REVIEW URRENT C OPINION

Acute pancreatitis Rupjyoti Talukdar a and Santhi S. Vege b

Purpose of review To summarize recent data on classification systems, cause, risk factors, severity prediction, nutrition, and drug treatment of acute pancreatitis. Recent findings Comparison of the Revised Atlanta Classification and Determinant Based Classification has shown heterogeneous results. Simvastatin has a protective effect against acute pancreatitis. Young black male, alcohol, smoldering symptoms, and subsequent diagnosis of chronic pancreatitis are risk factors associated with readmissions after acute pancreatitis. A reliable clinical or laboratory marker or a scoring system to predict severity is lacking. The PYTHON trial has shown that oral feeding with on demand nasoenteric tube feeding after 72 h is as good as nasoenteric tube feeding within 24 h in preventing infections in predicted severe acute pancreatitis. Male sex, multiple organ failure, extent of pancreatic necrosis, and heterogeneous collection are factors associated with failure of percutaneous drainage of pancreatic collections. Summary The newly proposed classification systems of acute pancreatitis need to be evaluated more critically. New biomarkers are needed for severity prediction. Further well designed studies are required to assess the type of enteral nutritional formulations for acute pancreatitis. The optimal minimally invasive method or combination to debride the necrotic collections is evolving. There is a great need for a drug to treat the disease early on to prevent morbidity and mortality. Keywords classification, cause, enteral nutrition, readmission, severity prediction

INTRODUCTION Significant advances in the understanding of the pathophysiology and clinical characteristics of acute pancreatitis have been observed in the recent years. A testimony to this is the development and validation of the Revised Atlanta Classification (RAC), proposal of the Determinant Based Classification (DBC), development and validation of newer severity prediction tools, utility of newer imaging modalities in risk stratification, and development of evidence-based official guidelines. In this review, we discuss the significant recent developments in acute pancreatitis. We searched Pubmed, Medline, Cochrane and Google Scholar databases with the search words ‘acute pancreatitis’, ‘classification’, ‘risk factors’, ‘prediction’, ‘imaging’, ‘treatment’, and ‘guidelines’. In view of the word restrictions of the journal we included only the most significant papers, in our opinion, in this review.

CLASSIFICATION SYSTEMS The RAC was published in 2013 [1]. This classification has provided discrete definitions of fluid www.co-gastroenterology.com

collections, namely acute peripancreatic fluid collection, pancreatic pseudocyst, acute necrotic collection (ANC), and walled-off necrosis, based on the pathophysiology and natural history. The severity of acute pancreatitis has also been classified into mild, moderately severe, and severe according to the presence or absence of local complication and transient/persistent organ failure. Around the same time, the four-tier DBC [2] was also published. This classification stratifies severity of acute pancreatitis based on factors that determine mortality. The four categories in this classification include mild, moderate, severe, and critical acute pancreatitis, based on the presence or absence of infected/noninfected a Asian Institute of Gastroenterology/Asian Healthcare Foundation, Hyderabad, Telangana, India and bDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, USA

Correspondence to Santhi S. Vege, Professor of Medicine & Director Pancreas Group, Division of Gastroenterology and Hepatology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. Tel: +1 507 284 2175; e-mail: [email protected] Curr Opin Gastroenterol 2015, 31:374–379 DOI:10.1097/MOG.0000000000000201 Volume 31  Number 5  September 2015

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Acute pancreatitis Talukdar and Vege

KEY POINTS  Simvastatin has a protective effect against acute pancreatitis.  Young black male, alcohol, smoldering symptoms, and subsequent diagnosis of chronic pancreatitis are risk factors associated with readmissions after acute pancreatitis.  A reliable clinical or laboratory marker or a scoring system to predict severity is still lacking.  Oral feeding with on demand nasoenteric tube feeding after 72 h is as good as nasoenteric tube feeding within 24 h in preventing infections in predicted severe acute pancreatitis.  In acute biliary pancreatitis with peripancreatic collections, cholecystectomy should be deferred till the collections resolve or if they persist beyond 6 weeks.

