Plasma hepatocyte growth factor levels are increased in systemic inflammatory response syndrome

Interleukin-1 (IL-1), a cytokine released from macrophages by endotoxin stimulation, has been shown to upregulate the genetic expression of the hepatocyte growth factor (HGF). The present study was conducted to determine whether plasma HGF is increased in patients with systemic inflammatory response syndrome (SIRS). The plasma levels of HGF, endotoxin, and beta-glucan were measured in 41 surgical patients without hepatic diseases, 18 of whom had been diagnosed with sepsis, and 33, with nonseptic SIRS. The plasma HGF was found to be significantly increased in the 18 patients with sepsis, at 0.69 +/- 0.47 ng/ml (mean +/- SD), and in the 23 patients with nonseptic SIRS, at 0.49 +/- 0.37 ng/ml, compared to values in 40 normal controls, at 0.10 +/- 0.03 ng/ml (P < 0.001). No significant correlations were observed between the plasma levels of HGF and endotoxin (r = 0.02) or beta-glucan (r = -0.05) in any of the patients; however, plasma HGF was significantly correlated with the WBC count (r = 0.34, P < 0.05) and with total bilirubin (r = 0.45, P < 0.01). Plasma HGF was also strongly correlated with alanine transaminase (ALT) in 8 patients with ALT levels higher than 50 U/l (r = 0.70), but there was no such correlation in 33 patients with ALT levels of 50 U/l or less (r = 0.30). Thus, although the clinicopathologic significance of HGF is not well understood, the present findings indicate that plasma HGF increases in response to infection or inflammation.