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Compartmentalization of the Inflammatory Response during Acute Pancreatitis

Correlation with Local and Systemic Complications

Department of Intensive Care and Emergency Medicine, and Experimental Immunology Unit, Department of Surgery, St. Luc University Hospital, Brussels, Belgium; and Division of Medical Intensive Care, University Hospital of Geneva, Geneva, Switzerland

Correspondence and requests for reprints should be addressed to Thierry Dugernier, M.D., Department of Intensive Care and Emergency Medicine, St. Luc University Hospital, Hippocrate Avenue, 10 B-1200 Brussels, Belgium. E-mail: thierry.dugernier{at}skynet.be

Local and systemic inflammation has been implicated in the pathogenesis of acute pancreatitis and secondary multisystem organ failure. To assess the pro- and antiinflammatory response, the site of mediator production, and their route of diffusion, we sampled simultaneously ascites, thoracic lymph, and blood at the onset of end-organ dysfunction and for the following 6 days in 60 patients with acute pancreatitis. We used immunoassays to measure pro- and antiinflammatory cytokines and cell-based bioassays to assess the net pro- and antiinflammatory activity elicited by the biological fluids. Tumor necrosis factor- and interleukin-1ß were detected in less than 15% of blood and lymph samples. Secondary pro- and antiinflammatory cytokines were found to be elevated early and throughout the sampling period in all compartments. Cytokine levels decreased from ascites to lymph to blood, suggesting a splanchnic origin. Prolonged diversion of ascites and lymph did not alter cytokine gradients, suggesting mediator transfer via the splanchnic blood circulation. Although a net proinflammatory activity ascribed to interleukin-1ß was detected in ascites, a net antiinflammatory activity was measured in virtually all lymph and blood samples, suggesting that the pancreas and the splanchnic area are sites of a proinflammatory response and that an early, dominant, and sustained antiinflammatory activity takes place in circulating compartments.

Key Words: acute necrotizing pancreatitis • cytokines • inflammation mediators • multiple organ failure • systemic inflammatory response syndrome

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