a1 MRC Secretary, Control Research Group, Department of Physiology, School of Biomedical Sciences, Crown Street, University of Liverpool, Liverpool L69 3BX, UK. E-mail: email@example.com
Excessive alcohol consumption is linked to a variety of major health problems, including the severe inflammation of the pancreas, which may lead to premature death of the individual.1 Hospital admissions in the United Kingdom due to acute pancreatitis were recently shown to have doubled over a 30 year period,2 in parallel with an estimated doubling of alcohol consumption in this country, and the incidence of the disease is dramatically increasing. Within the European Union, acute pancreatitis may attain an incidence of up to 1 per 1000 individuals per year. In accord with trends in drinking lifestyle in the UK, admissions of younger people and women have correspondingly escalated over the last few decades, and alcohol-related problems have placed a heavy financial burden on the healthcare system. So-called ‘binge drinking’, a prevalent feature of the current ‘drinking culture’, is commonly linked to patients presenting at clinic with episodes of acute pancreatitis, often manifested initially as excruciating abdominal pain and vomiting. Of these individuals, approximately 20% will develop a more extensive form of the disease with significant pancreatic necrosis triggering a systemic inflammatory response syndrome (SIRS) that may cause multiple organ failure; up to a third of these patients will die. The extent of necrotic cell death in these patients is a major determinant of the severity of acute pancreatitis and disease outcome.3 However, the precise way in which alcohol triggers the cellular damage that forms the basis of this severe and debilitating disease has remained elusive.