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Affiliation(s)
- Bing-Jun Yu
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China
| | - Nian-Shuang Li
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China
| | - Wen-Hua He
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China
| | - Cong He
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China
| | - Jian-Hua Wan
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China
| | - Yin Zhu
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China
| | - Nong-Hua Lu
- Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China
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17
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Omega-3 fatty acid exposure with a low-fat diet in patients with past hypertriglyceridemia-induced acute pancreatitis; an exploratory, randomized, open-label crossover study. Lipids Health Dis 2020; 19:117. [PMID: 32473640 PMCID: PMC7260759 DOI: 10.1186/s12944-020-01295-7] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/23/2019] [Accepted: 05/21/2020] [Indexed: 11/10/2022] Open
Abstract
BACKGROUND Omega-3 fatty acids (OM3-FAs) are recommended with a low-fat diet for severe hypertriglyceridemia (SHTG), to reduce triglycerides and acute pancreatitis (AP) risk. A low-fat diet may reduce pancreatic lipase secretion, which is required to absorb OM3-ethyl esters (OM3-EEs), but not OM3-carboxylic acids (OM3-CAs). METHODS In this exploratory, randomized, open-label, crossover study, 15 patients with SHTG and previous AP were instructed to take OM3-CA (2 g or 4 g) and OM3-EE 4 g once daily for 4 weeks, while adhering to a low-fat diet. On day 28 of each treatment phase, a single dose was administered in the clinic with a liquid low-fat meal, to assess 24-h plasma exposure. Geometric least-squares mean ratios were used for between-treatment comparisons of baseline (day 0)-adjusted area under the plasma concentration versus time curves (AUC0-24) and maximum plasma concentrations (Cmax) for eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). RESULTS Before initiating OM3-FA treatment, mean baseline fasting plasma EPA + DHA concentrations (nmol/mL) were 723 for OM3-CA 2 g, 465 for OM3-CA 4 g and 522 for OM3-EE 4 g. At week 4, mean pre-dose fasting plasma EPA + DHA concentrations increased by similar amounts (+ 735 - + 768 nmol/mL) for each treatment. During the 24-h exposure assessment (day 28), mean plasma EPA + DHA increased from pre-dose to the maximum achieved concentration by + 32.7%, + 45.8% and + 3.1% with single doses of OM3-CA 2 g, OM3-CA 4 g and OM3-EE 4 g, respectively. Baseline-adjusted AUC0-24 was 60% higher for OM3-CA 4 g than for OM3-EE 4 g and baseline-adjusted Cmax was 94% higher (both non-significant). CONCLUSIONS Greater 24-h exposure of OM3-CA versus OM3-EE was observed for some parameters when administered with a low-fat meal at the clinic on day 28. However, increases in pre-dose fasting plasma EPA + DHA over the preceding 4-week dosing period were similar between treatments, leading overall to non-significant differences in baseline (day 0)-adjusted AUC0-24 and Cmax EPA + DHA values. It is not clear why the greater 24-h exposure of OM3-CA versus OM3-EE observed with a low-fat meal did not translate into significantly higher pre-dose fasting levels of DHA + EPA with longer-term use. TRIAL REGISTRATION ClinicalTrials.gov, NCT02189252, Registered 23 June 2014.
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18
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Ru N, Zou WB, Wu H, Hu LH, Li XB, Liu GF, Li ZS, Liao Z. Chinese guidelines for the diagnosis and treatment of pancreatic exocrine insufficiency (2018 edition). J Dig Dis 2019; 20:567-571. [PMID: 31006979 DOI: 10.1111/1751-2980.12753] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/11/2019] [Revised: 04/16/2019] [Accepted: 04/16/2019] [Indexed: 12/11/2022]
Affiliation(s)
- Nan Ru
- Department of Gastroenterology, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, China
| | - Wen Bin Zou
- Department of Gastroenterology, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, China.,Department of Gastroenterology, Shanghai Institute of Pancreatic Diseases, Shanghai, China
| | - Hao Wu
- Department of Gastroenterology, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, China
| | - Liang Hao Hu
- Department of Gastroenterology, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, China
| | - Xiao Bin Li
- Department of General Surgery, Peking Union Medical College Hospital, Beijing, China
| | - Gai Fang Liu
- Department of Gastroenterology, Hebei People's Hospital, Shijiazhuang, China
| | - Zhao Shen Li
- Department of Gastroenterology, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, China.,Department of Gastroenterology, Shanghai Institute of Pancreatic Diseases, Shanghai, China
| | - Zhuan Liao
- Department of Gastroenterology, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, China.,Department of Gastroenterology, Shanghai Institute of Pancreatic Diseases, Shanghai, China
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19
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Mikó A, Erőss B, Sarlós P, Hegyi Jr P, Márta K, Pécsi D, Vincze Á, Bódis B, Nemes O, Faluhelyi N, Farkas O, Papp R, Kelemen D, Szentesi A, Hegyi E, Papp M, Czakó L, Izbéki F, Gajdán L, Novák J, Sahin-Tóth M, Lerch MM, Neoptolemos J, Petersen OH, Hegyi P. Observational longitudinal multicentre investigation of acute pancreatitis (GOULASH PLUS): follow-up of the GOULASH study, protocol. BMJ Open 2019; 9:e025500. [PMID: 31481363 PMCID: PMC6731920 DOI: 10.1136/bmjopen-2018-025500] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/21/2018] [Revised: 02/19/2019] [Accepted: 05/02/2019] [Indexed: 02/06/2023] Open
Abstract
BACKGROUND Acute pancreatitis (AP) is an inflammatory condition that can lead to late consequences. Recurrent AP (RAP) develops in 20% of patients and chronic pancreatitis (CP) occurs in 7%-12.8%. However, we do not have sufficient information to establish an evidence-based statement to define early CP, or how to prevent its development. AIM The aim of this study was to understand the influencing factors and to determine which parameters should be measured or used as a biomarker to detect the early phase of CP. METHODS/DESIGN This is an observational prospective follow-up study of the GOULASH-trial (ISRTCN 63827758) in which (1) all severity of pancreatitis are included; (2) patients receive only therapeutic modalities which are accepted by the evidence based medicine (EBM) guideline; (3) whole blood, serum and plasma samples are stored in our biobank; and (4) large amount of variables are collected and kept in our electronic database including anamnestic data, physical examination, laboratory parameters, imaging, therapy and complications. Therefore, this fully characterised patient cohort are well suitable for this longitudinal follow-up study. Patients' selection: patients enrolled in the GOULASH study will be offered to join to the longitudinal study. The follow-up will be at 1, 2, 3, 4, 5 and 6 years after the episode of AP. Anamnestic data will be collected by questionnaires: (1) diet history questionnaire, (2) 36-Item Short-Form Health Survey, (3) physical activity questionnaire and (4) stress questionnaire. Genetic tests will be performed for the genes associated with CP. The exocrine and endocrine pancreatic, liver and kidney functions will be determined by laboratory tests, stool sample analyses and imaging. Cost-effectiveness will be analysed to examine the relationship between events of interest and health-related quality of life or to explore subgroup differences. CONCLUSION This study will provide information about the risk and influencing factors leading to CP and identify the most useful measurable parameters. TRIAL REGISTRATION NUMBER ISRCTN63396106.
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Affiliation(s)
- Alexandra Mikó
- Institute for Translational Medicine, University of Pécs, Medical School, Pécs, Hungary
| | - Bálint Erőss
- Institute for Translational Medicine, University of Pécs, Medical School, Pécs, Hungary
| | - Patrícia Sarlós
- Division of Gastroenterology, First Department of Medicine, University of Pécs, Pécs, Hungary
| | - Péter Hegyi Jr
- Institute for Translational Medicine, University of Pécs, Medical School, Pécs, Hungary
- Gastroenterological Clinic, Faculty of Medicine, Slovak Medical University in Bratislava, Bratislava, Slovakia
| | - Katalin Márta
- Institute for Translational Medicine, University of Pécs, Medical School, Pécs, Hungary
- János Szentágothai Research Center, University of Pécs, Pécs, Hungary
| | - Dániel Pécsi
- Division of Gastroenterology, First Department of Medicine, University of Pécs, Pécs, Hungary
| | - Áron Vincze
- Division of Gastroenterology, First Department of Medicine, University of Pécs, Pécs, Hungary
| | - Beáta Bódis
- Division of Endocrinology and Metabolism, First Department of Medicine, University of Pécs, Pécs, Hungary
| | - Orsolya Nemes
- Division of Endocrinology and Metabolism, First Department of Medicine, University of Pécs, Pécs, Hungary
| | - Nándor Faluhelyi
- Department of Radiology, Medical School, University of Pécs, Pécs, Hungary
| | - Orsolya Farkas
- Department of Radiology, Medical School, University of Pécs, Pécs, Hungary
| | - Róbert Papp
- Surgery Clinic, University of Pécs, Pécs, Hungary
| | | | - Andrea Szentesi
- Institute for Translational Medicine, University of Pécs, Medical School, Pécs, Hungary
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Eszter Hegyi
- Institute for Translational Medicine, University of Pécs, Medical School, Pécs, Hungary
| | - Mária Papp
- Department of Internal Medicine, Division of Gastroenterology, University of Debrecen, Debrecen, Hungary
| | - László Czakó
- First Department of Medicine, University of Szeged, Szeged, Hungary
| | - Ferenc Izbéki
- First Department of Gastroenterology, Szent György University Teaching Hospital of Fejér County, Székesfehérvár, Hungary
| | - László Gajdán
- First Department of Gastroenterology, Szent György University Teaching Hospital of Fejér County, Székesfehérvár, Hungary
| | - János Novák
- First Department of Gastroenterology, Pándy Kálmán Hospital of Békés County, Gyula, Hungary
| | - Miklós Sahin-Tóth
- Department of Molecular and Cell Biology, Henry M Goldman School of Dental Medicine Boston University, Boston, Massachusetts, UK
| | - Markus M Lerch
- Department of Medicine A, Universitatsmedizin Greifswald, Greifswald, Germany
| | - John Neoptolemos
- Cancer Research UK Liverpool Cancer Trials Unit, University of Liverpool, Liverpool, UK
| | | | - Péter Hegyi
- Institute for Translational Medicine, University of Pécs, Medical School, Pécs, Hungary
- Surgery Clinic, University of Pécs, Pécs, Hungary
- Hungarian Academy of Sciences- University of Szeged, Momentum Gastroenterology Multidisciplinary Research Group, Szeged, Hungary
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20
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Infection rate among nutritional therapies for acute pancreatitis: A systematic review with network meta-analysis of randomized controlled trials. PLoS One 2019; 14:e0219151. [PMID: 31291306 PMCID: PMC6620007 DOI: 10.1371/journal.pone.0219151] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/04/2019] [Accepted: 06/17/2019] [Indexed: 12/12/2022] Open
Abstract
Background Infection in acute pancreatitis (AP) is associated with nutritional therapies including naso-gastric (NG), naso-jejunal (NJ), and total parenteral nutrition (TPN). To examine infections among NG, NJ, TPN, and no nutritional support (NNS) in treating patients with AP. Methods The investigators completed comprehensive search in the Cochrane library, EMBASE, PubMed, Web of Science, and ClinicalTrials.gov without restriction on language and publication date before January 21, 2019. They also searched the reference lists of relevant studies for randomized controlled trials (RCTs) comparing NG, NJ, TPN, and NNS among patients with AP. Quantitative synthesis was conducted in a contrast-based network meta-analysis. To clarify effects, a network meta-analysis was conducted to calculate the surface under the cumulative ranking curve (SUCRA). Beside of overall infections, the event rates of infected pancreatic necrosis, bacteremia, line infection, pneumonia, urinary tract infection, and other types of infections were measured. Results The network meta-analysis of 16 RCTs showed that NJ had significantly lower overall infection rates compared with TPN (risk ratio: 0.59; 95% confidence interval: 0.38, 0.90); and NG had a larger effect size and higher rank probability compared with NJ, TPN, and NNS (mean rank = 1.7; SUCRA = 75.8). TPN was the least preferred (mean rank = 3.2; SUCRA = 26.6). Conclusions NG and NJ may be preferred therapies for treating patients with AP. Clinicians may consider NG as a first-line treatment for patients with AP (including severe AP) and even in patients receiving prophylactic antibiotics. In addition, we found that NNS should be avoided when treating patients with severe AP.
