1.Clinical efficacy of Xuebijing injection for the treatment of sepsis: A retrospective cohort study.
Zhao-Tang GONG ; Hong-Xin YANG ; Ben-Ben ZHU ; Huan-Huan LIU ; Guleng SIRI
Journal of Integrative Medicine 2024;22(6):645-651
OBJECTIVE:
The objective of this study was to investigate the clinical efficacy and safety of treating sepsis patients with Xuebijing injection (XBJI).
METHODS:
We conducted a retrospective analysis of 418 patients who experienced severe infections and were treated with XBJI from June 2018 to June 2021. Propensity score matching was used to match the patient cases. The study population included 209 pairs of cases (418 individuals), and the analysis included data from before and after a 14-day course of treatment with carbapenem alone, or carbapenem with XBJI.
RESULTS:
There were no significant differences in the 14-day mortality or length of hospital stay (P > 0.05) between the two groups. The combined treatment group had more patients with C-reactive protein that returned to normal levels (compared to baseline) than the non-combined treatment group (14.4% vs 8.1%; odds ratio [OR]: 0.528; 95% confidence interval [CI]: 0.282-0.991; P = 0.026). Similarly, the combined treatment group had higher procalcitonin attainment rate (55.0% vs 39.7%; OR: 0.513; 95% CI: 0.346-0.759; P = 0.001) than the non-combined treatment group. Further, more patients in the combined treatment group achieved normal creatinine levels than in the non-combined treatment group (64.1% vs 54.1%; OR: 0.659; 95% CI: 0.445-0.975; P = 0.037).
CONCLUSION
The combination of XBJI with carbapenem did not reduce the 14-day mortality rate of patients with severe infection, but it was able to reduce the level of inflammatory factors in patients with sepsis, and had a protective effect on liver and kidney function. Please cite this article as: Gong ZT, Yang HX, Zhu BB, Liu HH, Siri GL. Clinical efficacy of Xuebijing injection for the treatment of sepsis: A retrospective cohort study. J Integr Med. 2024; 22(6): 645-651.
Humans
;
Drugs, Chinese Herbal/administration & dosage*
;
Sepsis/mortality*
;
Retrospective Studies
;
Male
;
Female
;
Middle Aged
;
Aged
;
Treatment Outcome
;
Anti-Bacterial Agents/administration & dosage*
;
C-Reactive Protein/analysis*
;
Carbapenems/therapeutic use*
;
Length of Stay
;
Injections
;
Adult
;
Drug Therapy, Combination
;
Procalcitonin/blood*
2.Single Center Clinical Analysis of Bloodstream Infection Pathogens in Children with Acute Leukemia.
Jin-Hua CHU ; Kang-Kang LIU ; Ning-Ling WANG ; Song-Ji TU ; Hua-Ju CAI ; Zheng-Yu WU ; Lin-Hai YANG ; Zhi-Wei XIE
Journal of Experimental Hematology 2022;30(2):357-360
OBJECTIVE:
To investigate the clinical features, distribution of pathogenic bacteria, and drug resistance of bloodstream infection in children with acute leukemia.
METHODS:
Clinical data of 93 blood culture-positive children with acute leukemia from January 2015 to December 2019 in Department of Pediatrics, The Second Hospital of Anhui Medical University were analyzed retrospectively.
RESULTS:
In these 93 cases, 78 cases were in the period of neutrophil deficiency. There were 54 Gram-negative bacteria (G-) (58.1%) found through blood culture, and the top 4 strains were Escherichia coli (15.1%), Klebsiella pneumoniae (13.9%), Pseudomonas aeruginosa (6.5%), and Enterobacter cloacae (6.5%). There were 39 Gram-positive bacteria (G+) (41.9%) detected, and the top 4 strains were Staphylococcus epidermidis (10.8%), Streptococcus pneumoniae (6.5%), Staphylococcus hemolyticus (5.4%), and Staphylococcus human (5.4%). Among 74 strains of pathogenic bacteria from acute lymphoblastic leukemia (ALL) children, there were 29 strains of G+ bacteria (39.2%) and 45 strains of G- bacteria (60.8%). While in 19 strains from acute myeloblastic leukemia (AML) patients, G- bacteria accounted for 47.4% and G+ bacteria accounted for 52.6%. In 15 ALL children without neutropenia, G+ bacteria made up the majority of the strains (66.7%). In the 93 strains of pathogenic bacteria, 13 (13.9%) strains were multidrug-resistant. Among them, extended-spectrum β-lactamases accounted for 42.9%, carbapenemase-resistant enzyme Klebsiella pneumoniae 15.4%, and carbapenemase-resistant enzyme Enterobacter cloacae strains 33.3%, which were detected from G- bacteria. While, 13.3% of methicillin-resistant coagulase-negative Staphylococci accounted for 13.3% detected from G+ bacteria, but linezolid, vancomycin, teicoplanin Staphylococcus and Enterococcus resistant were not found. The average procalcitonin (PCT) value of G- bacteria infection was (11.02±20.282) ng/ml, while in G+ infection it was (1.81±4.911) ng/ml, the difference was statistically significant (P<0.05). The mean value of C-reactive protein (CRP) in G- infection was (76.33±69.946) mg/L, and that in G+ infection was (38.34±57.951) mg/L. The prognosis of active treatment was good, and only one case died of septic shock complicated with disseminated intravascular coagulation (DIC) and gastrointestinal bleeding caused by carbapenemase-resistant enzyme enterobacteriaceae.
