Hanna Sternby

Early management of acute pancreatitis: A review of the best evidence

In the 20th century early management of acute pancreatitis often included surgical intervention, despite overwhelming mortality. The emergence of high-quality evidence (randomized controlled trials and meta-analyses) over the past two decades has notably shifted the treatment paradigm towards predominantly non-surgical management early in the course of acute pancreatitis. The present evidence-based review focuses on contemporary aspects of early management (which include analgesia, fluid resuscitation, antibiotics, nutrition, and endoscopic retrograde cholangiopancreatography) with a view to providing clear and succinct guidelines on early management of patients with acute pancreatitis in 2017 and beyond.

Predictive Capacity of Biomarkers for Severe Acute Pancreatitis.

Background: Early prediction of severe acute pancreatitis (SAP) substantially improves treatment of patients. A large amount of biomarkers have been studied with this objective. The aim of this work was to study predictive biomarkers using preset cut-off levels in an unselected population of patients with acute pancreatitis (AP). Methods: 232 patients (52.2% males, median age 66 years) with AP admitted to Skåne University Hospital, Malmö, were consecutively enrolled. Blood samples were collected upon admission and clinical data were gathered both prospectively at inclusion and through review of medical notes. Cut-off levels were defined based on the reports of prior studies, and through their results eight biomarkers (IL-1β, IL-6, IL-8, IL-10, TNF-α, MCP-1, procalcitonin and D-dimer) were selected for analysis. Results: Of the patients, 83.2% had mild AP and 16.8% had SAP. Levels of IL-1β, IL-6 and IL-10 were significantly (p < 0.05) higher upon admission in the group with SAP. When applying the preset cut-off levels on our material, sensitivity and specificity for prediction of severity were low. Receiver operating characteristic curves showed that selected cut-off levels were acceptable, but areas under the curves were inferior compared to other studies. The results did not improve when using the revised Atlanta 2012 classification. Conclusions: Previous studies on severity prediction of AP are difficult to compare due to large variations in setups and outcomes. Calculated cut-offs in our cohort were in acceptable range from preset levels, however areas under the curves were low, indicating suboptimal biomarkers for the unselected population investigated. For comparable results and possible clinical implementations, future studies need large consecutive series with a reasonable percentage of severe cases. Additionally, novel biomarkers need to be explored.

Lifetime and baseline alcohol intakes and risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition study

Recent evidence suggested a weak relationship between alcohol consumption and pancreatic cancer (PC) risk. In our study, the association between lifetime and baseline alcohol intakes and the risk of PC was evaluated, including the type of alcoholic beverages and potential interaction with smoking. Within the European Prospective Investigation into Cancer and Nutrition (EPIC) study, 1,283 incident PC (57% women) were diagnosed from 476,106 cancer‐free participants, followed up for 14 years. Amounts of lifetime and baseline alcohol were estimated through lifestyle and dietary questionnaires, respectively. Cox proportional hazard models with age as primary time variable were used to estimate PC hazard ratios (HR) and their 95% confidence interval (CI). Alcohol intake was positively associated with PC risk in men. Associations were mainly driven by extreme alcohol levels, with HRs comparing heavy drinkers (>60 g/day) to the reference category (0.1–4.9 g/day) equal to 1.77 (95% CI: 1.06, 2.95) and 1.63 (95% CI: 1.16, 2.29) for lifetime and baseline alcohol, respectively. Baseline alcohol intakes from beer (>40 g/day) and spirits/liquors (>10 g/day) showed HRs equal to 1.58 (95% CI: 1.07, 2.34) and 1.41 (95% CI: 1.03, 1.94), respectively, compared to the reference category (0.1–2.9 g/day). In women, HR estimates did not reach statistically significance. The alcohol and PC risk association was not modified by smoking status. Findings from a large prospective study suggest that baseline and lifetime alcohol intakes were positively associated with PC risk, with more apparent risk estimates for beer and spirits/liquors than wine intake.

