Published online Nov 7, 2014. doi: 10.3748/wjg.v20.i41.15200
Revised: May 21, 2014
Accepted: June 14, 2014
Published online: November 7, 2014
Processing time: 239 Days and 0.8 Hours
Acute pancreatitis (AP) is one of the most common diseases of the gastrointestinal tract, bearing significant morbidity and mortality worldwide. Current treatment of AP remains unspecific and supportive and is mainly targeted to aggressively prevent systemic complications and organ failure by intensive care. As acute pancreatitis shares an indistinguishable profile of inflammation with sepsis, therapeutic approaches have turned towards modulating the systemic inflammatory response. Targets, among others, have included pro- and anti-inflammatory modulators, cytokines, chemokines, immune cells, adhesive molecules and platelets. Even though, initial results in experimental models have been encouraging, clinical implementation of immune-regulating therapies in acute pancreatitis has had a slow progress. Main reasons include difficulty in clinical translation of experimental data, poor understanding of inflammatory response time-course, flaws in experimental designs, need for multimodal approaches and commercial drawbacks. Whether immune-modulation in acute pancreatitis remains a fact or just fiction remains to be seen in the future.
Core tip: Acute pancreatitis is a common entity with significant mortality worldwide. Treatment remains non-specific and mainly supportive, mostly focusing on intensive care. Presence of inflammatory response syndrome during AP has driven recent immune-modulating therapeutic attempts in experimental models, including cytokine, chemokine, immune cell and other inflammatory mediator blockade. Although initial data are promising, translation to clinical routine has been less encouraging. The authors attempt to elucidate whether and to what extent tampering with the immune burst triggered by acute pancreatitis could actually ensure better outcomes, or that remains a farfetched expectation.