Abstract
PurposeAcute pancreatitis (AP) is an inflammatory disease. AP starts with sterile inflammation and is often complicated with critical local or systemic infection or sepsis in severe cases. Septic AP activates peptidyl arginine deiminase (PAD) and citrullinates histone H3 (CitH3), leading to neutrophil extracellular trap (NET) formation. Investigating the role of NETs and underlying mechanisms in septic AP may facilitate developing diagnostic and therapeutic approaches. In this study, we sought to identify the expression of CitH3 in septic AP patients and to analyze the correlation of CitH3 concentration with NET components as well as clinical outcomes.MethodsSeventy AP patients with or without sepsis (40 septic cases, 30 nonseptic cases) and 30 healthy volunteers were recruited in this study. Concentration of NET components (CitH3 and double-strain DNA) and key enzymes (PAD2/4) were measured. Clinical and laboratory characteristics of patients were recorded and analyzed.ResultsLevels of CitH3 were elevated significantly in septic AP patients compared with those in nonseptic AP and healthy volunteers. The area under the curve (AUC, 95% confidence interval) for diagnosing septic AP was 0.93 (0.86–1.003), and the cutoff was 43.05 pg/ml. Among septic AP cases (n = 40), the concentration of CitH3 was significantly increased in those who did not survive or were admitted to the intensive care unit, when compared with that in those who survived or did not require intensive care unit. Association analysis revealed that CitH3 concentration was positively correlated with PAD2, PAD4, dsDNA concentration, and Sequential Organ Failure Assessment scores.ConclusionCitH3 concentration increased in septic AP patients and was closely correlated with disease severity and clinical outcomes. CitH3 may potentially be a diagnostic and prognostic biomarker of septic AP.
Highlights
Acute pancreatitis (AP) is an inflammatory disease caused by digestive enzyme activation and self digestion [1]
Forty septic AP patients (SP), 30 noninfectious AP patients (NIP), and 30 healthy volunteers (HV) who were admitted into Xiangya Hospital, Central South University were enrolled in this study
A total of 100 individuals were enrolled in this study, including 40 septic AP patients, 30 noninfectious AP patients and 30 healthy volunteers (SP, NIP, and HV groups, respectively) from Xiangya Hospital, Central South University
Summary
Acute pancreatitis (AP) is an inflammatory disease caused by digestive enzyme activation and self digestion [1]. AP causes local or systemic sterile inflammation at early stages; up to 40%–70% of AP patients develop pancreatitis-related infection during the late stage or sepsis in severe cases [2]. Sepsis is the leading cause of death in AP; early diagnosis of septic AP and prompt initiation of treatments are the key to improving outcomes [3]. Identification of reliable circulating biomarkers to diagnose sepsis is highly desirable. Procalcitonin (PCT) has been recognized as a promising sepsis biomarker and is widely used in the clinic [6]. Diagnostic efficacy of PCT is compromised significantly because of its nonspecificity [7]. Novel strategies to identify key pathological signal pathways and improve the rapid diagnosis of septic AP are desperately needed
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