Cytokines have been shown to play a pivotal role in multiple organ dysfunct
ion, a major cause of death in severe acute pancreatitis. Moreover, the two
-hit hypothesis of the cytokine-induced systemic inflammatory response synd
rome explains the variable individual response to severe acute pancreatitis
and the impact of secondary events such as sepsis or therapeutic intervent
ion. Many experimental anti-cytokine therapies have been administered follo
wing induction of experimental pancreatitis, and have proved to be therapeu
tic. Patients with severe pancreatitis present early because of pain. Clear
ly then a window for therapeutic intervention is available between onset of
symptoms and peak pro-inflammatory cytokine expression. It is this fundame
ntal observation that convinces many in the field that the treatment of AP
will be one of the first clinical successes for novel drugs or therapy that
seek to modulate the inflammatory response.