Pancreatic inflammatory disease can be classified as acute pancreatitis (AP) and chronic pancreatitis (CP) primarily by clinical criteria, with an obvious difference by restoration of normal function in the former or by permanent residual damage in the latter. Gallstones and alcohol are the most common causes of AP. Recent investigations have established that AP from all cause may disrupt normal stimulus-secretion coupling function within the acinar cell. This disruption within the acinar cell leads to an event termed 'co-localization' in which the digestive and lysosomal enzymes merge resulting in a premature activation of proteases. The mechanisms of inflammatory cells which adhere to endothelial cell are determined by a variety of mediators of cytokines released at the site of tissue damage. Cytokines hold the key for both local and systemic inflammatory response in AP. Besides, CP is a debilitating disease characterized by progressive and irreversible destruction of pancreatic tissue leading to exocrine and endocrine insufficiencies. Alcohol intake is the most common cause of CP. Mutations in the cationic trypsinogen gene were identified as causative gene for hereditary pancreatitis. The recognition of frequent cystic fibrosis transmembrane conductance regulator (CFTR) mutations and serine protease inhibitor, Kazal type 1 (SPINK1) mutations in idiopathic CP has hightened the awareness of importance of genetic mutations in CP. Pancreatic stellate cells represent the main cellular source of extracellular matrix in CP and play a key role in pancreatic fibrosis.
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