Acute pancreatitis (AP) is described as activation of pancreas enzymes inside the pancreas and digestion of pancreas tissue via its
own enzymes (autodigestion). Acute pancreatitis is diagnosed according to criteria indicated in Atlanta symposium in 1992, namely
abdominal pain accompanied by three-fold increase in serum amylase or lipase levels. According to this symposium, acute pancreatitis is
classified into two groups, as mild and severe disease states. While rate of mild disease is 70-80% in acute pancreatitis, severe cases present with
a rate of 20-30%. Though certain variations in etiology are seen in different countries, gallbladder stones and alcohol is held responsible in approximately 70-
80% of cases. Various scoring systems are being used to determine clinical severity and prognosis in acute pancreatitis. Ranson is a
specific scoring system for acute pancreatitis and is based on certain clinical and laboratory findings of patients at referral and at 48th hour.
APACHE II is rather a general scoring system; beginning from initial referral to hospital, it provides evaluation of certain physiological
functions and general health status of patients at 24-hour intervals. BISAP score are also newer scoring system for pancreatitis. Balthazar
scoring describes anatomic structures more precisely and may indicate complications like pancreatic inflammation and necrosis. Endogenous
inflammatory mediators play a significant role in pathogenesis of AP . Best known among these mediators is interleukin-6 (IL-6) and
itâs released at an early stage as a response to inflammation, enabling the synthesis of acute phase proteins, primarily C-reactive protein (CRP),
in liver. While measuring IL-6 levels are beneficial in determining early reaction of the organism to inflammation, serum CRP levels will be
helpful in evaluating early phase response.
Last date updated on July, 2014