followed patients [10]. The authors evaluated the utility of the RAC and DBC to predict mortality, need for ICU admission, need for interventions, length of stay in the ICU, and total hospital stay. Mild, moderately severe, and severe acute pancreatitis was observed in 49, 25.5, and 25.5% patients, respectively, according to the RAC; 67, 7, 19, and 7% patients, respectively, had mild, moderate, severe, and critical acute pancreatitis according to the DBC. Although both the RAC and DBC were similar in predicting mortality, ICU stay and length of stay in the ICU, the RAC appeared to predict hospital stay better and DBC appeared to predict need for intervention better. It is noteworthy that the RAC and the DBC were developed to categorize the disease severity and not to predict outcomes. Furthermore, using different systems to predict different outcomes may not be clinically appealing. Interestingly, a subsequent community-based comparative study [11 ] involving 459 patients who had 543 episodes of acute pancreatitis over 5 years did not find any significant differences in the frequencies of the severity categories and outcomes between the two classifications. This difference in results needs to be clarified in larger prospective studies. Furthermore, it is important to identify the clinical need at different levels of healthcare before implementing prediction or classification systems. For instance, at the primary care or community level, wherein a substantial proportion of patients report first after the onset of acute pancreatitis, early prediction of adverse outcomes would be more important from a therapeutic standpoint (including early referral and drug therapy if one becomes available). On the contrary, in the tertiary care referral centers, use of severity classification systems could guide selection of the appropriate intervention based on the type of complication. &

(peri)pancreaticnecrosis and transient/persistent organ failure. Details of these two classifications are presented in Table 1. Both of these have been evaluated and validated in several subsequent studies. To date, the largest study that validated the RAC retrospectively evaluated 553 patients over 7 years [3]. In this study, mortality was significantly higher in patients with infected necrosis and organ failure compared with organ failure alone (32.2 versus 8%). Mortality was similar in patients who had either infected necrosis or organ failure alone (7.1 versus 8%). Another prospective validation study that evaluated 163 directly admitted consecutive patients with acute pancreatitis reported persistent organ failure in 44.4% (of all persistent organ failures) within the first week of disease onset, and mortality was high (37.5%) among these patients [4 ]. The clinical behavior of these patients was similar to the previously described entity called early severe acute pancreatitis (ESAP) [5–7]. However, ESAP has not been addressed in the two classification systems. The DBC was initially validated in a prospective study that included 151 patients over a 2-year period [8]. The severity-wise distribution of acute pancreatitis was mild in 13.9% patients, moderate in 41.7%, severe in 39.1%, and critical in 5.3%; and there was a stepwise increase in frequency of adverse outcomes across the groups. The moderate category of the DBC was validated in a small study of 92 consecutive patients [9]. However, this group was not compared with the moderately severe group in the RAC. The RAC and the DBC were compared in two recent large studies. In the first study post-hoc analysis was conducted on 256 prospectively &&

CAUSE Apart from gallstones and ethanol, several other causes including drugs have been implicated in the causation of acute pancreatitis. Among the drugs, simvastatin was earlier classified as a Class Ia agent associated with acute pancreatitis [12]. However, a recent retrospective study on a cohort of 3 967 859 adult patients from an integrated US healthcare system demonstrated that use of simvastatin was independently associated with a significantly lower risk of developing acute pancreatitis (risk ratio of 0.29 [95% confidence interval (CI) 0.27–0.31]) after adjusting for age, sex, race/ethnicity, gallstone disorders, alcohol dependence, smoking, and hypertriglyceridemia [13 ]. This observation holds merit because individuals receiving simvastatin were more likely to have risk factors for acute pancreatitis, such as gallstones, &&

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Pancreas Table 1. Similarities and differences between the Revised Atlanta and Determinant-Based Classifications of acute pancreatitis Revised Atlanta Classification

Determinant-Based Classification

Definitions:

Definitions:

Mild AP

Mild AP

No organ failure

No organ failure

No local or systemic complications

No (peri)pancreatic necrosis

Moderately severe AP

Moderate AP

Transient organ failure and/or local or systemic complication OR exacerbation of preexisting co-morbidities.

