Determination of the Immunoglobulin E Postoperative Variation as a Measure of Surgical Injury

Abstract

The aim of this study was to ascertain postoperative changes in immunoglobulin E (IgE) in patients undergoing different types of surgery and the possible correlation with the duration and type of surgery. Evidence suggests that surgery induces a predominant activation pattern through the T-helper-2 (Th2) cell pathway, increasing interleukins (IL-4, IL-5, IL-10, IL-13), inhibiting Th1 cell activation, and promoting B and Th2 cell activation. IgE production may indicate predominant Th2 pathway activation and may be a more persistent and easily measurable postoperative marker than IL-6 for measuring surgical trauma. Altogether, 180 patients undergoing different types of surgery for nonneoplastic and nonparasitic diseases were studied. All patients received the same type of anesthesia. Before surgery and on the first (1PO) and 7th (7PO) postoperative days we determined in peripheral blood the CD3, CD4, CD8, CD16, and CD19 cell percentages; IL-1, IL-2, IL-4, IL-6, and tumor necrosis factor (TNF) levels; and the IgA, IgG, IgM, total IgE, C3, C4, and CIC levels. On 1PO, all variables decreased except IgE, IL-1, IL-2, IL-4, IL-6, CIC, and CD19. Only IgE, IL-6, and CD19 increases showed a significantly statistical (ss) difference regarding preoperative values (0.01, 0.05, 0.001, respectively). Relations between the IL-4 and IgE increases (p < 0.01) and between the IgG decrease and IgE increase (p < 0.001) were found. On 7PO, only IgE was increased (p < 0.001). The IgE increase correlated with surgical trauma intensity (p < 0.05). We concluded that IgE increases during the early postoperative period, correlating with surgical injury intensity. The increase in the IgE level may be detected 24 hours after surgery and during the first 7 postoperative days depending on the type of surgery.

Differential effects of propofol and isoflurane on the activation of T‐helper cells in lung cancer patients

“…Our finding that propofol up-regulated the expression of CD28 on CD4 + T lymphocytes suggested that propofol might facilitate costimulatory-molecule expression on T-helper cells by unidentified mechanisms. However, we were unable to clarify if this propofol effect is a direct one, or indirect via the modulation of the cortisol response [29,30].…”

Insights into the Role of Chemokines, Damage-Associated Molecular Patterns, and Lymphocyte-Derived Mediators from Computational Models of Trauma-Induced Inflammation

“…We and others (86,111) have focused significant efforts on identifying how trauma might suppress CD4 + T-cell activation and push the adaptive immune response toward a counter-inflammatory phenotype. Early studies suggested that the counter-inflammatory behavior of that adaptive immune system may be a result of a shift toward high Th2 and low Th1 responses in mice and in patients.…”

Effect of age on cytokine response in an experimental model of osteomyelitis

“…As such mediators can be produced by multiple cell types, it is difficult to identify the cellular source of the different cytokines involved in the variations of inflammation associated with ageing. At the same time, the immune dysfunction associated with age may be added to the immunological alterations produced by surgery (Navarro-Zorraquino et al 2001). Indeed, age modulates the immune response to surgery (Zenilman 1988;Navarro-Zorraquino et al 1993;Ono et al 2001).…”