Features of cytokine profile in patients with local and generalized soft tissue infections

Aim. To determine the features of cytokine profile in patients with local and generalized soft tissue infections. Methods. The treatment results of 2350 patients with soft tissues infections since 1998 to 2012 were analyzed. ELISA test was used to measure tumor necrosis factor alpha and interleukin-1 receptor antagonist levels in 300 randomly picked patients with local (75 patients, comparison group) and generalized (225 patients, main group) forms of soft tissue infections. Results. In patients with generalized infections, tumor necrosis factor alpha level was 1.5 times higher in patients with mild systemic inflammatory response, 3.5 times higher - in patients with moderate and 6.7 times higher in patients with severe systemic inflammatory response compared to healthy controls. Interleukin-1 receptor antagonist levels were also elevated and related to the degree of inflammatory response, thus, it was the highest (2 times higher compared to controls) in patients with moderate systemic inflammatory response, while in patients with mild and severe inflammation it was only 30-40% higher. The significant increase in tumor necrosis factor alpha level associated with normal interleukin-1 receptor antagonist level is characteristic for different forms of sepsis. At the same time, increase in interleukin-1 receptor antagonist level associated with minimal changes in tumor necrosis factor alpha level can be used as a diagnostic criteria for compensated inflammatory response I patients with local infections cytokine profile was normal. The severity of systemic inflammation and clinical course of generalized infection depended not only on the absolute increase of cytokine levels, but on pro-inflammatory (tumor necrosis factor alpha) and anti-inflammatory (interleukin-1 receptor antagonist) cytokine levels misbalance. Conclusion. Examining the serum cytokine levels allows to confirm the diagnosis of generalized infection on early stages and to differentiate between compensated and non-ompensated systemic inflammatory response.

infection, sepsis, systemic inflammatory response, cytokines, tumor necrosis factor alpha, interleukin-1 receptor antagonist