Coagulation Abnormalities in Acute Pancreatitis

Acute pancreatitis (AP) is a potentially lethal disorder with no specific medical treatment. AP is characterized by a spectrum of symptoms, ranging from a local inflammatory process to the more severe form (acute necrotizing pancreatitis) which is associated with a systemic inflammatory response and a mortality rate of 27-45%. A number of risk factors have been identified for AP including alcohol abuse, gallstones, abdominal surgery/injury, cigarette smoking, cystic fibrosis, endoscopic retrograde cholangiopancreatography, hypercalcemia, hyperparathyroidism, hypertriglyceridemia, infection, pancreatic cancer, and injury to the abdomen (Pandol et al., 2007). Alcohol abuse and the development of gallstones account for the majority of AP cases. In AP, inappropriate intracellular activation of digestive enzymes within the pancreas (e.g. trypsin, chymotrypsin, elastase) is the main initiating event. The development of acute necrotizing pancreatitis is usually associated with pancreatic glandular necrosis. Acinar cell apoptosis, the release of cytokines, activation of coagulation, tissue ischemia, and tissue necrosis are key factors in the progression of the condition, as well as in the development of associated extrapancreatic complications (Steinberg & Tenner, 1994; McKay & Buter, 2003; Pandol et al., 2007).