• M Braunstein, T Kusmenkov, W Böcker, and V Bogner-Flatz.
• Klinik für Allgemeine, Unfall- und Wiederherstellungschirurgie, Klinikum der Universität München, LMU München, Nußbaumstr. 20, 80336, München, Deutschland. Mareen.Braunstein@med.uni-muenchen.de.
• Unfallchirurg. 2019 Dec 1; 122 (12): 967-976.

BackgroundThe morbidity and mortality of polytrauma patients are substantially influenced by the extent of the posttraumatic inflammatory reaction. Studies have shown that TIMP‑1 and MMP‑9 play a major role in posttraumatic immune disorder in genome-wide mRNA microarray analyses. Furthermore, both showed differential gene expression profiles depending on the clinical parameters massive blood transfusion and traumatic brain injury.ObjectiveThe aim of this study was to evaluate TIMP‑1 and MMP‑9 serum concentrations in polytraumatized patients depending on the clinical parameters massive blood transfusion and traumatic brain injury in the early posttraumatic phase.Material And MethodsPolytrauma patients (≥18 years) with an "Injury Severity Score" (ISS) ≥ 16 points were enrolled in this prospective study. Serum levels of TIMP‑1 and MMP‑9 were quantified (at 0 h, 6 h, 12 h, 24 h, 48 h and 72 h) using an enzyme-linked immunosorbent assay (ELISA). Groups were divided according to the clinical parameter massive blood transfusion (≥10 red blood cell units [RBC units] in the first 24-hour posttrauma) and traumatic brain injury (CCT postive [cranial computed tomography]).ResultsFollowing massive blood transfusion (n = 21; 50 ± 15.7 years; ISS 39 ± 12.8 points) patients showed overall significantly increased TIMP‑1 levels (p = 0.003) and significantly higher TIMP‑1 values after 12-72 h. Traumatic brain injury patients (n = 28; 44 ± 19 years; ISS 42 ± 10 points) showed significantly higher MMP‑9 levels (p = 0.049) in the posttraumatic period.ConclusionPolytraumatized patients who received massive blood transfusions following major trauma showed significantly higher TIMP‑1 levels than patients who did not receive massive transfusions. This seems to be an expression of a massively excessive inflammatory reaction and therefore represents a substantial factor in the pathogenesis of severe posttraumatic immune dysfunction in this collective. Furthermore, the significant increase in MMP‑9 with accompanying traumatic brain injury reflects the pivotal role of matrix metalloproteinases in the pathophysiology of traumatic brain injury.

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