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Ramsey ML, Heald B, Gokun Y, Baker J, Groce JR, Han S, Hart PA, Krishna SG, Lara LF, Lee PJ, Papachristou GI, Pearlman R, Poll S, Roberts ME, Stanich PP. Germline multigene panel testing in acute and chronic pancreatitis. PLoS One 2024; 19:e0307076. [PMID: 39172977 PMCID: PMC11341018 DOI: 10.1371/journal.pone.0307076] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/17/2024] [Accepted: 06/29/2024] [Indexed: 08/24/2024] Open
Abstract
BACKGROUND/OBJECTIVES Germline genetic testing is recommended for younger patients with idiopathic pancreatitis but there has been a lack of consensus in recommendations for those over age 35. We aimed to analyze the results of genetic testing among subjects of varying ages. METHODS Individuals who underwent germline multigene testing for pancreatitis susceptibility genes (CASR, CFTR, CPA1, CTRC, PRSS1, SPINK1) through a large commercial laboratory between 2017 and 2022 were included. Test results and information collected from test requisition forms were evaluated. Multivariable logistic regression models were performed to identify factors associated with a positive pancreatitis panel (pathogenic, likely pathogenic, and/or increased risk variants) in pancreatitis-related genes. RESULTS Overall, 2,468 subjects with primary indication of acute pancreatitis (AP) (n = 401), chronic pancreatitis (CP) (n = 631), pancreatic cancer (n = 128), or other indications (n = 1,308) completed germline testing. Among patients with AP or CP, the prevalence of any positive result for those <35 versus ≥35 years of age was 32.1% and 24.5% (p = 0.007), and the prevalence of a clinically meaningful result was 10.8% and 5.4%, respectively (p = 0.001). Positive family history of pancreatitis was associated with increased odds ratio (OR) of 8.59 (95% confidence interval (CI) 2.92-25.25) for a clinically significant panel result while each 5-year increase in age at test completion had lower odds (OR 0.89, 95% CI 0.83-0.95). CONCLUSIONS The highest prevalence of pathogenic variants is seen in younger individuals with a positive family history of pancreatitis. However, clinically meaningful results are identified in older subjects, suggesting that genetic counseling and testing should be considered for all age groups.
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Affiliation(s)
- Mitchell L. Ramsey
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Brandie Heald
- Medical Affairs, Invitae Corporation, San Francisco, California, United States of America
| | - Yevgeniya Gokun
- Department of Biomedical Informatics, Center for Biostatistics, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Josie Baker
- Division of Human Genetics, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - J. Royce Groce
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Samuel Han
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Phil A. Hart
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Somashekar G. Krishna
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Luis F. Lara
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Peter J. Lee
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Georgios I. Papachristou
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Rachel Pearlman
- Division of Human Genetics, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Sarah Poll
- Medical Affairs, Invitae Corporation, San Francisco, California, United States of America
| | - Maegan E. Roberts
- Division of Human Genetics, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
| | - Peter P. Stanich
- Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States of America
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Panchoo AV, VanNess GH, Rivera-Rivera E, Laborda TJ. Hereditary pancreatitis: An updated review in pediatrics. World J Clin Pediatr 2022; 11:27-37. [PMID: 35096544 PMCID: PMC8771313 DOI: 10.5409/wjcp.v11.i1.27] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/31/2021] [Revised: 08/08/2021] [Accepted: 11/28/2021] [Indexed: 02/06/2023] Open
Abstract
Hereditary Pancreatitis (HP) has emerged as a significant cause of acute, acute recurrent and chronic pancreatitis in the pediatric population. Given that it presents similarly to other causes of pancreatitis, a positive family history and/or isolation of a gene mutation are vital in its designation. Inheritance patterns remain complex, but mutations involving the PRSS1, SPINK1, CFTR and CTRC genes are commonly implicated. Since being first described in 1952, dozens of genetic alterations that modify the action of pancreatic enzymes have been identified. Among children, these variants have been isolated in more than 50% of patients with chronic pancreatitis. Recent research has noted that such mutations in PRSS1, SPINK1 and CFTR genes are also associated with a faster progression from acute pancreatitis to chronic pancreatitis. Patients with HP are at increased risk of developing diabetes mellitus, exocrine pancreatic insufficiency, and pancreatic adenocarcinoma. Management follows a multi-disciplinary approach with avoidance of triggers, surveillance of associated conditions, treatment of pancreatic insufficiency and use of endoscopic and surgical interventions for complications. With significant sequela, morbidity and a progressive nature, a thorough understanding of the etiology, pathophysiologic mechanisms, diagnostic evaluation, current management strategies and future research considerations for this evolving disease entity in pediatrics is warranted.