Sterile (peri)pancreatic necrosis AND/OR transient organ failure

Severe AP

Severe AP

Persistent organ failure (single or multiple)

Infected (peri)pancreatic necrosis OR persistent organ failure Critical AP Infected (peri)pancreatic necrosis AND persistent organ failure

Considers the natural course of the disease (early and late phases)

Does not consider the natural course of the disease (early and late phases)

Distinguishes between transient and persistent organ failure

Distinguishes between transient and persistent organ failure

Recommends use of Modified Marshall Scoring system to define organ failure

Recommends use of Sequential Organ Failure Assessment system to define organ failure

Defines pancreatic and peripancreatic necrosis

Defines pancreatic and peripancreatic necrosis

Provides discrete definitions of fluid collections [acute (peri)pancreatic fluid collections, pancreatic pseudocyst, acute necrotic collection and walled off necrosis]

Does not define fluid collections

Includes gastric outlet dysfunction, portal and splenic vein thrombosis, and colonic necrosis as local complications

Does not consider gastric outlet dysfunction, portal and splenic vein thrombosis, and colonic necrosis as local complications

Defines systemic complications as exacerbation of preexisting conditions such as coronary artery disease, congestive cardiac failure, chronic obstructive pulmonary disease, diabetes, and chronic liver disease

Does not consider systemic complications

AP, acute pancreatitis.

alcohol, and hypertriglyceridemia. Similar results were also observed with atorvastatin (a class III drug associated with acute pancreatitis by earlier classification), in the same study thereby implying a classeffect. Even though it was earlier believed that smoking was cofactor in alcohol-related acute pancreatitis, it is now known that smoking is an independent risk factor of the disease [14]. This was further reiterated in two recent meta-analyses [15 ,16 ], of which the study by Sun et al. [16 ] also demonstrated a doseresponse effect in the form of a 40% (95% CI: 30– 51%) increased risk of acute pancreatitis for every 10 additional cigarettes per day. &

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HOSPITAL READMISSIONS Hospital readmissions after the sentinel attack of acute pancreatitis incur additional financial burden. Two recent studies have addressed the pattern of readmissions for acute pancreatitis and the risk factors associated. In a population-based study [17 ] from Allegheny County, Pennsylvania by Yadav et al. that included 6010 patients, the absolute risk &

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for readmission was 21.9%. Young black males, alcohol use, and subsequent diagnosis of chronic pancreatitis emerged as risk factors associated with readmissions. A more elaborate subsequent study [18 ] involving a cohort of patients from the prospectively maintained Severe Acute Pancreatitis Study database aimed to evaluate the determinants of early and late readmissions. Readmissions were defined as early and late with a cutoff of 30 days. The overall readmission rate was 34%. Although the most common causes of early readmissions were smoldering symptoms and local complications, late readmissions were associated with recurrent disease. Readmissions due to recurrence of acute pancreatitis were seen in a significantly higher proportion of male patients and those with alcohol cause. Majority of patients with early readmissions had idiopathic acute pancreatitis. Other determinants associated with an increased risk of readmissions included unstable vital signs on discharge, semisolid diet, poor pain or other symptom control, and placement of a percutaneous catheter drain. Another recent retrospective study involving 606 hospital admissions from Germany evaluated &

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the incidence and risk factors for hospital readmissions. The results suggested concomitant liver disease, pseudocysts, alcohol, tobacco, and substance abuse was associated with readmissions. However, this study included patients with both acute and chronic pancreatitis and did not stratify either of them separately [19].

SEVERITY PREDICTION Even though several clinical and laboratory markers and many scoring systems for predicting the severity of acute pancreatitis have been evaluated over the years, no reliable marker or system is currently available. Yet another recent report described the change in amylase and BMI (CAB) score [20], which has been modeled on the percentage change in serum amylase within 24 h of admission and BMI. Multivariable analyses identified this score, among other variables, to have the highest area under receiver operating characteristic (AUROC) values to predict persistent organ failure (defined by the Modified Marshall system) in both the discovery and the validation cohorts [0.79 (95% CI 0.71– 0.87) and 0.73 (95% CI 0.61–0.84) respectively]. However, the number of patients with severe acute pancreatitis was 21/182 in the discovery cohort and 35/140 in the validation. Furthermore, the predictive accuracy of the system did not appear to be dramatically higher than the earlier scoring systems. From the recent and previous data on severity prediction of acute pancreatitis, it appears that the current predictors have reached a saturation point [21]. Most of the predictors have a low-positive predictive value, which could be the result of a low prevalence of SAP. Therefore, unless novel molecular or genetic biomarkers, or novel tools like machine learning and high efficiency artificial neural networks to analyze various data sets are developed, predicting severity is no better than the flip of a coin.

