Trauma causes sustained elevation of soluble tumor necrosis factor receptors

Soluble tumor necrosis factor receptors (sTNF-R) are thought to modulate the systemic effects of tumor necrosis factor (TNF) by binding to serum TNF and preventing its interaction with target organs. Recently, it has been shown that traumatic injury causes the early release of the soluble forms of the 55 and 75 kDa membrane receptors for TNF. This study was done to determine the magnitude of TNF receptor elevation after trauma, to delineate the duration of this elevation, and to determine if sTNF-R levels correlate with severity of injury and outcome.

One hundred injured patients treated at a Level I Trauma Center were included in the study (74 males, 26 females, mean age of 29.4 years [range of ten to 72 years], mean injury severity score of 16.8 [range of zero to 75]). Serum samples were drawn from these patients beginning within one hour of injury and continuing for as many as 15 days. Samples were analyzed using polyclonal ELISA assays for TNF and sTNF 55 and 75 kDa receptor levels; control levels of receptor were determined from healthy volunteers.

Tumor necrosis factor was not measurable, but trauma caused immediate elevation of both receptor levels (within one hour of injury). Receptor levels remained elevated for as many as 15 days after injury. Late variations in levels were related to complications, that is, hypoxia, infection, and sepsis. Levels were significantly more elevated in critically ill patients and nonsurvivors.

We conclude that sTNF-R levels are significantly elevated after trauma, in the absence of measurable TNF. Levels are elevated for variable periods of time, which seem to depend on the severity of injury and complications.