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Affiliation(s)
- Arvind Vasant Panchoo
- Division of Gastroenterology, Hepatology and Nutrition, The Children’s Hospital of San Antonio, San Antonio, TX 78207, United States
- Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, United States
| | - Grant H VanNess
- Faculty of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, United States
| | - Edgardo Rivera-Rivera
- Department of Pediatric Gastroenterology, Parkview Health, Fort Wayne, IN 46845, United States
| | - Trevor J Laborda
- Division of Gastroenterology, Hepatology and Nutrition, The Children’s Hospital of San Antonio, San Antonio, TX 78207, United States
- Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, United States
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Abstract
Hereditary pancreatitis (HP) is a rare inherited chronic pancreatitis (CP) with strong genetic associations, with estimated prevalence ranging from 0.3 to 0.57 per 100,000 across Europe, North America, and East Asia. Apart from the most well-described genetic variants are PRSS1, SPINK1, and CFTR, many other genes, such as CTRC, CPA1, and CLDN2 and CEL have been found to associate with HP, typically in one of the 3 main mechanisms such as altered trypsin activity, pancreatic ductal cell secretion, and calcium channel regulation. The current mainstay of management for patients with HP comprises genetic testing for eligible individuals and families, alcohol and tobacco cessation avoidance, pain control, and judicious screening for complications, including exocrine and endocrine insufficiency and pancreatic cancer.
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Affiliation(s)
- Yichun Fu
- Henry D. Janowitz Division of Gastroenterology, One Gustave L. Levy Place, Box 1069, New York, NY 10029, USA; Samuel Bronfman Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, USA
| | - Aimee L Lucas
- Henry D. Janowitz Division of Gastroenterology, One Gustave L. Levy Place, Box 1069, New York, NY 10029, USA; Samuel Bronfman Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, USA.
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Noor MT, Sudan R, Goyal V, Kosta S, Kumar R, Singh Thakur B. PREVALENCE OF SPINK 1 AND CASR GENE MUTATIONS IN ACUTE AND RECURRENT ACUTE PANCREATITIS : A STUDY FROM CENTRAL INDIA. INDIAN JOURNAL OF APPLIED RESEARCH 2021:62-65. [DOI: 10.36106/ijar/2508292] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 09/01/2023]
Abstract
Background: Genetic factors may play an important role in the pathogenesis of acute pancreatitis. It has been observed
in various studies that the presence of risk factors alone like alcohol abuse or gall bladder stones does not lead to attacks of
pancreatitis in all the patients. This leads to assumption that genetic factors may decrease the threshold for the development of pancreatitis in
presence of one or more risk factors. We observed that there is a paucity of data regarding the role of genetics in acute pancreatitis (AP) and
recurrent acute pancreatitis (RAP) in our part of the world and we aimed at studying the prevalence of genetic mutations in such patients.
Methods: Our study intended to nd the prevalence of SPINK1 N34S (Serine protease inhibitor kazal type 1) and CaSR (Calcium sensing
receptor) gene mutations in patients of AP and RAP. A total of 50 patients and 25 age and gender matched controls entered our study. Blood
samples were obtained from all the cases and controls for routine investigations and genetic analysis. SPINK 1 N34S and CaSR gene mutation
studies were done in all the patients and controls.
Results: Alcohol (64%) followed by gallbladder stone disease (20%) was the most common aetiology of pancreatitis. SPINK 1 N34S mutation
was present in 21 patients and 2 controls whereas CaSR gene mutation was present in 13 patients and 2 controls. Patients with SPINK 1 N34S and
CaSR gene mutations were younger than the patients without these mutations. Prevalence of both SPINK1 N34S and CaSR gene mutations was
higher in patients of RAP than AP. These mutations were not associated with aetiology or severity of pancreatitis.