TREATMENT There has been increasing discussion in the recent years on domiciliary care for patients with mild acute pancreatitis; a recent randomized controlled trial has demonstrated the feasibility of this paradigm shift in management of acute pancreatitis [22 ]. In this study, 84 patients with nonalcoholic acute pancreatitis were randomized into home monitoring and hospital admission groups after initial assessment in the hospital. Mild acute pancreatitis was defined using the Imrie [23] and the Harmless Acute Pancreatitis scores [24–26]; and patients presenting within 48 h of onset of symptoms and with hematocrit less &&

than 44% were included. Patients in the home monitoring arm stayed in the hospital for less than 24 h; and were monitored at home by a visiting nurse on second, third, and fifth day. These patients visited the hospital on seventh, 14th, and 30th day. The study outcomes (i.e., time from presentation to resolution of pain, time from presentation to resumption of oral solid food intake, and 30 days hospital readmission rates) were similar in both arms; whereas total expense was significantly lower in the home monitoring arm. Even though this study makes home monitoring of mild nonalcoholic acute pancreatitis a promising option, this needs to be validated in a substantially larger sample size. It would also be important to have data on serial morphological evaluation of the pancreas in the patients who are monitored at home to rule out any subclinical morphologic alterations that could potentially lead to late readmissions. Nutrition in acute pancreatitis has long been a topic of discussion. The current recommendation is to begin early oral feeding in order to maintain the gut mucosal barrier function [27,28]. A recently published systematic review reiterated the importance of enteral nutrition in reducing infections and mortality [29]. However, the optimal time cutoff is still under debate. A recent study [30 ] evaluated the effect of early (within 72 h) and delayed (beyond 72 h but within 7days) enteral feeding on clinical outcomes of acute pancreatitis. Hospital mortality, length of stay, number of patients requiring mechanical ventilation, and incidence of pancreatic infection in the early enteral nutrition group were significantly lower than those in the delayed enteral nutrition group. The optimal duration for enteral feeding to prevent infection was further evaluated in the PYTHON trial [31 ]. This was a multicenter trial in which patients were randomized to nasoenteric tube feeding within 24 h after randomization (early group) or to an oral diet initiated 72 h after presentation. In the latter group tube feeding was provided if the oral diet was not tolerated (on demand group). The results did not reveal any significant differences in the rate of major infection (25% and 26%, respectively; P ¼ 0.87) or death (11% and 7%, respectively; P ¼ 0.33) between the early group and the on demand group. This study concludes that the efficacy of early nasoenteric tube feeding is similar to that of an oral diet after 72 h in reducing the rate of infection or death in patients with acute pancreatitis at high risk for complications. Different types of nutritional preparations, for example, elemental and semielemental formulations, immunomodulatory agents, and glutamine have been used in clinical trials. A recent Cochrane meta-analysis [32 ] that evaluated 15 randomized