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Cho J, Walia M, Scragg R, Petrov MS. Frequency and risk factors for mental disorders following pancreatitis: a nationwide cohort study. Curr Med Res Opin 2019; 35:1157-1164. [PMID: 30614299 DOI: 10.1080/03007995.2018.1560748] [Citation(s) in RCA: 23] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
Objective: To investigate the frequency and risk factors for mental disorders following pancreatitis. Methods: Patients with acute pancreatitis (AP) and chronic pancreatitis (CP) were identified (n = 18,074) from a nationwide database in New Zealand (1998-2015). They were followed from their first hospital admissions for AP or CP to incident mental disorders. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated using multivariable Cox regression analyses. Results: CP (vs AP) was associated with a significantly higher risk of mental disorders (adjusted HR = 2.00 [95% CI = 1.53-2.62]). Pre-existing diabetes (adjusted HR = 8.99 [95% CI = 6.23-12.96] for AP and adjusted HR = 3.42 [95% CI = 2.37-4.96] for CP) and post-pancreatitis diabetes mellitus (adjusted HR = 7.10 [95% CI = 4.14-12.19] for AP and adjusted HR = 2.97 [95% CI = 1.83-4.82] for CP) were risk factors for mental disorders in individuals following pancreatitis. Severe (adjusted HR = 2.07 [95% CI = 1.39-3.06] vs mild) and recurrent (adjusted HR = 1.62 [95% CI = 1.07-2.45] vs single episode) attacks were associated with significantly higher risks of mental disorders following AP. Conclusions: Patients following CP, recurrent AP, severe AP, and those with diabetes are at high risk for developing mental disorders.
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Affiliation(s)
- Jaelim Cho
- a School of Medicine , University of Auckland , Auckland , New Zealand
| | - Monika Walia
- a School of Medicine , University of Auckland , Auckland , New Zealand
| | - Robert Scragg
- b School of Population Health , University of Auckland , Auckland , New Zealand
| | - Maxim S Petrov
- a School of Medicine , University of Auckland , Auckland , New Zealand
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22
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Zhi M, Zhu X, Lugea A, Waldron RT, Pandol SJ, Li L. Incidence of New Onset Diabetes Mellitus Secondary to Acute Pancreatitis: A Systematic Review and Meta-Analysis. Front Physiol 2019; 10:637. [PMID: 31231233 PMCID: PMC6558372 DOI: 10.3389/fphys.2019.00637] [Citation(s) in RCA: 74] [Impact Index Per Article: 12.3] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/14/2019] [Accepted: 05/06/2019] [Indexed: 12/14/2022] Open
Abstract
Background and Aims: Patients who have an episode of acute pancreatitis (AP) frequently develop diabetes mellitus (DM) over time. The reported incidence of DM after AP varies depending on the severity, etiology and the extent of pancreatic necrosis during AP. We performed a systematic review to determine the incidence of new-onset DM after AP episode (s), and compared the rate of DM in AP patients based upon different disease characteristics. Methods: A total of 31 relevant studies with 13894 subjects were collected from Medline, Embase, and Web of Science. Stata 15 software was used for data analyses in the meta-analysis. Results: The random-effects pooled incidence was 23.0% for DM (95% CI 16.0-31.0%) and 15.0% (95% CI 9.0-23.0%) for DM treated with insulin. We noted substantial heterogeneity in incidence estimates for DM and DM treated with insulin (I 2 = 95.61 and 71.78%; both p < 0·001). The DM incidence was higher in the populations that had a severe AP (SAP) episode than in those with mild acute pancreatitis (MAP) (39 vs. 14%). Patients that displayed pancreatic necrosis during the AP attack(s) had a higher frequency of DM than those without necrosis (37 vs. 11%). In addition, the pooled incidence of DM was higher after alcoholic compared to biliary AP (28 vs. 12%). The incidence of insulin use after SAP and alcoholic AP was 21 and 18%, respectively, with very low heterogeneities. According to duration of follow-up, the pooled rate of DM and insulin use within 5 years after AP was 20 and 14%, while the rate associated with follow-up duration of more than 5 years was elevated to 37 and 25%, respectively. On meta-regression, year of publication, male proportion, age at DM test, and duration of follow-up were neither positively nor negatively associated with the incidence of DM and DM treated with insulin in patients who had a prior AP attack. Conclusion: Patients with AP developed DM after discharge from hospital with a frequency of about 23%. SAP, alcoholic AP and acute necrotizing pancreatitis (ANP) were associated with increased incidence of DM. Assessments of severity, etiology, and pancreatic necrosis are critical for predicting DM development after AP.
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Affiliation(s)
- Mengmeng Zhi
- Department of Endocrinology, Affiliated ZhongDa Hospital, School of Medicine, Southeast University, Nanjing, China
| | - Xiangyun Zhu
- Department of Endocrinology, Affiliated ZhongDa Hospital, School of Medicine, Southeast University, Nanjing, China
| | - Aurelia Lugea
- Division of Gastroenterology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Richard T. Waldron
- Division of Gastroenterology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Stephen J. Pandol
- Division of Gastroenterology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States
| | - Ling Li
- Department of Endocrinology, Affiliated ZhongDa Hospital, School of Medicine, Southeast University, Nanjing, China
- Institute of Pancreas, Southeast University, Nanjing, China
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23
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Huang W, de la Iglesia-García D, Baston-Rey I, Calviño-Suarez C, Lariño-Noia J, Iglesias-Garcia J, Shi N, Zhang X, Cai W, Deng L, Moore D, Singh VK, Xia Q, Windsor JA, Domínguez-Muñoz JE, Sutton R. Exocrine Pancreatic Insufficiency Following Acute Pancreatitis: Systematic Review and Meta-Analysis. Dig Dis Sci 2019; 64:1985-2005. [PMID: 31161524 PMCID: PMC6584228 DOI: 10.1007/s10620-019-05568-9] [Citation(s) in RCA: 66] [Impact Index Per Article: 11.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/23/2018] [Accepted: 02/26/2019] [Indexed: 02/07/2023]
Abstract
BACKGROUND/OBJECTIVES The epidemiology of exocrine pancreatic insufficiency (EPI) after acute pancreatitis (AP) is uncertain. We sought to determine the prevalence, progression, etiology and pancreatic enzyme replacement therapy (PERT) requirements for EPI during follow-up of AP by systematic review and meta-analysis. METHODS Scopus, Medline and Embase were searched for prospective observational studies or randomized clinical trials (RCTs) of PERT reporting EPI during the first admission (between the start of oral refeeding and before discharge) or follow-up (≥ 1 month of discharge) for AP in adults. EPI was diagnosed by direct and/or indirect laboratory exocrine pancreatic function tests. RESULTS Quantitative data were analyzed from 370 patients studied during admission (10 studies) and 1795 patients during follow-up (39 studies). The pooled prevalence of EPI during admission was 62% (95% confidence interval: 39-82%), decreasing significantly during follow-up to 35% (27-43%; risk difference: - 0.34, - 0.53 to - 0.14). There was a two-fold increase in the prevalence of EPI with severe compared with mild AP, and it was higher in patients with pancreatic necrosis and those with an alcohol etiology. The prevalence decreased during recovery, but persisted in a third of patients. There was no statistically significant difference between EPI and new-onset pre-diabetes/diabetes (risk difference: 0.8, 0.7-1.1, P = 0.33) in studies reporting both. Sensitivity analysis showed fecal elastase-1 assay detected significantly fewer patients with EPI than other tests. CONCLUSIONS The prevalence of EPI during admission and follow-up is substantial in patients with a first attack of AP. Unanswered questions remain about the way this is managed, and further RCTs are indicated.
