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Tamura T, Ashida R, Emori T, Itonoga M, Yamashita Y, Hatamaru K, Kawaji Y, Koutani H, Maekita T, Kitano M. Serum trypsin as an early predictor of post-endoscopic retrograde cholangiopancreatography pancreatitis. JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES 2024; 31:917-925. [PMID: 39183624 DOI: 10.1002/jhbp.12063] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 08/27/2024]
Abstract
BACKGROUND Serum amylase (AMY) levels measured 2-6 h after ERCP are a predictor of post-ERCP pancreatitis (PEP). Trypsin is one of the pancreatic enzymes elevated in the development of PEP. The study assessed whether serum trypsin (TRY) can predict early-stage PEP. METHODS This prospective study included patients who underwent ERCP from June 2022 to May 2023. TRY, AMY, serum pancreatic AMY (P-AMY), and serum lipase (LIP) levels were measured immediately after ERCP and 2 h later. The primary outcome was the diagnostic abilities of TRY levels measured immediately (0 h-TRY) and 2 h after (2 h-TRY) ERCP to predict PEP (compared with the other serum pancreatic enzymes). RESULTS Of 130 patients analyzed, 18 developed PEP. The sensitivity and specificity of 0 h-TRY were 83.3% and 69.6%, respectively, and those of 2 h-TRY were 88.9% and 72.3%, respectively. The area under the curve (AUC) for 0 h-TRY was significantly higher than that for 0 h-AMY (p = .006) and 0 h-P-AMY (p = .012), whereas the AUCs for 0 h-TRY and 0 h-LIP did not differ significantly (p = .563). The AUC for 2 h-TRY for predicting PEP was significantly higher than that for 2 h-AMY (p = .025), whereas there was no significant differences between the AUCs for 2 h-TRY and 2 h-P-AMY(p = .146), or between those for 2 h-TRY and 2 h-LIP (p = .792). The median increase ratio (expressed as a ratio relative to baseline) in TRY was highest among all of serum pancreatic enzymes tested immediately after ERCP (5.35, 1.72, 1.94, and 4.44 for TRY, AMY, P-AMY, and LIP, respectively). CONCLUSION Measuring TRY immediately after ERCP is useful for the early prediction of PEP.
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Affiliation(s)
- Takashi Tamura
- Second Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan
| | - Reiko Ashida
- Second Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan
| | - Tomoya Emori
- Department of Gastroenterology, Wakayama Rosai Hospital, Wakayama, Japan
| | - Masahiro Itonoga
- Second Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan
| | - Yasunobu Yamashita
- Second Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan
| | - Keiichi Hatamaru
- Second Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan
| | - Yuki Kawaji
- Second Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan
| | - Hiromu Koutani
- Second Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan
| | - Takao Maekita
- Second Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan
| | - Masayuki Kitano
- Second Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan
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Chen C, Xu Y, Lai Z, Li Z, Sun Q. Case Report: Exploration of changes in serum immunoinflammation-related protein complexes of patients with metastatic breast cancer. Front Oncol 2023; 13:1207991. [PMID: 37546392 PMCID: PMC10401826 DOI: 10.3389/fonc.2023.1207991] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/27/2023] [Accepted: 06/26/2023] [Indexed: 08/08/2023] Open
Abstract
Patients with advanced breast cancer are difficult to treat and have poor prognosis. At present, the commonly used methods to monitor the disease progression of breast cancer are imaging examinations such as breast ultrasound, mammography and peripheral blood tumor markers such as carcinoembryonic antigen (CEA) and carbohydrate antigen 15-3 (CA15-3). However, none of them can detect tumor progression at an early stage. Serum immunoinflammation-related protein complexes (IIRPCs) showed potential to indicate cancer progression. Therefore, we attempted to monitor the level of IIRPCs in peripheral blood of patients with metastatic breast cancer and compare it with patients' treatment and disease progression, and here we performed case reports of two of them.
