Potential role of reactive oxygen species in pancreatitis-associated multiple organ dysfunction

Severe acute pancreatitis is still associated with substantial morbidity and mortality. Experimental and clinical studies have demonstrated that reactive oxygen species (ROS) represent early occurring inflammatory mediators contributing to cell dysfunction, both locally in the pancreas and remote organs.

A systematic literature review was conducted to investigate the potential roles of intra- and intercellular, as well as interorgan signaling of ROS in the development of pancreatitis-associated multiple organ dysfunction syndrome (MODS). A text word search of the Medline, PubMed and Cochrane databases, and a manual search of the citations from these references, was performed.

ROS directly compromise cellular damage and regulate intercellular signals in pancreatitis-associated MODS. ROS are involved in leukocyte activation, production of cytokines, endothelial barrier dysfunction, and microcirculatory barrier dysfunction in acute pancreatitis. Beside effects on intercellular signaling, ROS also affect intracellular events and activate the transcription factor nuclear factor kappa B that regulates inflammatory cytokine expression.

ROS is a critical factor responsible for the development of pancreatitis-induced remote organ dysfunction via intercellular and interorgan signaling. The role of antioxidant treatment, included as a part of multimodal management, remains to be investigated.