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Affiliation(s)
- Wei Huang
- 0000 0004 1770 1022grid.412901.fDepartment of Integrated Traditional Chinese and Western Medicine, Sichuan Provincial Pancreatitis Center and West China-Liverpool Biomedical Research Center, West China Hospital, Sichuan University, Chengdu, China
| | - Daniel de la Iglesia-García
- 0000 0000 8816 6945grid.411048.8Department of Gastroenterology and Hepatology, Health Research Institute of Santiago (IDIS), University Hospital of Santiago de Compostela, Santiago de Compostela, Spain
| | - Iria Baston-Rey
- 0000 0000 8816 6945grid.411048.8Department of Gastroenterology and Hepatology, Health Research Institute of Santiago (IDIS), University Hospital of Santiago de Compostela, Santiago de Compostela, Spain
| | - Cristina Calviño-Suarez
- 0000 0000 8816 6945grid.411048.8Department of Gastroenterology and Hepatology, Health Research Institute of Santiago (IDIS), University Hospital of Santiago de Compostela, Santiago de Compostela, Spain
| | - Jose Lariño-Noia
- 0000 0000 8816 6945grid.411048.8Department of Gastroenterology and Hepatology, Health Research Institute of Santiago (IDIS), University Hospital of Santiago de Compostela, Santiago de Compostela, Spain
| | - Julio Iglesias-Garcia
- 0000 0000 8816 6945grid.411048.8Department of Gastroenterology and Hepatology, Health Research Institute of Santiago (IDIS), University Hospital of Santiago de Compostela, Santiago de Compostela, Spain
| | - Na Shi
- 0000 0004 1770 1022grid.412901.fDepartment of Integrated Traditional Chinese and Western Medicine, Sichuan Provincial Pancreatitis Center and West China-Liverpool Biomedical Research Center, West China Hospital, Sichuan University, Chengdu, China
| | - Xiaoying Zhang
- 0000 0004 1770 1022grid.412901.fDepartment of Integrated Traditional Chinese and Western Medicine, Sichuan Provincial Pancreatitis Center and West China-Liverpool Biomedical Research Center, West China Hospital, Sichuan University, Chengdu, China ,0000 0004 1936 8470grid.10025.36Liverpool Pancreatitis Research Group, Royal Liverpool University Hospital, Institute of Translational Medicine, University of Liverpool, Liverpool, UK
| | - Wenhao Cai
- 0000 0004 1770 1022grid.412901.fDepartment of Integrated Traditional Chinese and Western Medicine, Sichuan Provincial Pancreatitis Center and West China-Liverpool Biomedical Research Center, West China Hospital, Sichuan University, Chengdu, China
| | - Lihui Deng
- 0000 0004 1770 1022grid.412901.fDepartment of Integrated Traditional Chinese and Western Medicine, Sichuan Provincial Pancreatitis Center and West China-Liverpool Biomedical Research Center, West China Hospital, Sichuan University, Chengdu, China
| | - Danielle Moore
- 0000 0004 1936 8470grid.10025.36Liverpool Pancreatitis Research Group, Royal Liverpool University Hospital, Institute of Translational Medicine, University of Liverpool, Liverpool, UK
| | - Vikesh K. Singh
- 0000 0001 2171 9311grid.21107.35Pancreatitis Center, Division of Gastroenterology, Johns Hopkins Medical Institutions, Baltimore, USA
| | - Qing Xia
- 0000 0004 1770 1022grid.412901.fDepartment of Integrated Traditional Chinese and Western Medicine, Sichuan Provincial Pancreatitis Center and West China-Liverpool Biomedical Research Center, West China Hospital, Sichuan University, Chengdu, China
| | - John A. Windsor
- 0000 0004 0372 3343grid.9654.eSurgical and Translational Research Center, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
| | - J. Enrique Domínguez-Muñoz
- 0000 0000 8816 6945grid.411048.8Department of Gastroenterology and Hepatology, Health Research Institute of Santiago (IDIS), University Hospital of Santiago de Compostela, Santiago de Compostela, Spain
| | - Robert Sutton
- 0000 0004 1936 8470grid.10025.36Liverpool Pancreatitis Research Group, Royal Liverpool University Hospital, Institute of Translational Medicine, University of Liverpool, Liverpool, UK
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Khatkov IE, Maev IV, Abdulkhakov SR, Alekseenko SA, Alikhanov RB, Bakulin IG, Bakulina NV, Baranovskiy AY, Beloborodova EV, Belousova EA, Voskanyan SE, Vinokurova LV, Grinevich VB, Darvin VV, Dubtsova EA, Dyuzheva TG, Egorov VI, Efanov MG, Izrailov RE, Korobka VL, Kotiv BN, Kokhanenko NY, Kucheryavyy YA, Livzan MA, Lyadov VK, Nikolskaya KA, Osipenko MF, Pasechnikov VD, Plotnikova EY, Sablin OA, Simanenkov VI, Tsvirkun VV, Tsukanov VV, Shabunin AV, Bordin DS. Russian consensus on exo- and endocrine pancreatic insufficiency after surgical treatment. TERAPEVT ARKH 2018; 90:13-26. [PMID: 30701935 DOI: 10.26442/terarkh201890813-26] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
The Russian consensus on exo- and endocrine pancreatic insufficiency after surgical treatment was prepared on the initiative of the Russian "Pancreatic Club" on the Delphi method. His goal was to clarify and consolidate the opinions of specialists on the most relevant issues of diagnosis and treatment of exo- and endocrine insufficiency after surgical interventions on the pancreas. An interdisciplinary approach is provided by the participation of leading gastroenterologists and surgeons.
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Affiliation(s)
- I E Khatkov
- A.S. Loginov Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russia
- A.I. Evdokimov Moscow State University of Medicine and Dentistry, Ministry of Health of Russia, Moscow, Russia
| | - I V Maev
- A.I. Evdokimov Moscow State University of Medicine and Dentistry, Ministry of Health of Russia, Moscow, Russia
| | - S R Abdulkhakov
- Kazan State Medical University, Ministry of Health of Russia, Kazan, Russia
| | - S A Alekseenko
- The Far Eastern State Medical University, Ministry of Health of Russia, Khabarovsk, Russia
| | - R B Alikhanov
- A.S. Loginov Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russia
| | - I G Bakulin
- I.I. Mechnikov North-Western State Medical University, Ministry of Health of Russia, Saint-Petersburg, Russia
| | - N V Bakulina
- I.I. Mechnikov North-Western State Medical University, Ministry of Health of Russia, Saint-Petersburg, Russia
| | | | - E V Beloborodova
- Siberian State Medical University, Ministry of Health of Russia, Tomsk, Russia
| | - E A Belousova
- M.F. Vladimirskiy Moscow Regional Research and Clinical Institute, Moscow, Russia
| | - S E Voskanyan
- A.I. Burnasyan Federal Medical Biophysical Center of Federal Medical Biological Agency, Moscow, Russia
| | - L V Vinokurova
- A.S. Loginov Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russia
| | - V B Grinevich
- S.M. Kirov Military Medical Academy, Ministry of Defence of Russia, Saint-Petersburg, Russia
| | - V V Darvin
- Medical Institute of Surgut State University, Surgut, Russia
| | - E A Dubtsova
- A.S. Loginov Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russia
| | - T G Dyuzheva
- I.M. Sechenov First Moscow State Medical University (Sechenov University), Ministry of Health of Russia, Moscow, Russia
| | - V I Egorov
- City Clinical Hospital named after the Bakhrushin Brothers, Moscow, Russia
| | - M G Efanov
- A.S. Loginov Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russia
| | - R E Izrailov
- A.S. Loginov Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russia
| | - V L Korobka
- Rostov State Medical University, Ministry of Health of Russia, Rostov-on-Don, Russia
| | - B N Kotiv
- S.M. Kirov Military Medical Academy, Ministry of Defence of Russia, Saint-Petersburg, Russia
| | - N Yu Kokhanenko
- Saint-Petersburg State Pediatric Medical University, Ministry of Health of Russia, Saint-Petersburg, Russia
| | - Yu A Kucheryavyy
- A.I. Evdokimov Moscow State University of Medicine and Dentistry, Ministry of Health of Russia, Moscow, Russia
| | - M A Livzan
- Omsk State Medical University, Ministry of Health of Russia, Omsk, Russia
| | - V K Lyadov
- Russian Medical Academy of Continuous Professional Education, Ministry of Health of Russia, Moscow, Russia
| | - K A Nikolskaya
- A.S. Loginov Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russia
| | - M F Osipenko
- Novosibirsk State Medical University, Ministry of Health of Russia, Novosibirsk, Russia
| | - V D Pasechnikov
- Stavropol State Medical University, Ministry of Health of Russia, Stavropol, Russia
| | - E Yu Plotnikova
- Kemerovo State Medical University, Ministry of Health of Russia, Kemerovo, Russia
| | - O A Sablin
- A.M. Nikiforov All-Russian Center for Emergency and Radiation Medicine, Russian Ministry for Emergency Situations, Saint-Petersburg, Russia
| | - V I Simanenkov
- I.I. Mechnikov North-Western State Medical University, Ministry of Health of Russia, Saint-Petersburg, Russia
| | - V V Tsvirkun
- A.S. Loginov Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russia
| | - V V Tsukanov
- Krasnoyarsk Scientific Center of Siberian Branch in Russian Academy of Sciences, Krasnoyarsk, Russia
| | - A V Shabunin
- S.P. Botkin City Hospital, Moscow Healthcare Department, Moscow, Russia
| | - D S Bordin
- A.S. Loginov Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russia
- Tver State Medical University, Ministry of Health of Russia, Tver, Russia
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25
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Whitcomb DC, Shimosegawa T, Chari ST, Forsmark CE, Frulloni L, Garg P, Hegyi P, Hirooka Y, Irisawa A, Ishikawa T, Isaji S, Lerch MM, Levy P, Masamune A, Wilcox CM, Windsor J, Yadav D, Sheel A, Neoptolemos JP. International consensus statements on early chronic Pancreatitis. Recommendations from the working group for the international consensus guidelines for chronic pancreatitis in collaboration with The International Association of Pancreatology, American Pancreatic Association, Japan Pancreas Society, PancreasFest Working Group and European Pancreatic Club. Pancreatology 2018; 18:516-527. [PMID: 29793839 PMCID: PMC6748871 DOI: 10.1016/j.pan.2018.05.008] [Citation(s) in RCA: 106] [Impact Index Per Article: 15.1] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/26/2018] [Accepted: 05/14/2018] [Indexed: 02/07/2023]
Abstract
BACKGROUND Chronic pancreatitis (CP) is a progressive inflammatory disorder currently diagnosed by morphologic features. In contrast, an accurate diagnosis of Early CP is not possible using imaging criteria alone. If this were possible and early treatment instituted, the later, irreversible features and complications of CP could possibly be prevented. METHOD An international working group supported by four major pancreas societies (IAP, APA, JPS, and EPC) and a PancreasFest working group sought to develop a consensus definition and diagnostic criteria for Early CP. Ten statements (S1-10) concerning Early CP were used to gauge consensus on the Early CP concept using anonymous voting with a 9 point Likert scale. Consensus required an alpha ≥0.80. RESULTS No consensus statement could be developed for a definition of Early-CP or diagnostic criteria. There was consensus on 5 statements: (S2) The word "Early" in early chronic pancreatitis is used to describe disease state, not disease duration. (S4) Early CP defines a stage of CP with preserved pancreatic function and potentially reversible features. (S8) Genetic variants are important risk factors for Early CP and can add specificity to the likely etiology, but they are neither necessary nor sufficient to make a diagnosis. (S9) Environmental risk factors can provide evidence to support the diagnosis of Early CP, but are neither necessary nor sufficient to make a diagnosis. (S10) The differential diagnosis for Early CP includes other disorders with morphological and functional features that overlap with CP. CONCLUSIONS Morphology based diagnosis of Early CP is not possible without additional information. New approaches to the accurate diagnosis of Early CP will require a mechanistic definition that considers risk factors, biomarkers, clinical context and new models of disease. Such a definition will require prospective validation.
