To measure plasma interleukin-1β (IL-1β) and tumor necrosis factor-α (TNFα) concentrations after burn injury and to determine if these concentrations relate to clinical status.
Hospital burn unit
Thirty-one patients with second- or third-degree burns, covering 10% to 95% of body surface area.
Measurements and Main Results
Initial concentrations of IL-1β were increased (mean 188 ±PT 31 pg/mL), and the concentrations for each patient correlated with body temperature at the time of the blood sample (rho = 0.51, p <.015) (rho is a nonparametric statistical measure; a non-parametric analysis is mandatory for data that is categorical [Acute Physiology and Chronic Health Evaluation, APACHE, scores] and data that are not normally distributed [IL-1β and tumor necrosis factor, TNF, data]). Mean TNFα concentrations were initially 264 ±PT 132 pg/mL, and these concentrations were positively related to body temperature (rho = 0.41, p <.05) and inversely related to the total WBC count (rho = −0.45, p <.025). Through the course of hospitalization, plasma cytokine levels fluctuated, but transient increases (sometimes into the nanogram/mL range) did not consistently correspond to changes in clinical signs or severity of illness, as determined by APACHE II scores. The maximum plasma cytokine levels in any patient were not related to age, but maximum IL-1β concentrations were inversely related to burn size (rho = −0.46, p <.015). The final IL-1β concentrations measured in the patients who died (n = 7) were significantly less than measurements in surviving patients matched for burn size and age taken at approximately the same time after admission.
These results indicate that early after burn injury there is a correspondence of IL-1β and TNFα with certain host responses, but these correlations disappear with the progression of illness. In general, IL-1β and TNFα appear to be poor indicators of prognosis during burn injury; however, the association of mortality with low circulating IL-1β values supports the concept of IL-1β as being an essential mediator of host defenses.