Copyright ©2009 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Nov 14, 2009; 15(42): 5260-5265
Published online Nov 14, 2009. doi: 10.3748/wjg.15.5260
Experimental evidence of obesity as a risk factor for severe acute pancreatitis
Jean-Louis Frossard, Pierre Lescuyer, Catherine M Pastor
Jean-Louis Frossard, Service of Gastroenterology, Geneva University Hospitals, Geneva 1205, Switzerland
Jean-Louis Frossard, Catherine M Pastor, Laboratory of pathophysiology and molecular imaging, Geneva University Hospitals, Geneva 1205, Switzerland
Pierre Lescuyer, Service of Genetics and Central Laboratory, Geneva University Hospitals, Geneva 1205, Switzerland
Author contributions: Frossard JL, Lescuyer P and Pastor CM have contributed equally to the design and writing and revising the manuscript.
Supported by (In part) The Swiss National Foundation for Sciences (to JLF), grant 320000-113225/1
Correspondence to: Jean-Louis Frossard, MD, Service of Gastroenterology, Geneva University Hospitals, Geneva 1205, Switzerland. jean-louis.frossard@hcuge.ch
Telephone: +41-22-3729340 Fax: +41-22-3729366
Received: July 8, 2009
Revised: September 25, 2009
Accepted: October 9, 2009
Published online: November 14, 2009

The incidence of acute pancreatitis, an inflammation of the pancreas, is increasing worldwide. Pancreatic injury is mild in 80%-90% of patients who recover without complications. The remaining patients may develop a severe disease with local complications such as acinar cell necrosis, abscess and remote organ injury including lung injury. The early prediction of the severity of the disease is an important goal for physicians in management of patients with acute pancreatitis in order to optimize the therapy and to prevent organ dysfunction and local complications. For that purpose, multiple clinical scale scores have been applied to patients with acute pancreatitis. Recently, a new problem has emerged: the increased severity of the disease in obese patients. However, the mechanisms by which obesity increases the severity of acute pancreatitis are unclear. Several hypotheses have been suggested: (1) obese patients have an increased inflammation within the pancreas; (2) obese patients have an increased accumulation of fat within and around the pancreas where necrosis is often located; (3) increase in both peri- and intra-pancreatic fat and inflammatory cells explain the high incidence of pancreatic inflammation and necrosis in obese patients; (4) hepatic dysfunction associated with obesity might enhance the systemic inflammatory response by altering the detoxification of inflammatory mediators; and (5) ventilation/perfusion mismatch leading to hypoxia associated with a low pancreatic flow might reduce the pancreatic oxygenation and further enhance pancreatic injury. Recent experimental investigations also show an increased mortality and morbidity in obese rodents with acute pancreatitis and the implication of the adipokines leptin and adiponectin. Such models are important to investigate whether the inflammatory response of the disease is enhanced by obesity. It is exciting to speculate that manipulation of the adipokine milieu has the potential to influence the severity of acute pancreatitis.

Keywords: Acute pancreatitis, Obesity, Adiponectin, Leptin