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Affiliation(s)
- David C Whitcomb
- Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Department of Human Genetics, University of Pittsburgh, Pittsburgh, PA, USA.
| | - Tooru Shimosegawa
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan
| | - Suresh T Chari
- Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA
| | - Christopher E Forsmark
- Division of Gastroenterology, Hepatology, and Nutrition, University of Florida, Gainesville, FL, USA
| | - Luca Frulloni
- Gastroenterology Unit, Department of Medicine and the Pancreas Institute, University of Verona, Verona, Italy
| | - Pramod Garg
- Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi, India
| | - Peter Hegyi
- Institute for Translational Medicine, Medical School, University of Pécs, Pécs, Hungary and MTA-SZTE Translational Gastroenterology Research Group, Szeged, Hungary
| | - Yoshiki Hirooka
- Department of Endoscopy, Nagoya University Hospital, Nagoya, Japan
| | - Atsushi Irisawa
- Department of Gastroenterology, Dokkyo Medical University, Mibu, Tochigi, Japan
| | - Takuya Ishikawa
- Department of Gastroenterology, Nagoya University Graduate School of Medicine, Nagoya, Japan
| | - Shuiji Isaji
- Department of Hepatobiliary Pancreatic and Transplant Surgery, Mie University, Tsu, Japan
| | - Markus M Lerch
- Department of Medicine A, University Medicine Greifswald, Germany
| | - Philippe Levy
- Service de pancréatologie, Pôle des Maladies de l'Appareil Digestif, DHU UNITY, Centre de référence des maladies rares du pancréas (PAncreatic RAre DISeases), Centre de référence européen des tumeurs neuroendocrines digestives et pancréatiques, Hôpital Beaujon, Faculté Denis Diderot, APHP, Clichy, France
| | - Atsushi Masamune
- Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan
| | - Charles M Wilcox
- Division of Gastroenterology & Hepatology, University of Alabama Birmingham, Birmingham, AL, USA
| | - John Windsor
- Department of Surgery, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
| | - Dhiraj Yadav
- Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA
| | - Andrea Sheel
- Department of Molecular and Clinical Cancer Medicine, Institute of Translational Medicine, University of Liverpool, Liverpool, L69 3GE, UK
| | - John P Neoptolemos
- Department of General, Visceral and Transplantation Surgery, University of Heidelberg, Heidelberg, Germany
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26
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Leerhøy B, Shabanzadeh DM, Nordholm-Carstensen A, Novovic S, Hansen MB, Jørgensen LN. Pancreatic function following post-endoscopic retrograde cholangiopancreatography pancreatitis: A controlled cohort study with long-term follow-up. United European Gastroenterol J 2018; 6:586-594. [PMID: 29881614 DOI: 10.1177/2050640617742498] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/17/2017] [Accepted: 10/17/2017] [Indexed: 12/21/2022] Open
Abstract
Background Acute pancreatitis is one of the most common causes of gastrointestinal-related hospitalization and the incidence is increasing. Endo- and exocrine pancreatic function can be compromised after acute pancreatitis. Objective The purpose of this study was to explore the long-term consequences of post-endoscopic retrograde cholangiopancreatography pancreatitis (PEP) on pancreatic function. Methods A follow-up study was carried out with prospective assessment of endo- and exocrine pancreatic function among cases with previous PEP and matched controls from a Danish cohort consisting of 772 patients undergoing first-time ERCP. Pancreatic function was evaluated by faecal-elastase-1 test, blood levels of haemoglobin A1c, C-peptide, vitamin B12, vitamin D and indirectly by changes in body weight. Results Twenty-nine cases and 49 controls participated in the study. Mean follow-up time (standard deviation) was 58 (21) months. Twelve (41%), eight (28%) and nine (31%) patients had mild, moderate and severe PEP, respectively. There was no difference between cases and controls with regard to pancreatic function parameters and PEP severity was not associated with pancreatic function. Factors associated with pancreatic function impairment included body mass index, alcohol consumption, age and smoking. Conclusion This study suggests that long-term pancreatic function following PEP is similar to the pancreatic function of other patients with comparable gallstone-related morbidity.
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Affiliation(s)
- Bonna Leerhøy
- Digestive Disease Center, Bispebjerg Hospital, University of Copenhagen, Denmark
| | - Daniel M Shabanzadeh
- Digestive Disease Center, Bispebjerg Hospital, University of Copenhagen, Denmark
| | | | - Srdan Novovic
- 2Department of Gastroenterology and Gastrointestinal Surgery, Hvidovre Hospital, University of Copenhagen, Denmark
| | - Mark B Hansen
- Digestive Disease Center, Bispebjerg Hospital, University of Copenhagen, Denmark.,Zealand Pharma, Research and Development, Glostrup, Denmark
| | - Lars N Jørgensen
- Digestive Disease Center, Bispebjerg Hospital, University of Copenhagen, Denmark
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Tu J, Yang Y, Zhang J, Yang Q, Lu G, Li B, Tong Z, Ke L, Li W, Li J. Effect of the disease severity on the risk of developing new-onset diabetes after acute pancreatitis. Medicine (Baltimore) 2018; 97:e10713. [PMID: 29851776 PMCID: PMC6392884 DOI: 10.1097/md.0000000000010713] [Citation(s) in RCA: 27] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023] Open
Abstract
Endocrine pancreatic insufficiency secondary to acute pancreatitis (AP) drew increasing attention in the recent years. The aim of the present study was to assess the impact of pancreatic necrosis and organ failure on the risk of developing new-onset diabetes after AP.The follow-up study was conducted for patients recovered from AP in the treatment center of Jinling Hospital. Endocrine function was evaluated by simplified oral glucose tolerance test (OGTT). Pancreatic necrosis was examined by abdominal contrast-enhanced CT (CECT) scan during hospitalization. The data including APACHE II score, Balthazar's score, organ failure (AKI and ARDS) was also collected from the medical record database. All patients were divided into group diabetes mellitus (DM) and group non-DM according to the endocrine function and group pancreatic necrosis (PN) and persistent organ failure (OF), group PN and non-OF, group non-PN and OF, and group non-PN and non-OF according to the occurrence of pancreatic necrosis and persistent organ failure.Around 256 patients were included for the final analysis. 154 patients (60.2%) were diagnosed with DM (include impaired glucose tolerance, IGT), while 102 patients (39.8%) were deemed as normal endocrine function. APACHE II score and Balthazar score of the patients in the group DM were significant higher than those in the non-DM group (F = 6.09, P = .01; F = 10.74, P = .001). The incidence of pancreatic necrosis in group DM and group non-DM was, respectively, 64.7% and 53.0% (χ = 3.506, P = .06). The patients underwent necrosis debridement by percutaneous catheter drainage (PCD) and/or the operative necrosectomy (ON) were more likely to developed new onset DM than the patients without PCD or ON (χ = 2.385, P = .02). The morbidity of new-onset DM after AP gradually increased from group non-PN and non-OF, group non-PN and OF, group PN and non-OF to group PN and OF in order (χ = 4.587, P = .03). The value of HOMA-IR of patients at follow-up time was significant higher in group DM than group non-DM (F = 13.414, P = .000).Patients with both PN and persistent OF may were at increased risk of developing new-onset diabetes after AP. Insulin resistance could be the pivotal mechanism of the development of diabetes.
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Affiliation(s)
- Jianfeng Tu
- Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing
- Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College
| | - Yue Yang
- Hangzhou Medical College, Hangzhou, China
| | - Jingzhu Zhang
- Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing
| | - Qi Yang
- Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing
| | - Guotao Lu
- Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing
| | - Baiqiang Li
- Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing
| | - Zhihui Tong
- Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing
| | - Lu Ke
- Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing
| | - Weiqin Li
- Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing
| | - Jieshou Li
- Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing
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Hollemans RA, Hallensleben NDL, Mager DJ, Kelder JC, Besselink MG, Bruno MJ, Verdonk RC, van Santvoort HC. Pancreatic exocrine insufficiency following acute pancreatitis: Systematic review and study level meta-analysis. Pancreatology 2018; 18:253-262. [PMID: 29482892 DOI: 10.1016/j.pan.2018.02.009] [Citation(s) in RCA: 100] [Impact Index Per Article: 14.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/03/2017] [Revised: 02/05/2018] [Accepted: 02/18/2018] [Indexed: 12/11/2022]
Abstract
OBJECTIVES This study systematically explores the prevalence of pancreatic exocrine insufficiency (PEI) after acute pancreatitis in different subgroups of etiology (biliary/alcoholic/other), disease severity and follow-up time (<12, 12-36 and > 36 months after index admission). METHODS PubMed and EMBASE databases were searched, 32 studies were included in this study level meta-analysis. RESULTS In a total of 1495 patients with acute pancreatitis, tested at a mean of 36 months after index admission, the pooled prevalence of PEI was 27.1% (95%-confidence interval [CI]: 20.3%-35.1%). Patients from seven studies (n = 194) underwent direct tests with pooled prevalence of 41.7% [18.5%-69.2%]. Patients from 26 studies (n = 1305) underwent indirect tests with pooled prevalence of 24.4% [18.3%-31.8%]. In subgroup analyses on patients that underwent fecal elastase-1 tests, PEI occurred more often in alcoholic pancreatitis (22.7% [16.6%-30.1%]) than in biliary pancreatitis (10.2% [6.2%-16.4%]) or other etiology (13.4% [7.7%-22.4%]; P = 0.02). Pooled prevalence of PEI after mild and severe pancreatitis was 19.4% [8.6%-38.2%] and 33.4% [22.6%-46.3%] respectively in studies using fecal elaste-1 tests (P = 0.049). Similar results were seen in patients without (18.9% [9.3%-34.6%]) and with necrotizing pancreatitis (32.0% [18.2%-49.8%]; P = 0.053). Over time, the prevalence of PEI decreased in patients who underwent the fecal elastase-1 test and increased in patients who underwent the fecal fat analysis. CONCLUSIONS After acute pancreatitis, a quarter of all patients develop PEI during follow-up. Alcoholic etiology and severe and necrotizing pancreatitis are associated with higher risk of PEI. The prevalence of PEI may change as time of follow-up increases.
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Affiliation(s)
- Robbert A Hollemans
- Dept. of Surgery, St. Antonius Hospital, Nieuwegein, The Netherlands; Dept. of Research and Development, St. Antonius Hospital, Nieuwegein, The Netherlands
| | - Nora D L Hallensleben
- Dept. of Research and Development, St. Antonius Hospital, Nieuwegein, The Netherlands; Dept. of Gastroenterology and Hepatology, Erasmus Medical Center, Rotterdam, The Netherlands
| | | | - Johannes C Kelder
- Dept. of Research and Development, St. Antonius Hospital, Nieuwegein, The Netherlands
| | - Marc G Besselink
- Dept. of Surgery, Academic Gastroenterology and Metabolism, Amsterdam, The Netherlands
| | - Marco J Bruno
- Dept. of Gastroenterology and Hepatology, Erasmus Medical Center, Rotterdam, The Netherlands
| | - Robert C Verdonk
- Dept. of Gastroenterology and Hepatology, St. Antonius Hospital, Nieuwegein, The Netherlands
| | - Hjalmar C van Santvoort
- Dept. of Surgery, St. Antonius Hospital, Nieuwegein, The Netherlands; Dept. of Surgery, University Medical Center Utrecht, Utrecht, The Netherlands.
