Diagnosis and Staging of Acute Pancreatitis

Abstract

Determination of serum pancreatic enzymes remains the gold standard for the diagnosis of acute pancreatitis. Clinical symptoms and signs are of major importance in suspecting the disease, but they are not accurate enough to confirm the diagnosis. The different serum pancreatic enzymes have a similar accuracy in the diagnosis of acute pancreatitis. Total amylase, pancreatic isoamylase and lipase are preferred, since simple, rapid and inexpensive enzymatic methods are commercially available. More expensive and cumbersome methods (e.g. RIA or ELISA for pancreatic elastase) are useful only in special clinical circumstances. For early etiological classification of acute pancreatitis serum pancreatic enzymes and even different enzyme ratios are not reliable. For this purpose, determination of AST, bilirubin and alkaline phosphatase may make it possible to distinguish between biliary and nonbiliary origin of the disease. Ultrasonography and computed tomography provide very valuable information regarding not only etiology but also local complications of acute pancreatitis. Once the diagnosis of acute pancreatitis has been established, prognostic classification of the disease is required for adequate monitoring and treatment. Clinical symptoms and signs do not allow early assessment of the prognosis of acute pancreatitis. Multivariate scoring systems are sensitive but not sufficiently specific for the identification of severe pancreatitis. Among several biochemical markers commercially available for the assessment of severity, C-reactive protein and PMN-elastase appear to be the most valuable. These markers allow a proper selection of patients who need further investigation by contrast-enhanced CT (the gold standard for detection of pancreatic necrosis).

Hyperlipaemia intensifies the course of acute oedematous and acute necrotising pancreatitis in the rat.

“…A prevalence of hyperlipaemia in acute pancreatitis of between 4.5% and 47% has been reported in previous studies.' [1][2][3][4][5][6] This wide range of hyperlipaemia in acute pancreatitis seems to result from the patient populations, because patients with alcoholic pancreatitis have hyperlipaemia more frequently than patients with biliary pancreatitis.11 [14][15] Serum triglyceride values higher than 10 to 20 mmol/l seem to be a serious risk factor for developing acute pancreatitis. 14 15 Particularly in patients suffering from familial hyperlipoproteinaemia (types I, IV, and V according to the classification of Frederickson), acute pancreatitis occurs with an incidence of up to 21%.11 1219 In those cases, patients have increased serum concentrations of chylomicrons and triglycerides.…”

Phospholipase A2 Isoforms in Acute Pancreatitis

“…1 The clinical course of this disease is either mild and self-limiting (edematous pancreatitis) or severe and lifethreatening (necrotizing pancreatitis), and the treatment of the latter continues to be a challenge to even the best clinicians. 2 Histomorphologically, acute pancreatitis is associated with varying degrees of inflammation and autodigestion.…”