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Pancreas

trials involving 1376 participants on enteral nutrition in patients with acute pancreatitis reported that even though immunonutrition decreased all-cause mortality (relative risk 0.49, 95% CI 0.29–0.80), the quality of evidence was low. Evidence for the effects of immunonutrition on efficacy and safety measures was also very low; results from studies using probiotic fortified nutrition yielded inconsistent results from a safety standpoint. On the basis of this metaanalysis, there is currently insufficient evidence to support any specific type of enteral nutritional formulation for patients with acute pancreatitis. On the contrary, another meta-analysis of 10 studies (433 patients) that evaluated the efficacy of glutamine for severe acute pancreatitis reported that intravenous infusion could be associated with a reduction in infectious complications and mortality [33]. Current guidelines recommend percutaneous or transmural endoscopic drainage as the first line of management in suspected or confirmed infected walled-off pancreatic necrosis [27]. Even though percutaneous drainage is technically feasible in over 95% of patients [34] and can prevent 23–50% [27,34] of surgical necrosectomies, factors determining its failure have not been studied in depth. These factors were evaluated in a recent post-hoc analysis of 130 prospectively recruited patients with acute pancreatitis (113 underwent percutaneous and 17 endoscopic drainage) by the Dutch Pancreatitis Research Group [35 ]. Using multivariate regression analysis, the study group demonstrated that lower chances of success of catheter drainage was associated with male sex [odds ratio (OR) ¼ 0.27; 95% CI: 0.09–0.55; P < 0.01], multiple organ failure (OR ¼ 0.15; 95% CI: 0.04–0.62; P < 0.01), percentage of pancreatic necrosis (50%: OR ¼ 0.54; 95% CI: 0.30–0.96; P ¼ 0.03), and heterogeneous collection (OR ¼ 0.21; 95% CI: 0.06–0.67; P < 0.01). When these four factors were collated into a prediction model, the AUROC was found to be 0.76. This means the model is just fairly accurate especially in view of a low sample size. The other frequently discussed aspect regarding the management of acute (biliary) pancreatitis is the optimal timing for performing cholecystectomy. Current guidelines recommend laparoscopic cholecystectomy for mild biliary acute pancreatitis during the index admission [27]. In the presence of peripancreatic collections, cholecystectomy should be deferred till the collections resolve or if they persist beyond 6 weeks [27] (Grade 2C recommendation with strong agreement). These recommendations were based predominantly on cohort studies. Although the complete results of PONCHO, a randomized controlled parallel group superiority &

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trial is expected soon, a recent study by Borreca et al. [36] reiterated that there was a higher odds of developing an acute pancreatitis relapse (OR 10.28; P ¼ 0.02) when cholecystectomy is performed late. The recurrence rate in this study was 28.6%. Furthermore, the length of hospital stay was significantly lower for patients undergoing early laparoscopic cholecystectomy (9 versus 13 days, P ¼ 0.003). No difference was noticed in the other outcomes such as length of intervention, intraoperative complications, postoperative stay, and mortality. Even though an increasing understanding of the pathogenesis of acute pancreatitis and its complications has resulted in effective treatment modalities for the complications, there still does not exist any specific treatment for the primary disease. Experimental studies have targeted against the intraacinar mechanism of trypsin activation; however, these are unlikely to work in the clinical situation as these early events already occur by the time patients present to the emergency room (except for those with post-ERCP pancreatitis). The primary factor that determines adverse events is early and persistent systemic inflammatory response syndrome that is orchestrated by a complex interplay of cytokines. A recent pilot study from the Mayo Clinic addressed this aspect wherein the role of the tumor necrosis factor-a blocker pentoxifylline was evaluated in consecutive patients with predicted SAP in a randomized, double blinded, placebocontrolled, and allocation concealed study [37]. Pentoxifylline was administered orally at a dose of 400 mg thrice daily for 3 days in the treatment arm with matching placebo in the other. The pentoxifylline group had less patients requiring hospital stay more than 4 days and need for ICU. The sample size in this trial was small (n ¼ 28); nevertheless it opens up avenues for evaluating efficacy of anti-inflammatory agents early on in acute pancreatitis in a more elaborate manner.

CONCLUSION In this review, we summarized key updates in acute pancreatitis over the past year. Based on current data, it appears that the RAC and DBC may require further improvement. A reliable clinical or laboratory marker or a scoring system to predict severity is still lacking and requires further search for one. The ideal type of supplemental enteral nutrition is still not clear, and requires further evaluation. Acknowledgements None. Volume 31  Number 5  September 2015

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Acute pancreatitis Talukdar and Vege

Financial support and sponsorship None. Conflicts of interest There are no conflicts of interest.