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Faghih M, Gonzalez FG, Makary MA, Singh VK. Total pancreatectomy for recurrent acute and chronic pancreatitis: a critical review of patient selection criteria. Curr Opin Gastroenterol 2017; 33:330-338. [PMID: 28700371 PMCID: PMC5881167 DOI: 10.1097/mog.0000000000000390] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
PURPOSE OF REVIEW Critical review of the indications for total pancreatectomy and highlight limitations in current diagnostic criteria for chronic pancreatitis. RECENT FINDINGS The diagnosis of noncalcific chronic pancreatitis remains controversial because of an overreliance on nonspecific imaging and laboratories findings. Endoscopic ultrasound, s-magnetic resonance cholangiopancreatography, and/or endoscopic pancreatic function testing are often used to diagnose noncalcific chronic pancreatitis despite the fact that there is no gold standard for this condition. Abdominal pain is not specific for chronic pancreatitis and is more likely to be encountered in patients with functional gastrointestinal disorders based on the high incidence of these conditions. The duration of pain and opioid analgesic use results in central sensitization that adversely affects pain outcomes after total pancreatectomy. An alcoholic cause is associated with poorer pain outcomes after total pancreatectomy. SUMMARY The lack of a gold standard for noncalcific chronic pancreatitis limits the diagnostic accuracy of imaging and laboratory tests. The pain of chronic pancreatitis is nonspecific and is affected by duration, preoperative opioid use, and cause. These factors will need to be considered in the development of future selection criteria for this morbid surgery.
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Affiliation(s)
- Mahya Faghih
- Division of Gastroenterology, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
| | | | - Martin A. Makary
- Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
| | - Vikesh K. Singh
- Pancreatitis Center, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
- Division of Gastroenterology, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
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Risk Factors of Hyperglycemia in Patients After a First Episode of Acute Pancreatitis: A Retrospective Cohort. Pancreas 2017; 46:209-218. [PMID: 27846145 DOI: 10.1097/mpa.0000000000000738] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
OBJECTIVES The aim of this study was to evaluate the risk factors for hyperglycemia development after a first episode of acute pancreatitis (AP). METHODS Three hundred and ten patients treated for AP were retrospectively evaluated. Hyperglycemia was determined by fasting blood glucose. All data were collected from the medical records room database and a follow-up telephone call. RESULTS The incidence rate of hyperglycemia was obviously increased 5 years after the event. Hazard ratios (HRs) of developing hyperglycemia in patients with hyperlipidemia, fatty liver, and hypertension were 2.52 (P < 0.001), 1.87 (P = 0.01), and 1.78 (P = 0.017), respectively. Patients of biliary origin that underwent endoscopic retrograde cholangiopancreatography presented a 4.62-fold greater risk than those managed conservatively. Other risk factors were random blood glucose greater than 8.33 mmol/L (HR, 4.19; P < 0.001), lactate dehydrogenase greater than 350 U/L (HR, 1.99; P = 0.017), calcium less than 1.75 mmol/L (HR, 3.86; P = 0.004), and elevated creatine kinase (HR, 2.74; P = 0.001). Patients with AB blood type showed 2.92-fold greater risk compared with those with O blood type. Among them, hyperlipidemia and hyperglycemia on admission were the only independent risk factors (both P < 0.05). CONCLUSIONS Hyperlipidemia, fatty liver, hypertension, endoscopic retrograde cholangiopancreatography treatment, acute hyperglycemia, elevated lactate dehydrogenase and creatine kinase, decreased calcium, and AB blood type were risk factors for hyperglycemia development after AP.
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Umapathy C, Raina A, Saligram S, Tang G, Papachristou GI, Rabinovitz M, Chennat J, Zeh H, Zureikat AH, Hogg ME, Lee KK, Saul MI, Whitcomb DC, Slivka A, Yadav D. Natural History After Acute Necrotizing Pancreatitis: a Large US Tertiary Care Experience. J Gastrointest Surg 2016; 20:1844-1853. [PMID: 27619808 DOI: 10.1007/s11605-016-3264-2] [Citation(s) in RCA: 42] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/16/2016] [Accepted: 08/24/2016] [Indexed: 02/06/2023]
Abstract
BACKGROUND Most studies of acute necrotizing pancreatitis (ANP) focus on short-term outcomes. We evaluated long-term survival and outcomes following ANP. METHODS Patients treated for ANP at the University of Pittsburgh Medical Center from 2001 to 2008 were studied. Data on presentation and course during initial hospitalization and follow-up (median 34 months) was extracted. RESULTS Mean age of patients (n = 167) was 53 ± 16 years; 70 % were male, 94 % white, 71 % transfers, 52 % biliary etiology, and 78 % had first-attack of acute pancreatitis. Majority had severe disease with high Acute Physiology and Chronic Health Evaluation II (APACHE-II) score (median 11), length of stay (median 26 days), intensive care unit (ICU) admission (87 %), presence of systemic inflammatory response syndrome (SIRS) (90 %), persistent organ failure (60 %), and infected necrosis (50 %). Intervention was needed in 74 %. Eighteen (10.8 %) patients died during index hospitalization, 9 (5.4 %) during the first year, and 13 (7.8 %) after 1 year. Median survival was significantly shorter when compared with age- and sex-matched US general population (9.1 vs. 26.1 years, p < 0.001). Increasing age (HR 1.05), persistent organ failure (HR 4.5), and >50 % necrosis (HR 3.8) were independent predictors of death at 1 year. In eligible patients, new-onset diabetes, oral pancreatic enzyme replacement therapy, and disability were noted in 45, 25, and 53 %, respectively. CONCLUSION ANP significantly impacts long-term survival. A high proportion of patients develop functional derangement and disability following ANP.
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Affiliation(s)
| | - Amit Raina
- Division of Gastroenterology, Hepatology, and Nutrition, East Carolina University, Greenville, NC, USA
| | - Shreyas Saligram
- Division of Gastroenterology, Hepatology, and Motility, University of Kansas Medical Center, Kansas City, KS, USA
| | - Gong Tang
- Department of Biostatistics, University of Pittsburgh, Pittsburgh, PA, USA
| | - Georgios I Papachristou
- Division of Gastroenterology, Hepatology, and Nutrition, University of Pittsburgh School of Medicine, 200 Lothrop Street, M-2, C-Wing, Pittsburgh, PA, 15213, USA
| | - Mordechai Rabinovitz
- Division of Gastroenterology, Hepatology, and Nutrition, University of Pittsburgh School of Medicine, 200 Lothrop Street, M-2, C-Wing, Pittsburgh, PA, 15213, USA
| | - Jennifer Chennat
- Division of Gastroenterology, Hepatology, and Nutrition, University of Pittsburgh School of Medicine, 200 Lothrop Street, M-2, C-Wing, Pittsburgh, PA, 15213, USA
| | - Herbert Zeh
- Division of Surgical Oncology, University of Pittsburgh, Pittsburgh, PA, USA
| | - Amer H Zureikat
- Division of Surgical Oncology, University of Pittsburgh, Pittsburgh, PA, USA
| | - Melissa E Hogg
- Division of Surgical Oncology, University of Pittsburgh, Pittsburgh, PA, USA
| | - Kenneth K Lee
- Division of Surgical Oncology, University of Pittsburgh, Pittsburgh, PA, USA
| | - Melissa I Saul
- Department of Biomedical Informatics, University of Pittsburgh, Pittsburgh, PA, USA
| | - David C Whitcomb
- Division of Gastroenterology, Hepatology, and Nutrition, University of Pittsburgh School of Medicine, 200 Lothrop Street, M-2, C-Wing, Pittsburgh, PA, 15213, USA
| | - Adam Slivka
- Division of Gastroenterology, Hepatology, and Nutrition, University of Pittsburgh School of Medicine, 200 Lothrop Street, M-2, C-Wing, Pittsburgh, PA, 15213, USA
| | - Dhiraj Yadav
- Division of Gastroenterology, Hepatology, and Nutrition, University of Pittsburgh School of Medicine, 200 Lothrop Street, M-2, C-Wing, Pittsburgh, PA, 15213, USA.
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Smith RC, Smith SF, Wilson J, Pearce C, Wray N, Vo R, Chen J, Ooi CY, Oliver M, Katz T, Turner R, Nikfarjam M, Rayner C, Horowitz M, Holtmann G, Talley N, Windsor J, Pirola R, Neale R. Summary and recommendations from the Australasian guidelines for the management of pancreatic exocrine insufficiency. Pancreatology 2016; 16:164-180. [PMID: 26775768 DOI: 10.1016/j.pan.2015.12.006] [Citation(s) in RCA: 63] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/09/2015] [Revised: 12/01/2015] [Accepted: 12/10/2015] [Indexed: 02/06/2023]
Abstract
AIM Because of increasing awareness of variations in the use of pancreatic exocrine replacement therapy, the Australasian Pancreatic Club decided it was timely to re-review the literature and create new Australasian guidelines for the management of pancreatic exocrine insufficiency (PEI). METHODS A working party of expert clinicians was convened and initially determined that by dividing the types of presentation into three categories for the likelihood of PEI (definite, possible and unlikely) they were able to consider the difficulties of diagnosing PEI and relate these to the value of treatment for each diagnostic category. RESULTS AND CONCLUSIONS Recent studies confirm that patients with chronic pancreatitis receive similar benefit from pancreatic exocrine replacement therapy (PERT) to that established in children with cystic fibrosis. Severe acute pancreatitis is frequently followed by PEI and PERT should be considered for these patients because of their nutritional requirements. Evidence is also becoming stronger for the benefits of PERT in patients with unresectable pancreatic cancer. However there is as yet no clear guide to help identify those patients in the 'unlikely' PEI group who would benefit from PERT. For example, patients with coeliac disease, diabetes mellitus, irritable bowel syndrome and weight loss in the elderly may occasionally be given a trial of PERT, but determining its effectiveness will be difficult. The starting dose of PERT should be from 25,000-40,000 IU lipase taken with food. This may need to be titrated up and there may be a need for proton pump inhibitors in some patients to improve efficacy.
