Send to

Choose Destination
See comment in PubMed Commons below
Pancreas. 1988;3(2):159-61.

Correlation of serum amylase levels with pancreatic pathology and pancreatitis etiology.

Author information

Department of Surgery, Harbor/University of California at Los Angeles Medical Center, Torrance 90509.


Fifty-one patients, 35 men and 16 women, with acute pancreatitis were studied prospectively with early computed tomography (CT). Etiological factors for acute pancreatitis were alcohol abuse (n = 28), gallstones (n = 14), pancreas cancer (n = 3) and miscellaneous (n = 6). Admission serum amylase levels ranged between 68-5,856 U/L with a mean of 1,090 +/- 1,369 U/L. The mean serum amylase level was significantly different between patients with alcoholic pancreatitis (439 +/- 302 U/L) and gallstone pancreatitis (2,480 +/- 1,575) (p less than 0.001). The initial pancreatic CT findings and corresponding mean serum amylase levels were in CT grade A (pancreas normal) 1,499 +/- 1,569 U/L (n = 11), in CT grade B (pancreatic enlargement with inflammation confined to pancreas) 1,144 +/- 1,542 U/L (n = 18), in CT grade C (inflammatory extension into one peripancreatic space) 722 +/- 962 U/L (n = 13) and in CT grade D (inflammatory extension into two or more peripancreatic spaces) 590 +/- 369 U/L (n = 9). However, on separating the etiology subgroups, there was no increase or decrease in the serum amylase level with increasing pancreatic inflammatory involvement. Pancreatic complications (pseudocyst, abscess, necrosis) requiring surgical intervention developed only in patients with CT grades C and D. We conclude that within the etiologic subgroups there is no correlation between the initial serum amylase level and the extent of pancreatic involvement visualized by CT. These findings provide a pathological basis for the clinical observation that the initial serum amylase level cannot predict the outcome in acute pancreatitis.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wolters Kluwer
    Loading ...
    Support Center