Recent research into the cellular and biological mechanisms involved in the inflammatory response in acute pancreatitis has focused on cytokine interactions and their role in the systemic inflammatory response syndrome (SIRS) and the development of clinical complications in this disease. Platelet-activating factor (PAF) has been identified as a dominant cytokine in the SIRS of acute pancreatitis, and PAF antagonism has therefore been a target for therapeutic intervention. If a second phase III trial with lexipafant, a PAF antagonist is successful, then the first specific medical treatment for acute pancreatitis will become available. However, it is likely that lexipafant will ameliorate but not completely reverse the SIRS in acute pancreatitis, and alternative strategies require further study. This review discusses alternative approaches that have been recently investigated. These include modulation of the cellular immune response, manipulation of intracellular signalling mechanisms within the pancreatic acinar cell that initiate the cascade of damage resulting in acinar cell necrosis, and more conservative therapies such as enteral nutrition.
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