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Affiliation(s)
- Ross C Smith
- Department of Surgery, University of Sydney, NSW, Australia; Australasian Pancreatic Club, Australia.
| | | | | | - Callum Pearce
- Institute for Immunology and Infectious Diseases, Murdoch University, WA, Australia; Fremantle Hospital, WA, Australia
| | - Nick Wray
- Nutrition & Dietetics, School of Health Sciences, Flinders University, Adelaide, SA, Australia
| | - Ruth Vo
- Liverpool Hospital, University of NSW, Australia
| | - John Chen
- South Australian Liver Transplant & HPB Unit, RAH & Flinders Medical Centre, SA, Australia
| | - Chee Y Ooi
- School of Women's and Children's Health, Dept. of Medicine, University of NSW, Australia; Department of Gastroenterology, Sydney Children's Hospital, Randwick, NSW, Australia
| | - Mark Oliver
- Department of Gastroenterology and Clinical Nutrition, Royal Children's Hospital, Parkville, VIC, Australia
| | - Tamarah Katz
- Sydney Children's Hospital, Randwick, NSW, Australia
| | - Richard Turner
- Hobart Clinical School and Dept. Surgery, University of Tasmania, Australia
| | - Mehrdad Nikfarjam
- Dept. Surgery, University of Melbourne, VIC, Australia; Australasian Pancreatic Club, Australia
| | - Christopher Rayner
- School of Medicine, University of Adelaide, SA, Australia; Centre for Digestive Diseases, Royal Adelaide Hospital, SA, Australia
| | - Michael Horowitz
- Endocrine and Metabolic Unit, University of Adelaide and Royal Adelaide Hospital, SA, Australia
| | - Gerald Holtmann
- Faculty of Medicine and Biomedical Sciences, University of Queensland, Australia; Translational Research Institute, Department of Gastroenterology & Hepatology, Princess Alexandra Hospital, Qld, Australia
| | - Nick Talley
- Faculty of Health and Medicine, University of Newcastle, NSW, Australia; Royal Australasian College of Physicians, Australia
| | - John Windsor
- Dept. of Surgery, University of Auckland, New Zealand
| | - Ron Pirola
- Faculty of Medicine, SW Sydney Clinical School, University of NSW, Australia
| | - Rachel Neale
- Cancer Control Laboratory, Queensland Institute of Medical Research, Qld, Australia
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Development and Diagnostic Accuracy of a Breath Test for Pancreatic Exocrine Insufficiency in Chronic Pancreatitis. Pancreas 2016; 45:241-7. [PMID: 26390420 DOI: 10.1097/mpa.0000000000000434] [Citation(s) in RCA: 44] [Impact Index Per Article: 4.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
OBJECTIVE To develop a ¹³C-labeled substrate breath test by defining the optimal ¹³C-labeled substrate, substrate dose, test meal, and duration of the test and evaluating its accuracy for the diagnosis of pancreatic exocrine insufficiency (PEI) in chronic pancreatitis (CP). METHODS Five consecutive prospective comparative studies in patients with known advanced CP and healthy controls were performed to develop the optimal breath test. Coefficient of fat absorption was used as the reference method. The diagnostic accuracy of the optimized breath test was prospectively further evaluated in patients with advanced CP using coefficient of fat absorption as the reference method. RESULTS The optimal breath test protocol was that using 250 mg of ¹³C-mixed triglyceride as substrate together with a test meal containing 16 g of fat. Coefficient of fat absorption and breath test results correlated significantly (r = 0.736, P < 0.001). The test has sensitivity, specificity, and overall accuracy of 92.9%, 91.7%, and 92.3%, respectively, for the diagnosis of PEI. CONCLUSIONS The optimized ¹³C-mixed triglyceride breath test is an accurate and simple breath test for the diagnosis of PEI in patients with CP, easily applicable to the clinical routine.
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Lee YK, Huang MY, Hsu CY, Su YC. Bidirectional Relationship Between Diabetes and Acute Pancreatitis: A Population-Based Cohort Study in Taiwan. Medicine (Baltimore) 2016; 95:e2448. [PMID: 26765434 PMCID: PMC4718260 DOI: 10.1097/md.0000000000002448] [Citation(s) in RCA: 50] [Impact Index Per Article: 5.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022] Open
Abstract
The proposed bidirectional relationship between acute pancreatitis (AP) and diabetes has never been examined with the same source of data. Furthermore, the effects of disease severity on this relationship have not been fully evaluated. The present study employed the findings from a single database to measure the strength of the association between AP and diabetes.Findings from 1 million National Health Insurance beneficiaries were utilized. Two cohort studies with this database were selected to evaluate the linkage between diabetes and AP. The first cohort analysis addressed the risk of AP among diabetic patients and was comprised of 42,080 diabetic patients and 672,146 unexposed subjects. The second cohort analysis considered the risk of diabetes among patients with AP and enrolled 3187 patients with AP and 709259 unexposed subjects. All adult beneficiaries were followed from January 1, 2005 to December 31, 2012 to identify outcomes of interest. Cox regression models were applied to compare hazards adjusted for potential confounders.For the first cohort, the adjusted hazard ratio (HR) of AP was significantly increased by the presence of diabetes (1.72; 95% confidence interval [CI], 1.52-1.96). In diabetic patients with a history of hyperglycemic crisis episodes (HCEs), the HR was even higher (6.32; 95% CI, 4.54-8.81). For the second cohort, the adjusted HR of diabetes in patients with AP was increased compared to the general population (2.15; 95% CI, 1.92-2.41). For patients with severe AP, the HR was also higher (2.22; 95% CI, 1.50-3.29) but did not differ significantly from that for patients with nonsevere AP.The 2 cohort studies provided evidence for the bidirectional relationship between diabetes and AP. Moreover, diabetic patients with history of HCEs may be associated with higher risk of AP.
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Affiliation(s)
- Yi-Kung Lee
- From the School of Medicine, Tzu Chi University, Hualien, Taiwan, R.O.C. (Y-KL, Y-CS); Emergency Department, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan, R.O.C. (Y-KL, Y-CS); Department of Emergency Medicine, Mackay Memorial Hospital, Taipei, Taiwan, R.O.C. (M-YH); and Department of Public Heath, National Taiwan University, Taipei, Taiwan, R.O.C. (C-YH)
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Mansfield C, Beths T. Management of acute pancreatitis in dogs: a critical appraisal with focus on feeding and analgesia. J Small Anim Pract 2015; 56:27-39. [PMID: 25586804 DOI: 10.1111/jsap.12296] [Citation(s) in RCA: 24] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/06/2013] [Revised: 05/22/2014] [Accepted: 05/26/2014] [Indexed: 12/31/2022]
Abstract
Knowledge about acute pancreatitis has increased recently in both the medical and veterinary fields. Despite this expansion of knowledge, there are very few studies on treatment interventions in naturally occurring disease in dogs. As a result, treatment recommendations are largely extrapolated from experimental rodent models or general critical care principles. General treatment principles involve replacing fluid losses, maintaining hydrostatic pressure, controlling nausea and providing pain relief. Specific interventions recently advocated in human medicine include the use of neurokinin-1 antagonists for analgesia and early interventional feeding. The premise for early feeding is to improve the health of the intestinal tract, as unhealthy enterocytes are thought to perpetuate systemic inflammation. The evidence for early interventional feeding is not supported by robust clinical trials to date, but in humans there is evidence that it reduces hospitalisation time and in dogs it is well tolerated. This article summarises the major areas of management of acute pancreatitis in dogs and examines the level of evidence for each recommendation.
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Affiliation(s)
- C Mansfield
- Faculty of Veterinary and Agricultural Sciences, The University of Melbourne, 250 Princes Highway, Werribee, Victoria 3030, Australia
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Prospective comparison of long term outcomes in patients with severe acute pancreatitis managed by operative and non operative measures. Pancreatology 2015; 15:478-484. [PMID: 26364168 DOI: 10.1016/j.pan.2015.08.006] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/19/2015] [Revised: 08/06/2015] [Accepted: 08/19/2015] [Indexed: 12/11/2022]
Abstract
AIM Present study reports the long term functional and morphological changes following severe acute pancreatitis and compares patients managed by operative and non-operative methods. Association between morphological changes and functional parameters were studied. MATERIALS AND METHODS 35 patients with one year of follow up after recovery from attack of acute pancreatitis were evaluated. RESULTS Etiology was alcohol in 19, gallstones in 11 and idiopathic in 5. Fourteen patients were managed non-operatively and 21 operatively. Patients in non-operative group had a mean follow-up of 18.4 ± 8.2 months while patients in necrosectomy group had 31.4 ± 20.6 months. 40% patients had exocrine insufficiency (abnormal fecal fat) while 48.5% patients (17/35) had new onset diabetes. 90% patients had morphological changes in pancreas. Exocrine abnormality was significantly higher in necrosectomy group compared to non-operative group (57.2% vs 14.1%, p = 0.01). Patients undergoing necrosectomy had higher incidence of endocrine dysfunction {61.9% in surgery and 28.5% in non-operative group (p = 0.053)}. Operative group had more number of patients with completely non-visualized main pancreatic duct (MPD) (p = 0.028) and non-operative group had significantly higher irregular MPD (p = 0.021). Exocrine dysfunction was more in patients with complete non-visualization of MPD and/or incompletely visualized MPD (p = 0.013). CONCLUSION Patients managed non-operatively had significantly less exocrine and endocrine dysfunction compared to operated patients. Exocrine dysfunction was significantly associated with complete non-visualization of MPD and/or incompletely visualized MPD.
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Vujasinovic M, Makuc J, Tepes B, Marolt A, Kikec Z, Robac N. Impact of a clinical pathway on treatment outcome in patients with acute pancreatitis. World J Gastroenterol 2015; 21:9150-9155. [PMID: 26290642 PMCID: PMC4533047 DOI: 10.3748/wjg.v21.i30.9150] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/18/2015] [Revised: 04/23/2015] [Accepted: 06/15/2015] [Indexed: 02/07/2023] Open
Abstract
AIM To determine the impact of a clinical pathway (CP) on acute pancreatitis (AP) treatment outcome. METHODS A retrospective analysis of medical records was performed. We compared the results of AP treatment outcome over two time periods in our centre, before (2006-2007) and after (2010-2012) the implementation of a CP. The CP comprised the following indicators of quality: performance of all laboratory tests on admission (including lipids and carbohydrate deficient transferrin), determination of AP aetiology, abdomen ultrasound (US) within the first 24 h after admission, contrast-enhanced computed tomography of the abdomen in all cases of suspected pancreatic necrosis, appropriately selected and sufficiently used antibiotic therapy (if necessary), pain control, adequate hydration, control of haemodynamic parameters and transfer to the Intensive Care Unit (ICU) (if necessary), endoscopic retrograde cholangiopancreatography (ERCP) in biliary AP, surgical treatment (if necessary), and advice on outpatient follow-up after discharge. A comparison of the length of stay with that in other Slovenian hospitals was also performed. RESULTS There were 139 patients treated in the three-year period after the introduction of a CP, of which 81 (58.3%) were male and 58 (41.7%) female. The patients' mean age was 59.6 ± 17.3 years. The most common aetiologies were alcoholism and gallstones (38.8% each), followed by unexplained (11.5%), drug-induced, hypertriglyceridemia, post ERCP (2.9% each) and tumours (2.2%). Antibiotic therapy was prescribed in 72 (51.8%) patients. Abdominal US was performed in all patients within the first 24 h after admission. Thirty-two (23.0%) patients were treated in the ICU. Four patients died (2.9%). In comparison to 2006-2007, we found an increased number of alcoholic and biliary AP and an associated decrease in the number of unexplained aetiology cases. The use of antibiotics also significantly decreased after the implementation of a CP (from 70.3% to 51.8%; P = 0.003). There was no statistically significant difference in mortality (1.8% vs 2.9%). The length of stay was significantly shorter when compared to the Slovenian average (P = 0.018). CONCLUSION The introduction of a CP has improved the treatment of patients with AP, as assessed by all of the observed parameters.