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Affiliation(s)
- Chang Chen
- Department of Breast Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
| | - Yali Xu
- Department of Breast Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
| | - Zhizhen Lai
- Department of Biophysics and Structural Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing, China
| | - Zhili Li
- Department of Biophysics and Structural Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing, China
| | - Qiang Sun
- Department of Breast Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
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Suzuki M, Minowa K, Isayama H, Shimizu T. Acute recurrent and chronic pancreatitis in children. Pediatr Int 2021; 63:137-149. [PMID: 32745358 DOI: 10.1111/ped.14415] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/13/2020] [Revised: 06/27/2020] [Accepted: 07/28/2020] [Indexed: 12/14/2022]
Abstract
Acute recurrent pancreatitis (ARP) is defined as two distinct episodes of acute pancreatitis (AP), whereas chronic pancreatitis (CP) is caused by persistent inflammation of the pancreas. In children they are caused by genetic mutations, autoimmune pancreatitis, congenital pancreatic abnormalities, and other conditions. Acute recurrent pancreatitis is frequently a precursor to CP, and both are thought to be on the same disease continuum. In particular, genetic factors are associated with early progression of ARP to CP. The diagnosis of CP, as in AP, is based on clinical findings, biochemical tests, and imaging studies. Findings of exocrine pancreatic dysfunction are also important in the diagnosis of CP. A step-up strategy has become increasingly standard for the treatment of patients with CP. This strategy starts with endoscopic treatment, such as pancreatic sphincterotomy and stenting, and progresses to surgery should endoscopic therapy fail or prove technically impossible. Non-opioid (e.g. ibuprofen / naproxen) and opioid (e.g. oxycodone) forms of analgesia are widely used in pediatric patients with AP or CP, whereas pancreatic enzyme replacement therapy may be beneficial for patients with abdominal pain, steatorrhea, and malnutrition. Despite the disparity in the age of onset, pediatric CP patients display some similarities to adults in terms of disease progress. To reduce the risk of developing pancreatic exocrine inefficiency, diabetes and pancreatic cancer in the future, clinicians need to be aware of the current diagnostic approach and treatment methods for ARP and CP and refer them to a pediatric gastroenterologist in a timely manner.
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Affiliation(s)
- Mitsuyoshi Suzuki
- Department of Pediatrics, Juntendo University Faculty of Medicine, Tokyo, Japan
| | - Kei Minowa
- Department of Pediatrics, Juntendo University Faculty of Medicine, Tokyo, Japan
| | - Hiroyuki Isayama
- Department of Gastroenterology, Juntendo University Graduate School of Medicine, Tokyo, Japan
| | - Toshiaki Shimizu
- Department of Pediatrics, Juntendo University Faculty of Medicine, Tokyo, Japan
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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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Stewart JA, Koistinen R, Lempiäinen A, Hotakainen K, Salminen US, Vakkuri A, Wennervirta J, Stenman UH, Koistinen H. Dramatic increase in serum trypsinogens, SPINK1 and hCGβ in aortic surgery patients after hypothermic circulatory arrest. Scandinavian Journal of Clinical and Laboratory Investigation 2020; 80:640-643. [PMID: 32967482 DOI: 10.1080/00365513.2020.1824297] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 10/23/2022]
Abstract
The concentrations of several diagnostic markers have been found to increase dramatically in critically ill patients with a severe disturbance of normal physiological homeostasis, without indication of the diseases they are normally associated with. To prevent false diagnoses and inappropriate treatments of critically ill patients, it is important that the markers aiding the selection of second-line treatments are evaluated in such patients and not only in the healthy population and patients with diseases the markers are associated with. The levels of trypsinogen isoenzymes, the trypsin inhibitor serine peptidase inhibitor Kazal type 1 (SPINK1), hCG and hCGβ, which are used as pancreatitis and cancer markers, were analyzed by immunoassays from serum samples of 17 adult patients who have undergone surgery of the ascending aorta during hypothermic circulatory arrest (HCA) with optional selective cerebral perfusion. Highly elevated levels of trypsinogen-1, -2 and -3, SPINK1 and hCGβ were observed in patients after HCA. This was accompanied by increased concentrations of S100β and NSE. In conclusion, this study highlights the importance of critically evaluating the markers used for aiding selection of second line of treatments in critically ill patients.
