Pancreatitis is an inflammatory disease of the pancreas characterized by acute and chronic condition as well as varying duration and severity. Acute pancreatitis (AP) is a severe abdominal inflammation, characterized by parenchymal edema, necrosis with occasional presence of pseudocysts, abscess, hemorrhage, and inflammatory cell infiltration (Chan & Leung, 2007a). Its disease spectrum varies from mild edematous to severe disease with fatal complications. Pancreatic acinar cells are very susceptible to inflammation during an episode of AP attack. It is believed that some initiating factors can lead to the premature transformation of inactive pro-proteases into active proteases within the pancreas. The active proteases degrade a number of cellular proteins such as the structural protein F-actin, thus leading to the collapse and malfunction of acinar and pancreatic damage, a process known as autodigestion of the pancreas (Singh et al., 2001).
Etiology and PrognosisSome AP-triggering environmental toxins are known to directly affect pancreatic acinar cells, leading to rupture and necrosis, and eventually an extensive inflammatory response. Epidemiological studies have revealed that the morbidity rate of the disease depends on which regions are examined, ranging from 50 to 800 cases per 1,000,000 people annually. Actually, AP is more prevalent in Caucasian than in Asian populations. The incidence rate is 700-800 and 150-420 per million annually in the USA and UK, respectively (Banks, 2002); however, it is just 106-205 per million annually in Japan (Sekimoto et al., 2006). Similar studies in China and Hong Kong have been inconsistent. In 2007, there were only 1976 patients with AP admitted to hospital from 15 Chinese tertiary care centres during the period from 1990 to (Bai et al., 2007. Despite this discrepancy, there are an increasing number of individuals with AP, probably due to life-style changes and increased exposure to risk factors in recent decades.