Abstract
Background/aimSepsis is a condition caused by infection followed by unregulated inflammatory response which may lead to organ dysfunction. The aim of this study is to be the first in the literature and it has been designed to show the thiol/disulphide changes in patients with sepsis and septic shock and their correlation with acute phase reactants.Material and methodsA total of 113 patients (septic shock 53 and sepsis 60) and 60 healthy control subjects have been enrolled in this study from the period February 2018 to 2019. The patients were divided in 2 groups: nonsurvivors (74) and survivors (39). The investigation includes measurements of native thiol, total thiol, dynamic disulphide bond, oxidized thiol ratio, reduced thiol ratio and thiol oxidation reduction ratio, erythrocyte sedimentation rate, C-reactive protein, and procalcitonin. ResultsThe findings of this study suggest that changes in thiol levels play a role in the pathogenesis of patients with sepsis and septic shock.ConclusionsThiol/disulphide homeostasis is impaired in patients with sepsis and septic shock. Understanding the role of thiol/disulphide homeostasis in sepsis and septic shock may provide different therapeutic intervention strategies for patients.
Highlights
Sepsis, an exaggerated response to infection by the body, is a frequent problem of intensive care units that respond to physiological and pathological biochemical changes [1]
The findings of this study suggest that changes in thiol levels play a role in the pathogenesis of patients with sepsis and septic shock
Thiol/disulphide homeostasis is impaired in patients with sepsis and septic shock
Summary
An exaggerated response to infection by the body, is a frequent problem of intensive care units that respond to physiological and pathological biochemical changes [1]. The actual incidence is unknown, it is known that sepsis is still an important cause of mortality in intensive care units worldwide [2]. Concomitant factors such as uncontrolled diabetes mellitus, organ transplantation, surgical history, cirrhosis, and congestive heart failure may increase patients’ susceptibility to sepsis. A breakdown in the mitochondrial electron transmission systems and an increase in the inducible nitric oxide synthesis are the most important changes that occur [3,6,7].
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