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Abstract
Sepsis, defined as a dysregulated host response to infection, causes the interruption of homeostasis resulting in metabolic changes. An examination of patient metabolites, such as amino acids, during the early stage of sepsis may facilitate diagnosing and assessing the severity of the sepsis. The aim of this study was to compare patterns of urine and serum amino acids relative to sepsis, septic shock and survival. Urine and serum samples were obtained from healthy volunteers (n = 15) once or patients (n = 15) within 24 h of a diagnosis of sepsis or septic shock. Concentrations of 25 amino acids were measured in urine and serum samples with liquid chromatography-electrospray mass spectrometry. On admission in the whole cohort, AAA, ABA, mHis, APA, Gly-Pro and tPro concentrations were significantly lower in the serum than in the urine and Arg, Gly, His, hPro, Leu, Ile, Lys, Orn, Phe, Sarc, Thr, Tyr, Asn and Gln were significantly higher in the serum than in the urine. The urine Gly-Pro concentration was significantly higher in septic shock than in sepsis. The serum Cit concentration was significantly lower in septic shock than in sepsis. The urine ABA, mHis and Gly-Pro, and serum Arg, hPro and Orn concentrations were over two-fold higher in the septic group compared to the control group. Urine and serum amino acids measured in septic patients on admission to the ICU may shed light on a patient’s metabolic condition during sepsis or septic shock.
Highlights
Sepsis, defined as a dysregulated host response to infection, causes the interruption of homeostasis resulting in metabolic changes
It has been suggested that sepsis could be diagnosed by detecting increased concentrations of the parameters that are commonly assessed in clinical practice, such as procalcitonin (PCT)[3], C-reactive protein (CRP)[4], lipopolisaccharide-binding protein (LBP)[5], and pro-atrial natriuretic peptide[6]
They regulate protein turnover, enzyme activity and ion fluxes and affect cell signaling and inflammatory reactions by participating in the regulation of gene expression and protein phosphorylation. They are responsible for maintaining organ and body protein homeostasis, which is severely disturbed in the course of sepsis and includes the immune-inflammatory aspect and the massively disrupted metabolic homeostasis associated with an overall catabolic s tate[16]
Summary
Sepsis, defined as a dysregulated host response to infection, causes the interruption of homeostasis resulting in metabolic changes. It has been suggested that sepsis could be diagnosed by detecting increased concentrations of the parameters that are commonly assessed in clinical practice, such as procalcitonin (PCT)[3], C-reactive protein (CRP)[4], lipopolisaccharide-binding protein (LBP)[5], and pro-atrial natriuretic peptide (pro-ANP)[6]. They are insufficiently sensitive or specific as standard tools for the early diagnosis of s epsis[4]. The metabolic changes occurring in sepsis represent both systemic and cellular alterations and result in aberrations in the entire metabolic r esponse[17,18]
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