REFERENCES AND RECOMMENDED READING Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest && of outstanding interest 1. Banks PA, Bollen TL, Dervenis C, et al., Acute Pancreatitis Classification Working Group. Classification of Acute Pancreatitis-2102: revision of the Atlanta classification and definitions by international consensus. Gut 2013; 62:102–111. 2. Dellinger EP, Forsmark CE, Layer P, et al. Determinant-based classification of acute pancreatitis severity: an international multidisciplinary consultation. Ann Surg 2012; 256:875–880. 3. Choi JH, Kim MH, Oh D, et al. Clinical relevance of the revised Atlanta classification focusing on severity stratification system. Pancreatology 2014; 14:324–329. 4. Talukdar R, Bhattacharrya A, Rao B, et al. Clinical utility of the revised Atlanta && classification of acute pancreatitis in a prospective cohort: have all loose ends been tied? Pancreatology 2014; 14:257–262. This study has validated the RAC and has identified early severe acute pancreatitis as a separate entity that needs to be recognized by the new classification. 5. Sharma M, Banerjee D, Garg PK. Characterization of newer subgroups of fulminant and subfulminant pancreatitis associated with a high early mortality. Am J Gastroenterol 2007; 102:2688–2695. 6. Isenmann R, Rau B, Beger HG. Early severe acute pancreatitis: characteristics of a new subgroup. Pancreas 2001; 22:274–278. 7. Talukdar R, Vege SS. Classification of the severity of acute pancreatitis. Am J Gastroenterol 2011; 106:1169–1170. 8. Thandassery RB, Yadav TD, Dutta U, et al. Prospective validation of 4-category classification of acute pancreatitis severity. Pancreas 2013; 42:392–396. 9. Jin T, Huang W, Yang XN, et al. Validation of the moderate severity category of acute pancreatitis defined by determinant-based classification. Hepatobiliary Pancreat Dis Int 2014; 13:323–327. 10. Nawaz H, Mounzer R, Yadav D, et al. Revised Atlanta and determinant-based classification: application in a prospective cohort of acute pancreatitis patients. Am J Gastroenterol 2013; 108:1911–1917. 11. Acevedo-Piedra NG, Moya-Hoyo N, Rey-Riveiro M, et al. Validation of the & determinant-based classification and revision of the Atlanta classification systems for acute pancreatitis. Clin Gastroenterol Hepatol 2014; 12:311–316. This study compares between the RAC and DBC in a community care setting. 12. Badalov N, Baradarian R, Iswara K, et al. Drug-induced acute pancreatitis: an evidence-based review. Clin Gastroenterol Hepatol 2007; 5:648–661. 13. Wu BU, Pandol SJ, Liu IL. Simvastatin is associated with reduced risk of acute && pancreatitis: findings from a regional integrated healthcare system. Gut 2015; 64:133–138. This study showed that simvastatin and atorvastatin have a protective role against development of acute pancreatitis after adjustment for age, sex, and cause. 14. Tolstrup JS, Kristiansen L, Becker U, Grønbaek M. Smoking and risk of acute and chronic pancreatitis among women and men: a population-based cohort study. Arch Intern Med 2009; 169:603–609. 15. Ye X, Lu G, Huai J, Ding J. Impact of smoking on the risk of pancreatitis: a & systematic review and meta-analysis. PLoS One 2015; 10:e0124075. This study reiterates smoking as an independent risk factor of acute pancreatitis. 16. Sun X, Huang X, Zhao R, et al. Meta-analysis: tobacco smoking may enhance & the risk of acute pancreatitis. Pancreatology 2015; 15:286–294. This study shows a dose dependent effect of smoking on development of acute pancreatitis. 17. Yadav D, Lee E, Papachristou GI, O’Connell M. A population-based evalua& tion of readmissions after first hospitalization for acute pancreatitis. Pancreas 2014; 43:630–637. This study evaluates the burden and pattern of pancreatitis-related readmissions after index hospitalization for acute pancreatitis in Allegheny County, Pennsylvania, USA.