Dietary folate intake and pancreatic cancer risk: Results from the European Prospective Investigation into Cancer and Nutrition: Dietary folate intake and pancreatic cancer risk

Pancreatic cancer (PC) has an exceptionally low survival rate and primary prevention strategies are limited. Folate plays an important role in one‐carbon metabolism and has been associated with the risk of several cancers, but not consistently with PC risk. We aimed to investigate the association between dietary folate intake and PC risk, using the standardised folate database across 10 European countries. A total of 477,206 participants were followed up for 11 years, during which 865 incident primary PC cases were recorded. Folate intake was energy‐adjusted using the residual method. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. In multivariable analyses stratified by age, sex, study centre and adjusted for energy intake, smoking status, BMI, educational level, diabetes status, supplement use and dietary fibre intake, we found no significant association between folate intake and PC risk: the HR of PC risk for those in the highest quartile of folate intake (≥353 μg/day) compared to the lowest (<241 μg/day) was 0.81 (95% CI: 0.51, 1.31; ptrend = 0.38). In current smokers, a positive trend was observed in PC risk across folate quartiles [HR = 4.42 (95% CI: 1.05, 18.62) for ≥353 μg/day vs. <241 μg/day, ptrend = 0.01]. Nonetheless, there was no significant interaction between smoking and dietary folate intake (pinteraction = 0.99). We found no association between dietary folate intake and PC risk in this large European study.

Short article : Presence, extent and location of pancreatic necrosis are independent of aetiology in acute pancreatitis

Objective The most common aetiologies of acute pancreatitis (AP) are gallstones, alcohol and idiopathic. The impact of the aetiology of AP on the extent and morphology of pancreatic and extrapancreatic necrosis (EXPN) has not been clearly established. The aim of the present study was to assess the influence of aetiology on the presence and location of pancreatic necrosis in patients with AP. Patients and methods We carried out a post-hoc analysis of a previously established multicentre cohort of patients with AP in whom a computed tomography was available for review. Clinical data were obtained from the medical records. All computed tomographies were revised by the same expert radiologist. The impact of aetiology on pancreatic and EXPN was calculated. Results In total, 159 patients with necrotizing pancreatitis were identified from a cohort of 285 patients. The most frequent aetiologies were biliary (105 patients, 37%), followed by alcohol (102 patients, 36%) and other aetiologies including idiopathic (78 patients, 27%). No relationship was found between the aetiology and the presence of pancreatic necrosis, EXPN, location of pancreatic necrosis or presence of collections. Conclusion We found no association between the aetiology of AP and the presence, extent and anatomical location of pancreatic necrosis.

Contents Vol. 56, 2016

I. Alwayn, Halifax D.K. Bartsch, Marburg C. Bassi, Verona W.O. Bechstein, Frankfurt am Main J.A. Bradley, Cambridge M. Cikirikcioglu, Geneva P.-A. Clavien, Zurich U. Dahmen, Jena R.W.F. de Bruin, Rotterdam S. Fichtner-Feigl, Regensburg H. Friess, Munich G. Galata, London D.J. Gouma, Hilversum J.K. Habermann, Lübeck M. Heberer, Basel M. Heger, Amsterdam T. Hubert, Lille W.R. Jarnagin, New York, N.Y. J.C. Kalff, Bonn M.W. Laschke, Homburg/Saar H.-A. Lehr, Friedrichshafen C.M. Malata, Cambridge T. Minor, Bonn M. Morino, Torino J. Pirenne, Leuven A. Schachtrupp, Melsungen T. Schmitz-Rixen, Frankfurt a.M. R. Schramm, Munich L. Steinstraesser, Oldenburg A. Szijártó, Budapest R.H. Tolba, Aachen M. van Griensven, Munich T.M. van Gulik, Amsterdam M.A. Venermo, Helsinki M.H. Wilhelmi, Hannover D.C. Winter, Dublin Y. Yamamoto, Akita Clinical and Experimental Surgery