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Affiliation(s)
- Juhani A Stewart
- Department of Cardiology, Helsinki University Hospital, Helsinki, Finland
| | - Riitta Koistinen
- Department of Clinical Chemistry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
| | - Anna Lempiäinen
- Department of Clinical Chemistry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
| | - Kristina Hotakainen
- Department of Clinical Chemistry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
| | - Ulla-Stina Salminen
- Department of Cardiac Surgery, Helsinki University Hospital, Helsinki, Finland
| | - Anne Vakkuri
- Department of Anesthesiology and Intensive Care, Helsinki University Hospital, Helsinki, Finland
| | - Johanna Wennervirta
- Department of Anesthesiology and Intensive Care, Helsinki University Hospital, Helsinki, Finland
| | - Ulf-Håkan Stenman
- Department of Clinical Chemistry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
| | - Hannu Koistinen
- Department of Clinical Chemistry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
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Wu HC, Wang HP, Chen CC, Wu CH, Liu TH, Wang CH, Shih LN, Liao WC. Urinary trypsinogen-2 level and local complications of acute pancreatitis. J Gastroenterol Hepatol 2019; 34:2043-2049. [PMID: 31039289 DOI: 10.1111/jgh.14698] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/01/2019] [Revised: 04/18/2019] [Accepted: 04/25/2019] [Indexed: 01/08/2023]
Abstract
BACKGROUND AND AIM Local complications of acute pancreatitis (AP) carry risks of morbidity/mortality. This study aimed to assess whether urinary trypsinogen-2 levels and Bedside Index for Severity in Acute Pancreatitis (BISAP) score on admission predicted subsequent local complications. METHODS One hundred and forty-four consecutive patients with AP were prospectively followed till 6 months after discharge. Urinary trypsinogen-2 levels were measured within 24 h of admission. Local complications (acute peripancreatic fluid collection, acute necrotic collection, pseudocyst, and walled-off necrosis) were diagnosed by abdominal computed tomography. Cut-off for trypsinogen-2 level was assessed using receiver operating characteristic curve, and predictors of local complications were analyzed by logistic regression. RESULTS Thirty-seven (25.7%) patients developed local complications. Urinary trypsinogen-2 levels were significantly higher in patients with local complications compared with those without local complications (median [interquartile range], 3210 [620-9764.4] μg/L vs 627.3 [72.3-5895] μg/L, P = 0.006). Urinary trypsinogen-2 significantly outperformed BISAP score in predicting local complications (area under the receiver operating characteristic curve 0.65 [95% CI: 0.55-0.75] vs 0.48 [95% CI: 0.38-0.58], P = 0.005). At the optimal cut-off of 500 μg/L, the sensitivity, specificity, positive predictive value, and negative predictive value of trypsinogen-2 level were 78.4%, 45.8%, 33.3%, and 86.0%, respectively. Urinary trypsinogen-2 level > 500 μg/L was an independent predictor of local complications (adjusted odds ratio, 3.72; 95% CI: 1.42-9.76; P = 0.007). By contrast, BISAP score ≥ 3 and pleural effusion predicted organ failure but not local complications. CONCLUSION In a prospective cohort, urinary trypsinogen-2 level > 500 μg/L independently predicted local complications of AP.