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Pezzilli R, Zerbi A, Campra D, Capurso G, Golfieri R, Arcidiacono PG, Billi P, Butturini G, Calculli L, Cannizzaro R, Carrara S, Crippa S, De Gaudio R, De Rai P, Frulloni L, Mazza E, Mutignani M, Pagano N, Rabitti P, Balzano G. Consensus guidelines on severe acute pancreatitis. Dig Liver Dis 2015; 47:532-543. [PMID: 25921277 DOI: 10.1016/j.dld.2015.03.022] [Citation(s) in RCA: 107] [Impact Index Per Article: 10.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/02/2015] [Revised: 03/17/2015] [Accepted: 03/24/2015] [Indexed: 02/07/2023]
Abstract
This Position Paper contains clinically oriented guidelines by the Italian Association for the Study of the Pancreas (AISP) for the diagnosis and treatment of severe acute pancreatitis. The statements were formulated by three working groups of experts who searched and analysed the most recent literature; a consensus process was then performed using a modified Delphi procedure. The statements provide recommendations on the most appropriate definition of the complications of severe acute pancreatitis, the diagnostic approach and the timing of conservative as well as interventional endoscopic, radiological and surgical treatments.
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Vujasinovic M, Tepes B, Makuc J, Rudolf S, Zaletel J, Vidmar T, Seruga M, Birsa B. Pancreatic exocrine insufficiency, diabetes mellitus and serum nutritional markers after acute pancreatitis. World J Gastroenterol 2014; 20:18432-18438. [PMID: 25561813 PMCID: PMC4277983 DOI: 10.3748/wjg.v20.i48.18432] [Citation(s) in RCA: 34] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/25/2014] [Revised: 06/22/2014] [Accepted: 08/13/2014] [Indexed: 02/07/2023] Open
Abstract
AIM To investigate impairment and clinical significance of exocrine and endocrine pancreatic function in patients after acute pancreatitis (AP). METHODS Patients with AP were invited to participate in the study. Severity of AP was determined by the Atlanta classification and definitions revised in 2012. Pancreatic exocrine insufficiency (PEI) was diagnosed by the concentration of fecal elastase-1. An additional work-up, including laboratory testing of serum nutritional markers for determination of malnutrition, was offered to all patients with low levels of fecal elastase-1 FE. Hemoglobin A1c or oral glucose tolerance tests were also performed in patients without prior diabetes mellitus, and type 3c diabetes mellitus (T3cDM) was diagnosed according to American Diabetes Association criteria. RESULTS One hundred patients were included in the study: 75% (75/100) of patients had one attack of AP and 25% (25/100) had two or more attacks. The most common etiology was alcohol. Mild, moderately severe and severe AP were present in 67, 15 and 18% of patients, respectively. The mean time from attack of AP to inclusion in the study was 2.7 years. PEI was diagnosed in 21% (21/100) of patients and T3cDM in 14% (14/100) of patients. In all patients with PEI, at least one serologic nutritional marker was below the lower limit of normal. T3cDM was more frequently present in patients with severe AP (P = 0.031), but was also present in some patients with mild and moderately severe AP. PEI was present in all degrees of severity of AP. There were no statistically significantly differences according to gender, etiology and number of AP attacks. CONCLUSION As exocrine and endocrine pancreatic insufficiency can develop after AP, routine follow-up of patients is necessary, for which serum nutritional panel measurements can be useful.
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Vipperla K, Papachristou GI, Easler J, Muddana V, Slivka A, Whitcomb DC, Yadav D. Risk of and factors associated with readmission after a sentinel attack of acute pancreatitis. Clin Gastroenterol Hepatol 2014; 12:1911-9. [PMID: 24815327 DOI: 10.1016/j.cgh.2014.04.035] [Citation(s) in RCA: 65] [Impact Index Per Article: 5.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/09/2014] [Revised: 04/27/2014] [Accepted: 04/29/2014] [Indexed: 02/07/2023]
Abstract
BACKGROUND & AIMS Few data are available on how many patients are readmitted to the hospital after attacks of acute pancreatitis. We aimed to determine the risk and factors that determine early (within 30 days) and late (after 30 days) readmission of patients with acute pancreatitis. METHODS In a retrospective study, we collected and analyzed data on 127 surviving patients (median age, 53 y; 52% male; 83% white) hospitalized at the University of Pittsburgh Medical Center for a sentinel attack of acute pancreatitis, enrolled in the Severe Acute Pancreatitis Study from June 2003 through April 2010, and who had follow-up data. Information was collected on demographics, clinical profile, risk score at discharge (based on a recently developed scoring system), and details of readmissions during the follow-up period (median, 36 mo). RESULTS Of the 127 patients, 52% were transfers from another care center and 32% required admission to the intensive care unit. Etiologies for pancreatitis were biliary (47%), idiopathic (13%), alcohol associated (12%), and others (28%). Pancreatic necrosis (28%), persistent organ failure (27%), and peripancreatic fluid collections (19%) were common. The median length of stay was 9 days. A total of 108 readmissions occurred for 43 patients (34%). Early readmissions (n = 21) occurred more frequently for patients with smoldering (ongoing) symptoms or local complications than for those without. Late readmissions (n = 22) occurred more frequently for patients with recurrent pancreatitis than for those without. Male sex, alcohol-associated disease, and severe disease increased the risks of readmission and recurrence. The risk for readmission was lower among nontransferred patients (23%) and patients without necrosis or organ failure (16%). Risk for readmission increased with the number of points on the weighted scoring system. CONCLUSIONS Approximately one-third of patients hospitalized for acute pancreatitis are readmitted, usually as a result of smoldering symptoms, local complications, or recurrent attacks. Studies are needed to determine whether individualized discharge planning, with consideration of the etiology of acute pancreatitis, can reduce the risk for readmission.
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Affiliation(s)
- Kishore Vipperla
- Division of Gastroenterology and Hepatology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
| | - Georgios I Papachristou
- Division of Gastroenterology and Hepatology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
| | - Jeffrey Easler
- Division of Gastroenterology and Hepatology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
| | - Venkata Muddana
- Division of Gastroenterology and Hepatology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
| | - Adam Slivka
- Division of Gastroenterology and Hepatology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
| | - David C Whitcomb
- Division of Gastroenterology and Hepatology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
| | - Dhiraj Yadav
- Division of Gastroenterology and Hepatology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
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Nasogastric nutrition is efficacious in severe acute pancreatitis: a systematic review and meta-analysis. Br J Nutr 2014; 112:1769-78. [DOI: 10.1017/s0007114514002566] [Citation(s) in RCA: 32] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
In patients with severe acute pancreatitis (AP), enteral nutrition is delivered by nasojejunal (NJ) tube to minimise pancreatic stimulation. Nasogastric (NG) feeding represents an alternative route. The primary objective of this systematic review and meta-analysis was to evaluate the efficacy of NG feeding. Secondary objectives were to compare the NG and NJ routes and assess the side effects of the former. The primary endpoint was exclusive NG feeding with delivery of 75 % of nutritional targets. Additional outcomes included change to total parenteral nutrition (TPN), increased pain or disease severity, vomiting, diarrhoea, delivery rate reduction and tube displacement. Among the retrieved studies, six were found to be eligible for the qualitative review and four for the meta-analysis. NG nutrition was received by 147 patients; exclusive NG feeding was achieved in 90 % (133/147). Of the 147 patients, 129 (87 %) received 75 % of the target energy. In studies where all subjects received exclusive NG nutrition, 82 % (seventy-four of the ninety patients) received >75 % of the intended energy. Compared with NJ nutrition, there was no significant difference in the delivery of 75 % of nutritional targets (pooled risk ratio (RR) 1·02; 95 % CI 0·75, 1·38.) or no increased risk of change to TPN (pooled RR 1·05; 95 % CI 0·45, 2·48), diarrhoea (pooled RR 1·28; 95 % CI 0·62, 2·66), exacerbation of pain (pooled RR 1·10; 95 % CI 0·47, 2·61) or tube displacement (pooled RR 0·44; 95 % CI 0·11, 1·73). Vomiting and diarrhoea were the most common side effects of NG feeding (13·3 and 12·9 %, respectively). With respect to the delivery of nutrition, 11·2 % of the patients required delivery rate reduction and 3·4 % dislodged the tube. Other side effects included elevated levels of aspirates (9·1 %), abdominal distension (1·5 %), pain exacerbation (7·5 %) and increased disease severity (1·6 %). In conclusion, NG feeding is efficacious in 90 % of patients. Further research is required to optimise the delivery of NG nutrition and examine ‘gut-rousing’ approaches to nutrition in patients with severe AP.
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Early oral refeeding based on hunger in moderate and severe acute pancreatitis: a prospective controlled, randomized clinical trial. Nutrition 2014; 31:171-5. [PMID: 25441594 DOI: 10.1016/j.nut.2014.07.002] [Citation(s) in RCA: 55] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/22/2014] [Revised: 06/16/2014] [Accepted: 07/08/2014] [Indexed: 02/05/2023]
Abstract
OBJECTIVE Early enteral nutrition is beneficial for acute pancreatitis (AP), but the optimal timing and criteria remain unclear. The aim of this study was to explore the feasibility and safety of early oral refeeding (EORF) based on hunger in patients with moderate or severe AP. METHODS In a prospective, single-center, controlled, randomized clinical trial (ChiCTR-TRC-12002994), eligible patients with moderate or severe AP were randomized to either EORF or conventional oral refeeding (CORF). Patients in the EORF group restarted an oral diet when they felt hungry, regardless of laboratory parameters. Those in the CORF group restarted an oral diet only when clinical and laboratory symptoms had resolved. Clinical outcomes were compared between the two groups. RESULTS In all, 146 eligible patients with moderate or severe AP were included and randomized to the EORF (n = 70) or CORF (n = 76) group. There were eight dropouts after randomization (three in EORF group; five in CORF group). The groups had similar baseline characteristics. The total length of hospitalization (13.7 ± 5.4 d versus 15.7 ± 6.2 d; P = 0.0398) and duration of fasting (8.3 ± 3.9 d versus 10.5 ± 5.1 d; P = 0.0047) were shorter in the EORF group than in the CORF group. There was no difference in the number of adverse events or complications between the two groups. The mean blood glucose level after oral refeeding was higher in the EORF group than in the CORF group (P = 0.0030). CONCLUSIONS This controlled, randomized clinical trial confirmed the effectiveness and feasibility of EORF based on hunger in patients with moderate or severe AP. EORF could shorten the length of hospitalization in patients with moderate or severe AP.