Conclusion: The prevalence SPINK 1 N34S and CaSR gene mutations was higher in patients of AP and RAP. Identication of these mutations
in patients of AP can help in the identication of patients who are at increased risk of recurrent attacks of AP
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Affiliation(s)
- Mohd Talha Noor
- MD, DM, Department of Gastroenterology, Sri Aurobindo Medical College and Postgraduate Institute, Indore-Ujjain State Highway, Indore, Madhya Pradesh, India453555
| | - Rahul Sudan
- MD, Department of Gastroenterology, Sri Aurobindo Medical College and Postgraduate Institute, Indore-Ujjain State Highway, Indore, Madhya Pradesh, India453555
| | - Vipin Goyal
- MD, DM, Department of Gastroenterology, Sri Aurobindo Medical College and Postgraduate Institute, Indore-Ujjain State Highway, Indore, Madhya Pradesh, India453555
| | - Susmit Kosta
- PhD, Molecular Medicine Lab, Sri Aurobindo Medical College and Postgraduate Institute, Indore-Ujjain State Highway, Indore, Madhya Pradesh, India-453555
| | - Ravindra Kumar
- PhD, Molecular Medicine Lab, Sri Aurobindo Medical College and Postgraduate Institute, Indore-Ujjain State Highway, Indore, Madhya Pradesh, India-453555
| | - Bhagwan Singh Thakur
- MD, DM, Department of Gastroenterology, Sri Aurobindo Medical College and Postgraduate Institute, Indore-Ujjain State Highway, Indore, Madhya Pradesh, India453555
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Genetic Abnormalities in Pancreatitis: An Update on Diagnosis, Clinical Features, and Treatment. Diagnostics (Basel) 2020; 11:diagnostics11010031. [PMID: 33375361 PMCID: PMC7824215 DOI: 10.3390/diagnostics11010031] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/04/2020] [Revised: 12/12/2020] [Accepted: 12/22/2020] [Indexed: 02/07/2023] Open
Abstract
Several pancreatitis susceptibility genes have been identified to date. A relationship between a mutation in the cationic trypsinogen (protease serine 1, PRSS1) gene and hereditary pancreatitis (HP) was first identified in 1996. Currently, HP has been defined as either two or more individuals within a family exhibiting pancreatitis for two or more generations, or pancreatitis linked to mutation of the PRSS1 gene. In 2000, a mutation in the serine protease inhibitor gene (Kazal type 1: SPINK1) was reported to be related to sporadic pancreatitis of unknown etiology. This paper reviews and summarizes the current published data on the pancreatitis susceptibility genes, mainly PRSS1 and SPINK1 genes, and introduces a diagnostic and therapeutic approach for dealing with patients with these gene mutations. Patients with these genetic predispositions, both children and adults, have often been initially diagnosed with idiopathic acute pancreatitis, in approximately 20-50% of pediatric cases and 28-80% of adult cases. In such patients, where the etiology is unknown, genetic testing, which requires pre-test and post-test genetic counselling, may prove helpful. Patients with chronic pancreatitis (CP) due to SPINK1 gene mutation and HP patients have a potentially high risk of pancreatic exocrine insufficiency, diabetes mellitus, and, of particular importance, pancreatic cancer. Thus, these patients require careful long-term follow-up and management. Specifically, symptomatic CP patients often need endoscopic therapy or surgery, often following a step-up approach beginning with endoscopic therapy and progressing to surgery if necessary, which is similar to the therapeutic approach for patients with CP due to other etiologies. It is important that clinicians are aware of the characteristics of patients with pancreatitis susceptibility genetic abnormalities.