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Affiliation(s)
- Hsing-Chien Wu
- Taipei Hospital, Ministry of Health and Welfare, Taipei, Taiwan
| | - Hsiu-Po Wang
- Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
| | - Chieh-Chang Chen
- Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
| | - Chien-Hsien Wu
- Taipei Hospital, Ministry of Health and Welfare, Taipei, Taiwan
| | - Ting-Hsu Liu
- Taipei Hospital, Ministry of Health and Welfare, Taipei, Taiwan
| | - Chih-Hsien Wang
- Taipei Hospital, Ministry of Health and Welfare, Taipei, Taiwan
| | - Ling-Na Shih
- Lo-Sheng Sanatorium and Hospital, Ministry of Health and Welfare, Taipei, Taiwan
| | - Wei-Chih Liao
- Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.,Department of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan
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Rompianesi G, Hann A, Komolafe O, Pereira SP, Davidson BR, Gurusamy KS, Cochrane Upper GI and Pancreatic Diseases Group. Serum amylase and lipase and urinary trypsinogen and amylase for diagnosis of acute pancreatitis. Cochrane Database Syst Rev 2017; 4:CD012010. [PMID: 28431198 PMCID: PMC6478262 DOI: 10.1002/14651858.cd012010.pub2] [Citation(s) in RCA: 34] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
BACKGROUND The treatment of people with acute abdominal pain differs if they have acute pancreatitis. It is important to know the diagnostic accuracy of serum amylase, serum lipase, urinary trypsinogen-2, and urinary amylase for the diagnosis of acute pancreatitis, so that an informed decision can be made as to whether the person with abdominal pain has acute pancreatitis. There is currently no Cochrane review of the diagnostic test accuracy of serum amylase, serum lipase, urinary trypsinogen-2, and urinary amylase for the diagnosis of acute pancreatitis. OBJECTIVES To compare the diagnostic accuracy of serum amylase, serum lipase, urinary trypsinogen-2, and urinary amylase, either alone or in combination, in the diagnosis of acute pancreatitis in people with acute onset of a persistent, severe epigastric pain or diffuse abdominal pain. SEARCH METHODS We searched MEDLINE, Embase, Science Citation Index Expanded, National Institute for Health Research (NIHR HTA and DARE), and other databases until March 2017. We searched the references of the included studies to identify additional studies. We did not restrict studies based on language or publication status, or whether data were collected prospectively or retrospectively. We also performed a 'related search' and 'citing reference' search in MEDLINE and Embase. SELECTION CRITERIA We included all studies that evaluated the diagnostic test accuracy of serum amylase, serum lipase, urinary trypsinogen-2, and urinary amylase for the diagnosis of acute pancreatitis. We excluded case-control studies because these studies are prone to bias. We accepted any of the following reference standards: biopsy, consensus conference definition, radiological features of acute pancreatitis, diagnosis of acute pancreatitis during laparotomy or autopsy, and organ failure. At least two review authors independently searched and screened the references located by the search to identify relevant studies. DATA COLLECTION AND ANALYSIS Two review authors independently extracted data from the included studies. The thresholds used for the diagnosis of acute pancreatitis varied in the trials, resulting in sparse data for each index test. Because of sparse data, we used -2 log likelihood values to determine which model to use for meta-analysis. We calculated and reported the sensitivity, specificity, post-test probability of a positive and negative index test along with 95% confidence interval (CI) for each cutoff, but have reported only the results of the recommended cutoff of three times normal for serum amylase and serum lipase, and the manufacturer-recommended cutoff of 50 mg/mL for urinary trypsinogen-2 in the abstract. MAIN RESULTS Ten studies including 5056 participants met the inclusion criteria for this review and assessed the diagnostic accuracy of the index tests in people presenting to the emergency department with acute abdominal pain. The risk of bias was unclear or high for all of the included studies. The study that contributed approximately two-thirds of the participants included in this review was excluded from the results of the analysis presented below due to major concerns about the participants included in the study. We have presented only the results where at least two studies were included in the analysis.Serum amylase, serum lipase, and urinary trypsinogen-2 at the standard threshold levels of more than three times normal for serum amylase and serum lipase, and a threshold of 50 ng/mL for urinary trypsinogen-2 appear to have similar sensitivities (0.72 (95% CI 0.59 to 0.82); 0.79 (95% CI 0.54 to 0.92); and 0.72 (95% CI 0.56 to 0.84), respectively) and specificities (0.93 (95% CI 0.66 to 0.99); 0.89 (95% CI 0.46 to 0.99); and 0.90 (95% CI 0.85 to 0.93), respectively). At the median prevalence of 22.6% of acute pancreatitis in the studies, out of 100 people with positive test, serum amylase (more than three times normal), serum lipase (more than three times normal), and urinary trypsinogen (more than 50 ng/mL), 74 (95% CI 33 to 94); 68 (95% CI 21 to 94); and 67 (95% CI 57 to 76) people have acute pancreatitis, respectively; out of 100 people with negative test, serum amylase (more than three times normal), serum lipase (more than three times normal), and urinary trypsinogen (more than 50 ng/mL), 8 (95% CI 5 to 12); 7 (95% CI 3 to 15); and 8 (95% CI 5 to 13) people have acute pancreatitis, respectively. We were not able to compare these tests formally because of sparse data. AUTHORS' CONCLUSIONS As about a quarter of people with acute pancreatitis fail to be diagnosed as having acute pancreatitis with the evaluated tests, one should have a low threshold to admit the patient and treat them for acute pancreatitis if the symptoms are suggestive of acute pancreatitis, even if these tests are normal. About 1 in 10 patients without acute pancreatitis may be wrongly diagnosed as having acute pancreatitis with these tests, therefore it is important to consider other conditions that require urgent surgical intervention, such as perforated viscus, even if these tests are abnormal.The diagnostic performance of these tests decreases even further with the progression of time, and one should have an even lower threshold to perform additional investigations if the symptoms are suggestive of acute pancreatitis.