CONCLUSION
G- is the major bacteria in acute leukemia children with bloodstream infection, but the distribution of ALL and AML strains is different. G- bacteria dominates in ALL, while G+ bacteria and G- bacteria are equally distributed in AML. Non-agranulocytosis accompanied by bloodstream infections is dominant by G+ bacteria. The mean value of PCT and CRP are significantly higher in G- bacteria infection than in G+ bacteria.
Acute Disease
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Anti-Bacterial Agents/therapeutic use*
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Bacteremia/microbiology*
;
Bacteria
;
Child
;
Drug Resistance, Bacterial
;
Humans
;
Leukemia, Myeloid, Acute/drug therapy*
;
Microbial Sensitivity Tests
;
Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy*
;
Procalcitonin
;
Retrospective Studies
;
Sepsis/drug therapy*
3.Effect of Tetrastigma hemsleyanum on sepsis and mechanism based on network pharmacology and experimental verification.
Jing-Ru ZHENG ; Chun-Lian JI ; Liang-Hui ZHAN ; Jin-Bao PU ; Li YAO
China Journal of Chinese Materia Medica 2022;47(17):4744-4754
Based on network pharmacology and in vivo experiment, this study explored the therapeutic effect of Tetrastigma hemsle-yanum(SYQ) on sepsis and the underlying mechanism. The common targets of SYQ and sepsis were screened out by network pharmacology, and the "SYQ-component-target-sepsis" network was constructed. The protein-protein interaction(PPI) network was established by STRING. Gene Ontology(GO) term enrichment and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment were performed based on DAVID to predict the anti-sepsis mechanism of SYQ. The prediction results of network pharmacology were verified by animal experiment. The network pharmacology results showed that the key anti-sepsis targets of SYQ were tumor necrosis factor(TNF), interleukin(IL)-6, IL-1β, IL-10, and cysteinyl asparate specific proteinase 3(caspase-3), which were mainly involved in Toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor kappaB(NF-κB) signaling pathway. The results of animal experiment showed that SYQ can decrease the content of C-reactive protein(CRP), procalcitonin(PCT), lactate dehydrogenase(LDH), IL-6, TNF-α, and IL-1β, increase the content of IL-10, and down-regulate the protein levels of Bcl-2-associa-ted X(Bax)/B-cell lymphoma 2(Bcl2), cleaved caspase-3, TLR4, MyD88, and p-NF-κB p65/NF-κB p65. In summary, SYQ plays an anti-inflammatory role in the treatment of sepsis by acting on the key genes related to inflammation and apoptosis, such as TNF-α, IL-6, IL-lβ, IL-10, Bax, Bcl2, and cleaved caspase-3. The mechanism is the likelihood that it suppresses the TLR4/MyD88/NF-κB signaling pathway, which verifies relative prediction results of network pharmacology.
Animals
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Anti-Inflammatory Agents/therapeutic use*
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C-Reactive Protein
;
Caspase 3/metabolism*
;
Interleukin-10
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Interleukin-6/metabolism*
;
Lactate Dehydrogenases/metabolism*
;
Myeloblastin/metabolism*
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Myeloid Differentiation Factor 88/metabolism*
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NF-kappa B/metabolism*
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Network Pharmacology
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Procalcitonin/therapeutic use*
;
Sepsis/genetics*
;
Toll-Like Receptor 4/metabolism*
;
Tumor Necrosis Factor-alpha/metabolism*
;
bcl-2-Associated X Protein/metabolism*

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