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Makaya T, Ali A, Basu S. Rare and unexpected cause of diabetes in a teenager. Arch Dis Child Educ Pract Ed 2020; 105:358-360. [PMID: 30894368 DOI: 10.1136/archdischild-2018-315857] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/09/2018] [Revised: 01/28/2019] [Accepted: 01/28/2019] [Indexed: 11/04/2022]
Affiliation(s)
- Taffy Makaya
- Department of Paediatric Endocrinology, Oxford University Hospitals NHS trust Foundation Trust, Oxford, Oxfordshire, UK
| | - Aishatu Ali
- Department of Paediatric Endocrinology, Oxford University Hospitals NHS Foundation Trust, Oxford, Oxfordshire, UK
| | - Supriyo Basu
- Department of Paediatric Endocrinology, Oxford University Hospitals NHS Foundation Trust, Oxford, Oxfordshire, UK
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Müller R, Aghdassi AA, Kruse J, Lerch MM, Simon P, Salloch S. Perceptions of genetic testing in patients with hereditary chronic pancreatitis and their families: a qualitative triangulation. Eur J Hum Genet 2020; 29:29-38. [PMID: 32788661 PMCID: PMC7852527 DOI: 10.1038/s41431-020-00705-9] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/30/2020] [Revised: 07/16/2020] [Accepted: 07/21/2020] [Indexed: 12/13/2022] Open
Abstract
Hereditary chronic pancreatitis (HCP) is a genetically determined condition characterized by intermittent acute episodes of pancreatitis and long-term impairment of the exocrine and endocrine pancreatic functions. Genetic test results can have substantial psychological and social consequences for the individuals tested and their families. Nevertheless, little is known so far about the subjective experience of individuals genetically tested for HCP. This qualitative study examines the viewpoints of HCP patients and their relatives in order to identify the psychosocial and ethical implications related to genetic testing within families. Semi-structured qualitative individual interviews and a focus group with HCP patients and their family members were conducted. Data were audio-recorded, transcribed verbatim and analysed using qualitative content analysis. A total of 28 individuals were enrolled in the study: 24 individuals (17 patients, 7 relatives) were interviewed in semi-structured one-on-one interviews and 4 individuals (2 patients, 2 life partners) participated in the focus group. Emerging topics covered (1) genetic testing in childhood, (2) genetic testing within the family and (3) family planning. The study reveals that genetic testing for HCP has a wide influence in familial contexts and is accompanied by normative issues, such as autonomy, reproductive decisions and sharing of information within the family. The results raise the awareness of the complexity of family contexts: familial relationships and dynamics can have great influence on the individual decisions related to genetic testing. Increased understanding of these relational contexts can help health professionals, for example, in counselling, to discuss genetic testing better with patients and families.
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Affiliation(s)
- Regina Müller
- Institute of Ethics and History of Medicine, University of Tübingen, Gartenstraße 47, 72074, Tübingen, Germany.
| | - Ali A Aghdassi
- Department of Medicine A, University Medicine Greifswald, Ferdinand-Sauerbruch-Straße, 17475, Greifswald, Germany
| | - Judith Kruse
- Institute of Ethics and History of Medicine, University Medicine Greifswald, Ellernholzstr. 1-2, 17487, Greifswald, Germany
| | - Markus M Lerch
- Department of Medicine A, University Medicine Greifswald, Ferdinand-Sauerbruch-Straße, 17475, Greifswald, Germany
| | - Peter Simon
- Department of Medicine A, University Medicine Greifswald, Ferdinand-Sauerbruch-Straße, 17475, Greifswald, Germany
| | - Sabine Salloch
- Institute of History, Ethics and Philosophy of Medicine, Hannover Medical School, Carl-Neuberg-Str. 1, 30625, Hannover, Germany
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8
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Abstract
Individuals with acute recurrent and chronic pancreatitis may have an inherited predisposition to the development of the disease. Pancreatitis in the setting of a significant family history of the disease can be classified as hereditary or familial pancreatitis. In this article, the authors closely examine the specific genes implicated in pancreatitis, investigate the role of genetic testing for diagnosis, and describe the impact of genetic testing results on clinical management.
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Affiliation(s)
- Aws Hasan
- Department of Internal Medicine, Columbia University Medical Center, 630 West 168 Street, New York, NY, 10032, USA
| | - Dagmara I Moscoso
- Division of Digestive and Liver Diseases, Columbia University Medical Center, 630 West 168 Street, New York, NY, 10032, USA
| | - Fay Kastrinos
- Division of Digestive and Liver Diseases, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, 161 Fort Washington Avenue, Suite 862, New York, NY 10032, USA.
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9
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Metastatic Pancreatic Adenocarcinoma in a Patient With Chronic Calcific Pancreatitis and a Heterozygous SPINK1 c.194+2T>C Mutation. Pancreas 2018. [PMID: 29521951 DOI: 10.1097/mpa.0000000000001015] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
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10
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Abstract
Hereditary pancreatitis (HP) is a rare cause of acute, recurrent acute, and chronic pancreatitis. It may present similarly to other causes of acute and chronic pancreatitis, and often there has been a protracted evaluation prior to the diagnosis of HP. Since it was first described in 1952, multiple genetic defects that affect the action of digestive enzymes in the pancreas have been implicated. The most common mutations involve the PRSS1, CFTR, SPINK1, and CTRC genes. New mutations in these genes and previously unrecognized mutations in other genes are being discovered due to the increasing use of next-generation genomic sequencing. While the inheritance pathways of these genetic mutations may be variable and complex, sometimes involving coinheritance of other mutations, the clinical presentation of patients tends to be similar. Interactions with environmental triggers often play a role. Patients tend to present at an early age (prior to the second decade of life) and have a significantly increased risk for the development of pancreatic adenocarcinoma. Patients with HP may develop sequelae of chronic pancreatitis such as strictures and fluid collections as well as exocrine and endocrine insufficiency. Management of patients with HP involves avoidance of environmental triggers, surveillance for pancreatic adenocarcinoma, medical therapy for endocrine and exocrine insufficiency, pain management, and endoscopic or surgical treatment for complications. Care for affected patients should be individualized, with an emphasis on early diagnosis and multidisciplinary involvement to develop a comprehensive treatment strategy.