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Affiliation(s)
- Gianluca Rompianesi
- University of Modena and Reggio EmiliaInternational Doctorate School in Clinical and Experimental MedicineModenaItaly
| | | | | | - Stephen P Pereira
- Royal Free Hospital CampusUCL Institute for Liver and Digestive HealthUpper 3rd FloorLondonUKNW3 2PF
| | - Brian R Davidson
- Royal Free Campus, UCL Medical SchoolDepartment of SurgeryPond StreetLondonUKNW3 2QG
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Role of Biomarkers in Diagnosis and Prognostic Evaluation of Acute Pancreatitis. J Biomark 2015; 2015:519534. [PMID: 26345247 PMCID: PMC4541003 DOI: 10.1155/2015/519534] [Citation(s) in RCA: 60] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/31/2015] [Revised: 07/14/2015] [Accepted: 07/15/2015] [Indexed: 02/07/2023] Open
Abstract
Acute pancreatitis is a potentially life threatening disease. The spectrum of severity of the illness ranges from mild self-limiting disease to a highly fatal severe necrotizing pancreatitis. Despite intensive research and improved patient care, overall mortality still remains high, reaching up to 30–40% in cases with infected pancreatic necrosis. Although little is known about the exact pathogenesis, it has been widely accepted that premature activation of digestive enzymes within the pancreatic acinar cell is the trigger that leads to autodigestion of pancreatic tissue which is followed by infiltration and activation of leukocytes. Extensive research has been done over the past few decades regarding their role in diagnosis and prognostic evaluation of severe acute pancreatitis. Although many standalone biochemical markers have been studied for early assessment of severity, C-reactive protein still remains the most frequently used along with Interleukin-6. In this review we have discussed briefly the pathogenesis and the role of different biochemical markers in the diagnosis and severity evaluation in acute pancreatitis.
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Suzuki M, Sai JK, Shimizu T. Acute pancreatitis in children and adolescents. World J Gastrointest Pathophysiol 2014; 5:416-26. [PMID: 25400985 PMCID: PMC4231506 DOI: 10.4291/wjgp.v5.i4.416] [Citation(s) in RCA: 52] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/28/2014] [Revised: 04/09/2014] [Accepted: 07/18/2014] [Indexed: 02/06/2023] Open
Abstract
In this Topic Highlight, the causes, diagnosis, and treatment of acute pancreatitis in children are discussed. Acute pancreatitis should be considered during the differential diagnosis of abdominal pain in children and requires prompt treatment because it may become life-threatening. The etiology, clinical manifestations, and course of acute pancreatitis in children are often different than in adults. Therefore, the specific features of acute pancreatitis in children must be considered. The etiology of acute pancreatitis in children is often drugs, infections, trauma, or anatomic abnormalities. Diagnosis is based on clinical symptoms (such as abdominal pain and vomiting), serum pancreatic enzyme levels, and imaging studies. Several scoring systems have been proposed for the assessment of severity, which is useful for selecting treatments and predicting prognosis. The basic pathogenesis of acute pancreatitis does not greatly differ between adults and children, and the treatments for adults and children are similar. In large part, our understanding of the pathology, optimal treatment, assessment of severity, and outcome of acute pancreatitis in children is taken from the adult literature. However, we often find that the common management of adult pancreatitis is difficult to apply to children. With advances in diagnostic techniques and treatment methods, severe acute pancreatitis in children is becoming better understood and more controllable.
