The effect of a tyrosyl-D-alanyl-glycyl-phenylalanyl-leucyl-arginine diacetate (Dalargin) on oxidative stress in patients with severe combined trauma: a prospective clinical study

INTRODUCTION: Severe combined trauma remains the leading cause of mortality and disability of the workable population. Under damaging factor influence, a whole cascade of pathological processes is triggered, leading to development of multiple organ failure. OBJECTIVE: Exploration of the effects synthetic analogue of tyrosyl-D-alanyl-glycyl-phenylalanyl-leucyl-arginine diacetate (Dalargin) on the dynamics of oxidative stress markers in patients with severe polytrauma and the development of organ dysfunction. MATERIALS AND METHODS: 104 patients with severe combined trauma were included in study. There were 38 patients in the Dalargin group and 66 patients in the control group. Patients from main group received Dalargin in the form of a constant infusion through a syringe dispenser at the dose of 10 mcg/kg/hour at first 12 hours of hospitalization and 5 mcg/kg/hour up to 72 hours from the moment of admission. The control group received standard treatment. Indicators of oxidative stress were evaluated at the time of admission (0 days), 1, 3, 5, 7, 10 and 14 days from the therapy onset. RESULTS: In the main group, there was a significant decrease in oxidative stress markers such as malondialdehyde from the first day of treatment (p < 0.05), normalization of stable nitric oxide metabolites at day 10, and a decrease in total antioxidant activity below normal throughout the observation period. Mortality was comparable in both groups (p > 0.05), but the length of hospital stay was lower in surviving patients in the Dalargin group (p < 0.05). The development of organ dysfunction (acute respiratory distress syndrome, acute kidney injury) was less frequent in the Dalargine group (p < 0.05), but infectious complications (pneumonia, meningitis, wound suppuration) were comparable. CONCLUSIONS: Dalargin leads to a decrease of oxidative stress markers and normalization of endothelial function indicators, which contributes to a decrease of organ dysfunction frequency.