Fortschritte in der Pankreatologie^[*]

Abstract

Prof. Dr. med. Joachim Mössner has always been committed to an honest, evidence-based medicine that focuses on the patient. To him, research has always been an important basis of good medicine: His research focuses on the physiological and pathophysiological processes of pancreatic diseases. He was successful in characterizing signaling pathways at the cellular level. Based on his findings, genetic association studies were conducted. He thus contributed to a better understanding of the development of acute and chronic pancreatitis.

Prof. Dr. med. Joachim Mössner setzte sich stets für eine ehrliche, evidenzbasierte Medizin ein, in deren Mittelpunkt der Patient steht. Sein Forschungsschwerpunkt waren die physiologischen und pathophysiologischen Prozesse der Pankreaserkrankungen. Indem er auf zellulärer Ebene Signalwege charakterisierte, auf denen später genetische Assoziationsstudien basierten, trug er zu einem besseren Verständnis der akuten und chronischen Pankreatitis bei.

Schlüsselwörter

Pankreas - Pankreatitis - akut - chronisch - Physiologie

Key words

pancreas - pancreatitis - acute - chronic - physiology

^* gewidmet Herrn Professor Dr. med. Joachim Mössner anlässlich seiner Verabschiedung als DMW-Herausgeber.

^** im Namen aller kurz- und langfristigen Mitarbeiterinnen und Mitarbeiter (von Aretin bis Zabel-Langhennig), Kolleginnen und Kollegen, Wegbegleiterinnen und Wegbegleitern von Herrn Professor Mössner.

• Literatur

• 1 Nagai H, Henrich H, Wunsch PH. et al. Role of pancreatic enzymes and their substrates in autodigestion of the pancreas. In vitro studies with isolated rat pancreatic acini. Gastroenterology 1989; 96: 838-847
• 2 Mössner J, Logsdon CD, Goldfine ID. et al. Do insulin and the insulin like growth factors (IGFs) stimulate growth of the exocrine pancreas?. Gut 1987; 28: 51-55
• 3 Mössner J, Logsdon CD, Goldfine ID. et al. Regulation of pancreatic acinar cell insulin receptors by insulin. Am J Physiol 1984; 247: G155-G160
• 4 Mössner J, Logsdon CD, Potau N. et al. Effect of intracellular Ca2+ on insulin-like growth factor II. internalization into pancreatic acini. Roles of insulin and cholecystokinin. J Biol Chem 1984; 259: 12350-12356
• 5 Mössner J, Secknus R, Meyer J. et al. Treatment of pain with pancreatic extracts in chronic pancreatitis: results of a prospective placebo-controlled multicenter trial. Digestion 1992; 53: 54-66
• 6 Halm U, Loser C, Lohr M. et al. A double-blind, randomized, multicentre, crossover study to prove equivalence of pancreatin minimicrospheres versus microspheres in exocrine pancreatic insufficiency. Aliment Pharmacol Ther 1999; 13: 951-957
• 7 Hoffmeister A, Mayerle J. Chronic Pancreatitis German Society of Digestive and Metabolic Diseases (DGVS). et al. S3-Consensus guidelines on definition, etiology, diagnosis and medical, endoscopic and surgical management of chronic pancreatitis German Society of Digestive and Metabolic Diseases (DGVS). Z Gastroenterol 2012; 50: 1176-1224
• 8 Kimura W, Mössner J. Role of hypertriglyceridemia in the pathogenesis of experimental acute pancreatitis in rats. Int J Pancreatol 1996; 20: 177-184
• 9 Teich N, Mössner J, Keim V. Mutations of the cationic trypsinogen in hereditary pancreatitis. Hum Mutat 1998; 12 (01) 39-43
• 10 Fjeld K, Weiss FU, Lasher D. et al. A recombined allele of the lipase gene CEL and its pseudogene CELP confers susceptibility to chronic pancreatitis. Nat Genet 2015; 47: 518-522
• 11 Rosendahl J, Landt O, Bernadova J. et al. CFTR, SPINK1, CTRC and PRSS1 variants in chronic pancreatitis: is the role of mutated CFTR overestimated?. Gut 2013; 62: 582-592
• 12 Rosendahl J, Witt H, Szmola R. et al. Chymotrypsin C (CTRC) variants that diminish activity or secretion are associated with chronic pancreatitis. Nat Genet 2008; 40: 78-82
• 13 Witt H, Beer S, Rosendahl J. et al. Variants in CPA1 are strongly associated with early onset chronic pancreatitis. Nat Genet 2013; 45: 1216-1220