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Swahn F, Regnér S, Enochsson L, Lundell L, Permert J, Nilsson M, Thorlacius H, Arnelo U. Endoscopic retrograde cholangiopancreatography with rendezvous cannulation reduces pancreatic injury. World J Gastroenterol 2013; 19:6026-34. [PMID: 24106403 PMCID: PMC3785624 DOI: 10.3748/wjg.v19.i36.6026] [Citation(s) in RCA: 15] [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: 09/11/2012] [Revised: 03/13/2013] [Accepted: 03/21/2013] [Indexed: 02/07/2023] Open
Abstract
AIM: To examine whether rendezvous endoscopic retrograde cholangiopancreatography (ERCP) is associated with less pancreatic damage, measured as leakage of proenzymes, than conventional ERCP.
METHODS: Patients (n = 122) with symptomatic gallstone disease, intact papilla and no ongoing inflammation, were prospectively enrolled in this case-control designed study. Eighty-one patients were subjected to laparoscopic cholecystectomy and if intraoperative cholangiography suggested common bile duct stones (CBDS), rendezvous ERCP was performed intraoperatively (n = 40). Patients with a negative cholangiogram constituted the control group (n = 41). Another 41 patients with CBDS, not subjected to surgery, underwent conventional ERCP. Pancreatic proenzymes, procarboxypeptidase B and trypsinogen-2 levels in plasma, were analysed at 0, 4, 8 and 24 h. The proenzymes were determined in-house with a double-antibody enzyme linked immunosorbent assay. Pancreatic amylase was measured by an enzymatic colourimetric modular analyser with the manufacturer’s reagents. All samples were blinded at analysis.
RESULTS: Post ERCP pancreatitis (PEP) occurred in 3/41 (7%) of the patients cannulated with conventional ERCP and none in the rendezvous group. Increased serum levels indicating pancreatic leakage were significantly higher in the conventional ERCP group compared with the rendezvous ERCP group regarding pancreatic amylase levels in the 4- and 8-h samples (P = 0.0015; P = 0.03), procarboxypeptidase B in the 4- and 8-h samples (P < 0.0001; P < 0.0001) and trypsinogen-2 in the 24-hour samples (P = 0.03). No differences in these markers were observed in patients treated with rendezvous cannulation technique compared with patients that underwent cholecystectomy alone (control group). Post procedural concentrations of pancreatic amylase and procarboxypeptidase B were significantly correlated with pancreatic duct cannulation and opacification.
CONCLUSION: Rendezvous ERCP reduces pancreatic enzyme leakage compared with conventional ERCP cannulation technique. Thus, laparo-endoscopic technique can be recommended with the ambition to minimise the risk for post ERCP pancreatitis.
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Abstract
Approximately 20% of patients with acute pancreatitis develop a severe disease associated with complications and high risk of mortality. The purpose of this study is to review pathogenesis and prognostic factors of severe acute pancreatitis (SAP). An extensive medline search was undertaken with focusing on pathogenesis, complications and prognostic evaluation of SAP. Cytokines and other inflammatory markers play a major role in the pathogenesis and course of SAP and can be used as prognostic markers in its early phase. Other markers such as simple prognostic scores have been found to be as effective as multifactorial scoring systems (MFSS) at 48 h with the advantage of simplicity, efficacy, low cost, accuracy and early prediction of SAP. Recently, several laboratory markers including hematocrit, blood urea nitrogen (BUN), creatinine, matrix metalloproteinase-9 (MMP-9) and serum amyloid A (SAA) have been used as early predictors of severity within the first 24 h. The last few years have witnessed a tremendous progress in understanding the pathogenesis and predicting the outcome of SAP. In this review we classified the prognostic markers into predictors of severity, pancreatic necrosis (PN), infected PN (IPN) and mortality.
