Purpose To investigate the association between body composition and adverse clinical outcomes in older patients with sepsis in the emergency department. Methods Body composition, including the skeletal muscle area, skeletal muscle index (SMI), mean skeletal muscle density (SMD), and intramuscular fat area, was measured at the level of the third lumbar vertebra (L3) on abdominal computed tomography scans. Clinical outcomes included 90-day mortality, 90-day readmission, and discharge to long-term care. According to sex-specific cut-off values of L3 SMI and SMD, patients were divided into low SMI, low SMD, both low SMI and low SMD, and neither low SMI nor low SMD groups. Results In total, 443 patients were included, 162 (36.6%) of whom died. Lower SMI and SMD, as continuous variables, were independent risk factors for 90-day mortality (adjusted hazard ratio [HR] = 0.947 and 0.963, respectively, both p < 0.001). Cut-off values of L3 SMI and L3 SMD were 32.24 cm2/m2 and 30.01 HU for men and 28.28 cm2/m2 and 28.20 HU for women, respectively. The both low SMI and low SMD group had an increased risk of 90-day mortality (adjusted HR=3.059, p < 0.001), 90-day readmission (adjusted odds ratio [OR]=2.859, p = 0.006), and discharge to long-term care (adjusted OR = 2.814, p = 0.007). Conclusions Lower muscle mass and muscle quality, as measured by skeletal muscle index and density, were independent risk factors for mortality among older patients with sepsis in the emergency department. Furthermore, patients with both low muscle mass and quality had an increased risk of mortality, readmission, and discharge to long-term care.
Objective: Monocyte dysfunction is critical to sepsis-induced immunosuppression. Programmed death ligand-1 (PD-L1) has shown a close relationship with inflammatory disorder among animal models and patients. We aimed to investigate the potential beneficial immunologic mechanisms of anti-PD-L1 on monocyte dysfunction of mice with sepsis. Methods: Firstly,we assessed the potential association between PD-L1 expression on monocyte subsets and sepsis severity as well as 28-day mortality. In thi study, 52 septic patients,28 septic shock patients and 40 healthy controls were enrolled and their peripheral whole blood were examined by Flow cytometry. Then Cecal ligation and puncture (CLP) were performed for establishing the mouse sepsis model. Subsequently, effect of anti-PD-L1 antibody on monocyte subset, major histocompatibility complex II(MHC II) expression, cytokine production, and survival were investigated. Results: PD-L1 expression on the classical monocytes (CD14++CD16−) was significantly upregulated among septic shock patients and the 28-d death group than non-septic shock group and 28-d survival group (P<0.05). Compared to septic mice, anti-PD-L1 treated mice had significantly elevated percentages of major histocompatibility complex (MHC) II on peripheral Ly6chi monocyte at 24 h after CLP. Our results showed that the anti-PD-L1 antibody markedly decreased the level of serum inflammatory cytokines serum interleukin (IL)-6, tumor necrosis factor (TNF)-a, and IL-10 in sepsis mice at 24h, 48h, and 72 h, respectively (P<0.05). The survival rate of CLP mice was significantly improved by anti-PD-L1 antibody treatment . Conclusion: Classical monocytes with high expression of PD-L1 was thought to be connected with sepsis progression. The PD-L1 blockade protects from sepsis, at least partially by inhibiting the reversal of monocyte dysfunction.
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