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Zeng YB, Zhan XB, Guo XR, Zhang HG, Chen Y, Cai QC, Li ZS. Risk factors for pancreatic infection in patients with severe acute pancreatitis: an analysis of 163 cases. J Dig Dis 2014; 15:377-85. [PMID: 24720587 DOI: 10.1111/1751-2980.12150] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
OBJECTIVE We aimed to identify the risk factors for predicting pancreatic infection in patients with severe acute pancreatitis (SAP). METHODS In all, 163 patients with SAP were included and divided into two groups based on the presence or absence of pancreatic infection. Their demographic and clinical characteristics, laboratory examination results, complications and treatment modalities were collected from their medical records. Variables were initially screened by univariate analysis and those with statistical significance were then filtered by multivariate analysis to determine the independent risk factors for pancreatic infection in SAP. RESULTS Patients having SAP with pancreatic infection had a lower partial pressure of arterial carbon dioxide (PaCO2 ), peripheral white blood cell count and alkaline phosphatase levels, together with a higher computed tomography severity index (CTSI) than those without pancreatic infection, while their lactate dehydrogenase (LDH) levels and blood urea nitrogen were much higher. Pancreatic infection was also more common in patients receiving late fluid resuscitation than in those receiving early fluid resuscitation. Multivariate analyses revealed that increased LDH level, high CTSI, delayed fluid resuscitation and hypoxemia were independent risk factors for pancreatic infection in SAP. The sensitivity, specificity, positive and negative predictive values for a model combining the parameters in predicting pancreatic infection were 84%, 97%, 88% and 96%, respectively, with a cut-off value of 0.393, and the area under the receiver operating characteristic curve was 0.923. CONCLUSION Increased LDH, high CTSI, delayed fluid resuscitation and hypoxemia are independent risk factors for predicting pancreatic infection in patients with SAP.
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Affiliation(s)
- Yan Bo Zeng
- Department of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, China
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Abstract
OBJECTIVE This study aimed to evaluate the burden and pattern of pancreatitis-related readmissions after index hospitalization for acute pancreatitis (AP). METHODS We identified all unique white or black Allegheny County residents with first hospital admission for AP from 1996 to 2005 using the Pennsylvania Health Care Cost Containment Council data set. The final study population consisted of patients (n = 6010) who survived index admission and had follow-up data on readmissions. The etiology was determined using associated diagnosis codes. We analyzed pancreatitis-related readmissions until the third quarter of 2007 (median follow-up time, 39 months). RESULTS The absolute risk and total burden of readmissions were 21.9% and 2947 for primary AP, respectively, 5.8% and 812 for primary chronic pancreatitis (CP), respectively, and 32.3% and 6612 for any pancreatitis diagnosis, respectively. Patients with alcohol etiology (etiology on index admission in 20.3%; responsible for 41.6%-50.4% readmissions) and subsequent diagnosis of CP (any CP diagnosis, 12.8%; responsible for 73% readmissions) accounted for a disproportionately higher fraction of readmissions. Readmission risk decreased with increasing age. A small fraction of patients accounted for most readmissions. CONCLUSIONS Readmission after AP is influenced by demographics, etiology, and subsequent CP diagnosis. Future studies should focus on understanding the factors driving readmissions in high-risk individuals to develop strategies for reducing pancreatitis-related readmissions and health care costs.
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Das SLM, Singh PP, Phillips ARJ, Murphy R, Windsor JA, Petrov MS. Newly diagnosed diabetes mellitus after acute pancreatitis: a systematic review and meta-analysis. Gut 2014; 63:818-31. [PMID: 23929695 DOI: 10.1136/gutjnl-2013-305062] [Citation(s) in RCA: 272] [Impact Index Per Article: 24.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
BACKGROUND Diabetes mellitus (DM) is common in the general population and it poses a heavy burden to society in the form of long-term disability, healthcare use and costs. The pancreas is a key player in glucose homeostasis, but the occurrence of newly diagnosed DM after acute pancreatitis (AP), the most frequent disease of the pancreas, has never been assessed systematically. The aim of this study was to conduct a systematic literature review to determine the prevalence and time course of DM and related conditions after the first attack of AP as well as the impact of covariates. METHODS Relevant literature cited in three electronic databases (Scopus, EMBASE and MEDLINE) was reviewed independently by two authors. The main outcome measures studied were newly diagnosed prediabetes, DM, or DM treated with insulin. Pooled prevalence and 95% CIs were calculated for all outcomes. RESULTS A total of 24 prospective clinical studies, involving 1102 patients with first episode of AP, met all the eligibility criteria. Prediabetes and/or DM was observed in 37% (95% CI 30% to 45%) individuals after AP. The pooled prevalence of prediabetes, DM and treatment with insulin after AP was 16% (95% CI 9% to 24%), 23% (95% CI 16% to 31%), and 15% (95% CI 9% to 21%), respectively. Newly diagnosed DM developed in 15% of individuals within 12 months after first episode of AP and the risk increased significantly at 5 years (relative risk 2.7 (95% CI 1.9 to 3.8)). A similar trend was observed with regard to treatment with insulin. The severity of AP, its aetiology, individuals' age and gender had minimal effect on the studied outcomes. CONCLUSIONS Patients with AP often develop prediabetes and/or DM after discharge from hospital, and have a greater than twofold increased risk of DM over 5 years. Further studies are warranted to determine the optimal strategy for its detection and whether the risk of developing DM after AP can be reduced.
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Affiliation(s)
- Stephanie L M Das
- Department of Surgery, The University of Auckland, , Auckland, New Zealand
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Nutrition, inflammation, and acute pancreatitis. ISRN INFLAMMATION 2013; 2013:341410. [PMID: 24490104 PMCID: PMC3893749 DOI: 10.1155/2013/341410] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 09/10/2013] [Accepted: 10/30/2013] [Indexed: 12/14/2022]
Abstract
Acute pancreatitis is acute inflammatory disease of the pancreas. Nutrition has a number of anti-inflammatory effects that could affect outcomes of patients with pancreatitis. Further, it is the most promising nonspecific treatment modality in acute pancreatitis to date. This paper summarizes the best available evidence regarding the use of nutrition with a view of optimising clinical management of patients with acute pancreatitis.
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Garip G, Sarandöl E, Kaya E. Effects of disease severity and necrosis on pancreatic dysfunction after acute pancreatitis. World J Gastroenterol 2013; 19:8065-8070. [PMID: 24307801 PMCID: PMC3848155 DOI: 10.3748/wjg.v19.i44.8065] [Citation(s) in RCA: 40] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/28/2013] [Revised: 07/03/2013] [Accepted: 09/17/2013] [Indexed: 02/06/2023] Open
Abstract
AIM: To evaluate the effects of disease severity and necrosis on organ dysfunctions in acute pancreatitis (AP).
METHODS: One hundred and nine patients treated as AP between March 2003 and September 2007 with at least 6 mo follow-up were included. Patients were classified according to severity of the disease, necrosis ratio and localization. Subjective clinical evaluation and fecal pancreatic elastase-I (FPE-I) were used for exocrine dysfunction evaluation, and oral glucose tolerance test was completed for endocrine dysfunction. The correlation of disease severity, necrosis ratio and localization with exocrine and endocrine dysfunction were investigated.
RESULTS: There were 58 male and 51 female patients, and mean age was 56.5 ± 15.7. Of the patients, 35.8% had severe AP (SAP) and 27.5% had pancreatic necrosis. Exocrine dysfunction was identified in 13.7% of the patients [17.9% were in SAP, 11.4% were in mild AP (MAP)] and 34.7% of all of the patients had endocrine dysfunction (56.4% in SAP and 23.2% in MAP). In patients with SAP and necrotizing AP (NAP), FPE-Ilevels were lower than the others (P < 0.05 and 0.001 respectively) and in patients having pancreatic head necrosis or near total necrosis, FPE-1 levels were lower than 200 μg/g stool. Forty percent of the patients who had undergone necrosectomy developed exocrine dysfunction. Endocrine dysfunction was more significant in patients with SAP and NAP (P < 0.001). All of the patients in the necrosectomy group had endocrine dysfunction.
CONCLUSION: Patients with SAP, NAP, pancreatic head necrosis and necrosectomy should be followed for pancreatic functions.
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Abstract
PURPOSE OF REVIEW Enteral nutrition has emerged as one of the most effective treatments in the early management of patients with acute pancreatitis. The original rationale for nutrition in acute pancreatitis, dating back to the mid-20th century, was to provide full nutritional requirements but avoid stimulating exocrine pancreatic secretion. The purpose of this article is to review the recent clinical studies of enteral nutrition in acute pancreatitis to revise the rationale and develop a contemporary conceptual framework for nutritional management of this disease. RECENT FINDINGS Several recent randomized controlled trials dispel the outdated concept of 'pancreatic rest', which equates with gut neglect, and offer 'gut rousing' as a preferred concept. The new concept postulates that gastrointestinal (dys)function has a discernible impact on the outcomes of patients with acute pancreatitis. Further, timely administration of appropriate intraluminal modalities prevents or mitigates the gastrointestinal dysfunction. SUMMARY Nutritional management in acute pancreatitis should aim primarily at maintaining the gastrointestinal function. Providing full nutritional requirements and avoiding pancreatic exocrine stimulation should be considered as secondary aims.
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Affiliation(s)
- Maxim S Petrov
- Department of Surgery, The University of Auckland, Auckland, New Zealand.
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[Nutritional therapy in acute pancreatitis]. Med Klin Intensivmed Notfmed 2013; 108:401-7. [PMID: 23681278 DOI: 10.1007/s00063-012-0202-2] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/30/2013] [Accepted: 04/17/2013] [Indexed: 01/18/2023]
Abstract
Acute pancreatitis is a frequent clinical entity in the West. About 80% of patients with acute pancreatitis develop edematous pancreatitis, while 20% develop necrotizing pancreatitis: The latter is a potentially life-threatening disease. In this case, early enteral nutrition has been shown to improve the course of the disease. Usually, gastric enteral nutrition with a polymeric formula via a nasogastric tube is possible; only in a minority of patients is jejunal feeding necessary owing to the high gastric residual volume. An elemental formula is useful for patients with significant intestinal maldigestion. If enteral feeding is not feasible within 5-7 days, (additional) parenteral nutrition has to be considered. Individualized--primary enteral--nutritional support is an essential part of a multimodal therapy in severe acute pancreatitis and it improves clinical outcome.
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Mansfield C. Pathophysiology of acute pancreatitis: potential application from experimental models and human medicine to dogs. J Vet Intern Med 2012; 26:875-87. [PMID: 22676262 DOI: 10.1111/j.1939-1676.2012.00949.x] [Citation(s) in RCA: 52] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/14/2011] [Revised: 04/05/2012] [Accepted: 04/24/2012] [Indexed: 12/18/2022] Open
Abstract
The cellular events leading to pancreatitis have been studied extensively in experimental models. Understanding the cellular events and inciting causes of the multisystem inflammatory cascades that are activated with this disease is of vital importance to advance diagnosis and treatment of this condition. Unfortunately, the pathophysiology of pancreatitis in dogs is not well understood, and extrapolation from experimental and human medicine is necessary. The interplay of the inflammatory cascades (kinin, complement, cytokine) is extremely complex in both initiating leukocyte migration and perpetuating disease. Recently, nitric oxide (NO) and altered microcirculation of the pancreas have been proposed as major initiators of inflammation. In addition, the role of the gut is becoming increasingly explored as a cause of oxidative stress and potentiation of systemic inflammation in pancreatitis.
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Affiliation(s)
- Caroline Mansfield
- Faculty of Veterinary Science, The University of Melbourne, Werribee, Vic., Australia.
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