Invited Lecture (JSGS)
November 4 (Fri.), 15:20–16:00, Room 3 (Portopia Hotel South Wing Portopia Hall)
Invited Lecture-12

Pancreatology 2016: What is new?

J. Mossner
Divisions of Gastroenterology and Rheumatology, University Hospitals of Leipzig
Acute Pancreatitis (AP)Pathogenesis: B-cell CLL/lymphoma 3 (BCL3), a transcription factor, is upregulated in patients with AP or cholangitis. BCL3 may reduce the inflammatory response (Gastroenterology 2016;150:499). Peripancreatic fat necrosis worsens AP via unsaturated fatty acids (Gut 2016;65:100). Diagnosis: Which classification should we use to determine severity of acute pancreatitis? A modified Determinant-Based Classification revealed a better discriminatory power in comparison to Determinant-Based Classification and Revised Atlanta Classification (Crit Care Med 2016;44:910). Therapy: In mild biliary pancreatitis cholecystectomy should be performed during the same hospital stay. Interval cholecystectomy increases the risk of complications while waiting (Lancet 2015;386:1261). Very early compared with normal start of enteral feeding (PYTHON trial) does not lead to a better outcome in severe AP (NEJM 2014;271:1983). A preliminary study suggests that pentoxifylline via blockade of TNFalpha may be beneficial in predicted severe AP (Gastroenterology 2015;149:318). Chronic Pancreatitis (CP)See German S3-consensus guidelines on chronic pancreatitis: Definition, aetiology, diagnostic examinations, medical, endoscopic and surgical management of chronic pancreatitis (Z Gastroenterol 2015;53:1447). Pathogenesis: A recombined allele of the lipase gene CEL and its pseudogene CELP may play a role in the pathogenesis (Nat Genet 2015;47:518). The potential mechanisms are not related to premature protease activation. Impairment of autophagy induces chronic atrophic pancreatitis in mice via sex- and nutrition dependent mechanisms (Gastroenterology 2015;148:626). These factors could play a role in humans as well. A disruption of the function of CFTR by ethanol may play a role in the pathogenesis of CP (Gastroenterology 2015;148:427). Acute relapsing alcohol induced pancreatitis may lead to CP (Gastroenterology 2015;149:1490). Diagnosis: Secretin stimulated MRCP is more sensitive than MRCP in detection of duct abnormalities (Gastroenterology 2014;147:646). Thus, decision making whether therapeutic ERCP should be performed, is improved. Therapy: Pregabalin improves treatment of pain (Pancreas 2016;45:381). Benign bile duct stenosis due to CP is best treated by SEMS (JAMA 2016:315:1250).Pancreatic CancerDiagnosis: Measurement of a cocktail of various parameters, such as GNAS, KIRAS, may help to differentiate benign from malignant cystic tumors (Gastroenterology 2015;149:1501). Therapy: The prognosis is still dismal. Nanoliposomal irinotecan may be another option for palliative treatment (Lancet 2016;387:545). Chemoradiotherapy does not improve survival compared with chemotherapy alone (JAMA 2016;315:1844). In adjuvant chemotherapy a combination of gemcitabine with capecitabine leads to a significant longer survival as compared to gemcitabine alone (ESPAC 4 trial; ASCO 2016).
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