One out of ten cases of
acute pancreatitis develops into severe
acute pancreatitis which is a life threatening disorder with a high mortality rate. The other nine cases are self limiting and need very little
therapy. The specificity of good clinical judgement on admission, concerning the prognosis of the attack, is high (high specificity) but misses a lot of severe cases (low sensitivity). The prediction of severity in
acute pancreatitis was first suggested by John HC Ranson in 1974. Much effort has been put into finding a simple scoring system or a good
biochemical marker for selecting the severe cases of
acute pancreatitis immediately on admission. Today
C-reactive protein is the method of choice although this marker is not valid until 48-72 hours after the onset of
pain. Inflammatory mediators upstream from CRP like
interleukin-6 and other
cytokines are likely to react faster and preliminary results for some of these mediators look promising. Another successful approach has been to study markers for the activation of
trypsinogen such as TAP and
CAPAP. This is based on studies showing that active
trypsin is the initial motor of the inflammatory process in
acute pancreatitis. In the near future a combined clinical and laboratory approach for early severity prediction will be the most reliable. Clinical judgement predicts 1/3 of the severe cases on admission and early markers for either
inflammation or
trypsinogen activation should accurately identify 50-60% of the mild cases among the rest, thus missing only 2-4% of the remaining severe cases. One problem is that there is no simple and fast method to analyze any of these parameters.