OBJECTIVETo investigate the dynamic activity of NF-kappaB at the early stage of injury in multiple trauma patients and the protective effects of ulinastain.

METHODSFrom January 2008 to May 2010, patients with multiple traumas admitted to our emergency department were enrolled in this study. Their age varied from 20-55 years. All enrolled patients were assigned randomly into control group (26 cases of multiple injury without ulinastain treatment), ulinastain group (25 cases of multiple injury with ulinastain treatment), and mild injury group (20 cases) for basic control. The inclusion criteria for mild injury group were AIS-2005 less than or equal to 3, single wound, previously healthy inhospital patients without the history of surgical intervention. In addition to routine treatment, patients in ulinastain group were intravenously injected 200 000 IU of ulinastain dissolved in 100 ml of normal saline within 12 hours after injury and subsequently injected at the interval of every 8 hours for 7 days. NF-kappaB activity in monocytes and the level of TNF-alpha,IL-1, IL-6 in serum on admission (day 0), day 1, 2, 3, 4, and 7 were measured. Data were compared and analyzed between different groups.

RESULTSNF-kappaB activity in monocytes and TNF-alpha,IL-1 and IL-6 of these patients reached peak levels at 24 hour after trauma, with gradual decrease to normal at 72 hour after trauma. NF-kappaB activity and levels of TNF-alpha,IL-1 and IL-6 were lower in ulinastain group than control one, without any significant difference between the two groups. The mean duration for systemic inflammatory response syndrome and multiple organ dysfunction syndrome was 7 d+/-3.1 d and 10 d+/-3.5 d in ulinastain group and control group respectively, and showed a significant difference.

CONCLUSIONSNF-kappaB activity in monocytes and the levels of inflammatory cytokines in multiply injured patients increased transiently at the early stage of trauma. Ulinastain may shorten the duration of systemic inflammatory response syndrome and multiple organ dysfunction syndrome, but does not show the ability to decrease the activity of NF-kappaB .