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Affiliation(s)
- Kara L Raphael
- Division of Digestive Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA
| | - Field F Willingham
- Division of Digestive Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA
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Flores K, Dinh K, Rouleau E, Whalen G, Wassef W, LaFemina J. Identification of genetic risk for pancreatic adenocarcinoma. Cancer Genet 2015; 208:559-63. [DOI: 10.1016/j.cancergen.2015.09.002] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/22/2015] [Revised: 08/30/2015] [Accepted: 09/01/2015] [Indexed: 12/11/2022]
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12
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Identification of a novel deletion of CFTR in a 13-year-old: patient with idiopathic chronic pancreatitis. Pancreas 2014; 43:659-60. [PMID: 24713676 DOI: 10.1097/mpa.0000000000000071] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
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Abstract
Hereditary pancreatitis shares a majority of clinical and morphologic features with chronic alcoholic pancreatitis, but may present at an earlier age. The term hereditary pancreatitis has primarily been associated with mutations in the serine protease 1 gene (PRSS1) which encodes for cationic trypsinogen. PRSS1 mutations account for approximately 68-81% of hereditary pancreatitis. Mutations in other genes, primarily serine protease inhibitor Kazal type 1 (SPINK1) and the cystic fibrosis transmembrane conductance regulator (CFTR) are also associated with hereditary pancreatitis. While chronic alcoholic pancreatitis may develop in the fourth or fifth decades, patients with hereditary pancreatitis may develop symptoms in the first or second decades of life. Hereditary pancreatitis is diagnosed either by detecting a causative gene mutation or by the presence of chronic pancreatitis in two first-degree or three second-degree relatives, in two or more generations, without precipitating factors and with a negative workup for known causes. Patients with hereditary pancreatitis may have recurrent acute pancreatitis and may develop pancreatic exocrine and endocrine insufficiency. Hereditary pancreatitis may involve premature trypsinogen activation or decreased control of trypsin. Recurrent inflammation can lead to acute pancreatitis and subsequently to chronic pancreatitis with parenchymal calcification. There is a markedly increased risk of pancreatic carcinoma compared with the general population. Patients are often referred for evaluation of pancreatitis, biliary or pancreatic ductal dilatation, jaundice, biliary obstruction, pancreatic duct stone or stricture, pancreatic pseudocysts, and for evaluation for malignancy. Medical treatment includes pancreatic enzyme supplementation, nutritional supplementation, diabetes management, and palliation of pain. Patients should avoid tobacco use and alcohol exposure. Hereditary pancreatitis is reviewed and recommendations for genetic testing are discussed.
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Affiliation(s)
- Milan R. Patel
- Division of Digestive Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA
| | - Amanda L. Eppolito
- Department of Human Genetics, Emory University School of Medicine, Atlanta, GA, USA
| | - Field F. Willingham
- Director of Endoscopy, Assistant Professor of Medicine, Division of Digestive Diseases, Department of Medicine, 1365 Clifton Road, NE, Atlanta, GA 30322, USA
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14
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Abstract
Acute pancreatitis is a relatively common disease that affects about 300,000 patients per annum in America with a mortality of about 7%. About 75% of pancreatitis is caused by gallstones or alcohol. Other important causes include hypertriglyceridemia, medication toxicity, trauma from endoscopic retrograde cholangiopancreatography, hypercalcemia, abdominal trauma, various infections, autoimmune, ischemia, and hereditary causes. In about 15% of cases the cause remains unknown after thorough investigation. This article discusses the causes, diagnosis, imaging findings, therapy, and complications of acute pancreatitis.
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Affiliation(s)
- Mitchell S Cappell
- Division of Gastroenterology, Department of Medicine, William Beaumont Hospital, MOB 233, 3535 West Thirteen Mile Road, Royal Oak, MI 48073, USA.
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