18. Vipperla K, Papachristou GI, Easler J, et al. Risk of and factors associated with readmission after a sentinel attack of acute pancreatitis. Clin Gastroenterol Hepatol 2014; 12:1911–1919. This study evaluates the factors that determine early (within 30 days) and late (after 30 days) readmission of patients with acute pancreatitis. 19. Suchsland T, Aghdassi A, Ku¨hn K, et al. Predictive factors for and incidence of hospital readmissions of patients with acute and chronic pancreatitis. Pancreatology 2015; 15:265–270. 20. Kumaravel A, Stevens T, Papachristou GI, et al. A model to predict the severity of acute pancreatitis based on serum level of amylase and body mass index. Clin Gastroenterol Hepatol 2015; Mar 25. pii: S1542-3565(15)00304-3. doi: 10.1016/j.cgh.2015.03.018. [Epub ahead of print] 21. Mounzer R, Langmead CJ, Wu BU, et al. Comparison of existing clinical scoring systems to predict persistent organ failure in patients with acute pancreatitis. Gastroenterology 2012; 142:1476–1482. 22. Ince AT, Senturk H, Singh VK, et al. A randomized controlled trial of && homemonitoring versus hospitalization for mild nonalcoholic acute interstitial pancreatitis: a pilot study. Pancreatology 2014; 14:174– 178. This study introduces a new paradigm of home-based treatment of acute pancreatitis. Results of this study indicates that home-based monitoring for patients with mild acute pancreatitis has similar outcomes as hospital-based treatment. 23. Imrie CW. Prognostic indicators in acute pancreatitis. Can J Gastroenterol 2003; 17:325–328. 24. Lankisch PG, Weber-Dany B, Habel K, et al. The harmless acute pancreatitis score: a clinical algorithm for rapid initial stratification of nonsevere disease. Clin Gastroenterol Hepatol 2009; 7:702–705. 25. Talukdar R, Sharma M, Deka A, et al. Utility of the Harmless acute pancreatitis score in predicting a nonsevere course of acute pancreatitis: a pilot study in an Indian cohort. Indian J Gastroenterol 2014; 33:316–321. 26. Oskarsson V, Mehrabi M, Orsini N, et al. Validation of the harmless acute pancreatitis score in predicting nonsevere course of acute pancreatitis. Pancreatology 2011; 11:464–468. 27. Working Group IAP/APA Acute Pancreatitis Guidelines. IAP/APA evidencebased guidelines for the management of acute pancreatitis. Pancreatology 2013; 13 (4 Suppl 2):e1–e15. 28. Tenner S, Baillie J, DeWitt J, Vege SS, et al. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol 2013; 108:1400–1415. 29. Ola´h A, Romics L Jr. Enteral nutrition in acute pancreatitis: a review of the current evidence. World J Gastroenterol 2014; 20:16123–16131. 30. Zou L, Ke L, Li W, et al. Enteral nutrition within 72 h after onset of & acute pancreatitis vs delayed initiation. Eur J Clin Nutr 2014; 68:1288– 1293. This study explores early (within 72 h) versus delayed enteral nutrition therapy for patients with acute pancreatitis. 31. Bakker OJ, van Brunschot S, van Santvoort HC, et al. Early versus on-demand && nasoenteric tube feeding in acute pancreatitis. N Engl J Med 2014; 371:1983–1993. doi: 10.1056/NEJMoa1404393. This study by the Dutch Pancreatic Research group has concluded that the outcome of early oral feeding is similar to that of delayed (after 72 h) enteral feeding. 32. Poropat G, Giljaca V, Hauser G, Sˇtimac D. Enteral nutrition formulations for & acute pancreatitis. Cochrane Database Syst Rev 2015; 3:CD010605. [Epub ahead of print] This systematic review concludes that current evidence in favor of any specific type nutritional supplement is not adequate. 33. Yong L, Lu QP, Liu SH, Fan H. Efficacy of glutamine-enriched nutrition support for patients with severe acute pancreatitis: a meta-analysis. JPEN J Parenter Enteral Nutr 2015; Feb 5. pii: 0148607115570391. [Epub ahead of print] 34. van Santvoort Hjalmar C, Besselink Marc G, Bakker Olaf J, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med 2010; 362:1491–1502. 35. Hollemans RA, Bollen TL, van Brunschot S, et al. Predicting success of & catheter drainage in infected necrotizing pancreatitis. Ann Surg 2015; Mar 13. [Epub ahead of print] This study reports the patient and disease-related factors that could be used as predictors for success of catheter drainage for necrotic collections. 36. Borreca D, Bona A, Bellomo MP, et al. Timing of cholecystectomy in acute biliary pancreatitis. is still reasonable to wait? Minerva Chir 2015; Mar 31. [Epub ahead of print] 37. Vege SS, Atwal T, Chari ST, et al. Pentoxifylline treatment in predicted severe acute pancreatitis: a randomized double-blind placebo-controlled trial. Gastroenterology 2011; 144:5. (S-111–S-112). &

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To summarize recent data on classification systems, cause, risk factors, severity prediction, nutrition, and drug treatment of acute pancreatitis...
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