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Abstract
Pancreatitis is the most common complication after endoscopic retrograde cholangio-pancreatography (ERCP); the reported incidence of this complication varies from less than 1% to 40%, but a rate of 4%-8% is reported in most prospective studies involving non-selected patients. Differences in criteria for defining pancreatitis, methods of data collection, and patient populations (i.e. number of high-risk patients included in the published series) are factors that are likely to affect the varying rates of post-ERCP pancreatitis. The severity of post-ERCP pancreatitis (PEP) can range from a minor inconvenience with one or two days of added hospitalization with full recovery to a devastating illness with pancreatic necrosis, multiorgan failure, permanent disability, and even death. Although, most episodes of PEP are mild (about 90%), a small percentage of patients (about 10%) develop moderate or severe pancreatitis. In the past, PEP was often viewed as an unpredictable and unavoidable complication, with no realistic strategy for its avoidance. New data have aided in stratification of patients into PEP risk categories and new measures have been introduced to decrease the risk of PEP. As most ERCPs are performed on an outpatient basis, the majority of patients will not develop PEP and can be discharged. Alternatively, early detection of those patients who will go on to develop PEP can guide decisions regarding hospital admission and aggressive management. In the last decade, great efforts have been addressed toward prevention of this complication. Points of emphasis have included technical measures, pharmacological prophylaxis, and patient selection. This review provides a comprehensive, evidence-based assessment of published data on PEP and current suggestions for its avoidance.
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Affiliation(s)
- Ayman M Abdel Aziz
- Division of Gastroenterology and Hepatology, Indiana University Medical Center, Indianapolis, IN 46202, USA
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Beauregard JM, Lyon JA, Slovis C. Using the literature to evaluate diagnostic tests: amylase or lipase for diagnosing acute pancreatitis? J Med Libr Assoc 2007; 95:121-6. [PMID: 17443244 PMCID: PMC1852619 DOI: 10.3163/1536-5050.95.2.121] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/03/2023] Open
Affiliation(s)
| | - Jennifer A. Lyon
- , Coordinator, Research Informatics Consult Service, Eskind Biomedical Library
| | - Corey Slovis
- , Professor of Emergency Medicine and Medicine, and Chairman, Department of Emergency Medicine; Vanderbilt University Medical Center, Nashville, Tennessee 37232
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Affiliation(s)
- Peter A Banks
- Division of Gastroenterology, Center for Pancreatic Disease, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
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Abstract
An ideal laboratory test in the evaluation of a patient with acute pancreatitis (AP) should, in addition to accurately establishing the diagnosis of AP, provide early assessment of its severity and identify the etiology. None of the tests available today meet all these criteria, and presently there is no biochemical test that can be considered the "gold standard" for the diagnosis and assessment of severity of AP. In the diagnosis of AP, serum amylase and lipase remain important tests. Advantages of amylase estimation are its technical simplicity, easy availability, and high sensitivity. However, its greatest disadvantage is its low specificity. A normal amylase would usually exclude the diagnosis of AP, with the exception of AP secondary to hyperlipidemia, acute exacerbation of chronic pancreatitis, and when the estimation of amylase is delayed in the course of the disease. The major advantage of lipase is an increased sensitivity in acute alcoholic pancreatitis and in patients who initially present to the emergency room days after the onset of the disease, as lipase remains elevated longer than amylase. Although once considered to be specific for AP, nonspecific elevations of lipase have been reported in almost as many disorders as amylase, thus decreasing its specificity. Simultaneous estimation of amylase and lipase does not improve the accuracy. Other enzymes for the diagnosis of AP--pancreatic isoamylase, immunoreactive trypsin, and elastase--are more cumbersome and expensive and have no clear role in the diagnosis of AP. No enzyme assay has a predictive role in determining the severity or etiology of AP. Once the diagnosis of AP is established, daily measurements of enzymes have no value in assessing the clinical progress of the patient or ultimate prognosis and should be discouraged. A host of new serological and urinary markers have been investigated in the last few years. Their main use is in predicting the severity of AP. At present, serum C-reactive protein at 48 h is the best available laboratory marker of severity. Urinary trypsinogen activation peptides within 12-24 h of onset of AP are able to predict the severity but are not widely available. Serum interleukins 6 and 8 seem promising but remain experimental.
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Affiliation(s)
- Dhiraj Yadav
- Department of Surgery, Our Lady of Mercy University Medical Center, New York Medical College, Bronx 10466, USA
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