*2.1.2 Congenital abnormalities*

Chole-dochal cyst constitutes the most principal cause of AP. In case of abnormal junction between pancreatic and biliary ducts the sphincter of Oddi encircles


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**Figure 1.**

*Pediatric Pancreatitis: Not a Rare Entity DOI: http://dx.doi.org/10.5772/intechopen.85370*

*2.1.3 Drugs and chemotherapeutic agents*

they could experience cancer recurrence [5].

mon channel [3].

*2.1.4 Trauma*

clinically silent [6].

**2.2 Pathophysiology**

inhibition of secretion [7].

*Pathophysiology of acute pancreatitis.*

a single channel leading to bile reflux into the Wirsung duct is communication between in course of sphincter contraction or bilestone impingement in the com-

Drug-induced acute pancreatitis accounts for 21% of all cases in pediatric population. Valproic acid, radiocontrast and corticosteroids can induce pancreatitis

L-asparaginase-associated pancreatitis (AAP) occurs in 0.7–24% of children treated for acute lymphoblastic leukemia with mortality rates of 2–5%. Older children demonstrate an high risk for developing acute pancreatitis and if it occurs

Pediatric pancreatic injuries are uncommon and can be mostly ascribed to vehicle accidents. Anyway because of its retroperitoneal location pancreas is preserved in case of minor abdominal traumas and a pancreatic transection can occur

Acute pancreatitis is due to an organ injury with a subsequent inflammatory response that may involve both adjacent and distant structures. The first pathogenetic event may be represented by an acinar cell injury (**Figure 1**) that produces pancreatic edema with the activation of the inflammatory pathway. The release of cytokines and chemokines leads to a systemic inflammatory response (SIRS) and to

Several hypotheses have been advanced explaining the mechanism of this acinar cell damage. The autodigestion model focused on a premature calcium-mediated intracellular trypsinogen activation in trypsin (**Figure 1**). Trypsin then activates digestive enzymes that mediate acinar cell injury. On the other hand, recent studies in animal models of AP highlight the pathogenetic role of colocalized zymogens and lysosomes, intra acinar activation of zymogens, nuclear factor-κb activation and

complications such as pancreatic necrosis, shock and distant organ failure.

in the context of epilepsy or inflammatory bowel diseases [4].
