Thrombocytosis that occurs during the first hours after tissue injury aids in hemostasis, and platelets release many growth factors, such as transforming growth factor beta (TGF-ß) and insulin-like growth factor (IGF-1), which regulate inflammation, immune response, and cell migration. In the inflammatory phase, the local effects of inflammation can be amplified to a systemic level due to production of cytokines, such as tumor necrosis factor (TNF), interferon-y, interleukin-1 (IL-1), IL-6, IL-8, and IL-12 associated with a Th1 proinflammatory pathway, or cytokines with anti-inflammatory type 2 helper cell (Th2), including IL-4 and IL-10, which may contribute to the immunosuppression in sepsis and burns (Table 11.1). Thus critically ill patients have a biphasic immunological response. An initial excessive systemic inflammatory response syndrome (SIRS) with increased TNF, IL-1, and IL-10, interferon (IFN)-y or an inadequate compensatory anti-inflammatory response syndrome (CARS) is
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