Leukocyte Activation in the Peripheral Blood of Patients With Cirrhosis of the Liver and SIRS

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Abstract
Objective. —Leukocyte adhesion plays an important role in inflammation. Adhesion molecules such as CD11b on polymorphonuclear neutrophil leukocytes (PMNs) up-regulate in response to tumor necrosis factor—α, interleukin-8 (IL-8), and other mediators that are involved in systemic inflammatory response syndrome (SIRS). This study examined the behavior of CD11b and other membrane molecules in SIRS in relation to serum cytokines and the severity of illness. Design. —Survey study. Setting. —Liver transplantation intensive care unit at a tertiary care center. Patients. —A consecutive sample of 22 patients admitted to the liver transplantation intensive care unit for complications related to cirrhosis of the liver in the absence of other disease. Sixteen of the patients developed SIRS and multiple organ dysfunction syndrome with suspected bacterial infections. Seven control subjects were also studied. Main Outcome Measures. —Modified Goris organ failure score and Acute Physiology and Chronic Health Evaluation II score. Results. —Mean serum IL-6 levels, but not IL-1 β or tumor necrosis factor—α levels, correlated with organ failure (r=0.79,P<.001). Leukocyte cell-surface markers fluctuated from day to day. The mean of several values was more stable. Mean CD11b and CD35 on PMNs correlated with serum IL-6 level (r=0.75,P<.001, andr=0.77,P<.005, respectively). Up-regulation of both CD11b and CD35 display on PMNs correlated with organ failure (r=0.74,P<.001, andr=0.71,P<.01, respectively). Polymorphonuclear neutrophil leukocyte L-selectin, CD31, and CD16 were simultaneously decreased, consistent with PMN activation. Monocytes appeared to be activated, but the pattern of surface molecule display was different. Conclusions. —In human SIRS, the circulating monocyte and PMN pools undergo alterations suggestive of leukocyte activation, including up-regulation of PMN CD11b in correlation with the serum IL-6 level and severity of organ dysfunction. (JAMA. 1995;274:58-65)