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1.
Yonsei Med J ; 61(2): 145-153, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31997623

RESUMO

PURPOSE: This study investigated multidrug-resistant (MDR) pathogens and antibiotic strategies of culture-positive spontaneous ascitic infection (SAI) in patients with acute decompensated cirrhosis. MATERIALS AND METHODS: We retrospectively analyzed 432 acute decompensated cirrhotic patients with culture-positive SAI from 11 teaching hospitals in China (January 2012 to May 2018). A Cox proportional hazards model analysis was conducted to identify independent predictors of 28-day mortality. RESULTS: A total of 455 strains were isolated from 432 ascitic culture samples. Gram-negative bacteria (GNB), gram-positive bacteria (GPB), and fungi caused 52.3, 45.5, and 2.2% of all SAI episodes, respectively. Episodes were classified as nosocomial (41.2%), healthcare-related (34.7%), and community-acquired (24.1%). Escherichia coli (13.4%) and Klebsiella pneumoniae (2.4%) were extended-spectrum ß-lactamase producing isolates. The prevalence of methicillin-resistant Staphylococcus aureus was 1.1%. Ceftazidime, cefepime, aztreonam, and amikacin were recommended as first-line antibiotics agents for non-MDR GNB infections; piperacillin/tazobactam and carbapenems for MDR GNB in community-acquired and healthcare-related or nosocomial infections, respectively; and vancomycin or linezolid for GPB infections, regardless of drug-resistance status. Multivariate analysis revealed days of hospital stay before SAI, upper gastrointestinal bleeding, white blood cell count, alanine aminotransferase, serum creatinine concentration, total bilirubin, and international normalized ratio as key independent predictors of 28-day mortality. CONCLUSION: MDR pathogens and antibiotic strategies were identified in patients with acute decompensated cirrhosis with culture-positive SAI, which may help optimize therapy and improve clinical outcomes.


Assuntos
Antibacterianos/uso terapêutico , Ascite/tratamento farmacológico , Ascite/microbiologia , Farmacorresistência Bacteriana Múltipla , Cirrose Hepática/tratamento farmacológico , Cirrose Hepática/microbiologia , Antibacterianos/farmacologia , China , Feminino , Bactérias Gram-Negativas/efeitos dos fármacos , Bactérias Gram-Positivas/efeitos dos fármacos , Humanos , Cirrose Hepática/mortalidade , Masculino , Staphylococcus aureus Resistente à Meticilina , Testes de Sensibilidade Microbiana , Pessoa de Meia-Idade , Estudos Retrospectivos , Sobreviventes
2.
J Ethnopharmacol ; 145(1): 175-81, 2013 Jan 09.
Artigo em Inglês | MEDLINE | ID: mdl-23127651

RESUMO

AIM OF THE STUDY: Fuzheng Huayu (FZHY) is a Chinese compound herbal preparation which consists of six Chinese herbs. This study examines the preventative effects of FZHY on liver fibrosis induced by carbon tetrachloride (CCl(4)) and explores its possible mechanisms of action. MATERIALS AND METHODS: Liver fibrosis was induced in male C57BL/6N mice by injecting a 10% CCl(4) solution intraperitoneal twice a week for six weeks. After 6 weeks of treatment, serum ALT and AST assay, liver tissue histological examination and immunostaining were carried out to examine the liver function and fibrosis degree. The expression levels of alpha-smooth muscle actin (SMA) were measured by quantitative real-time PCR and western blot. Hepatic natural killer (NK) cells were isolated from liver and evaluated by FACS. RESULTS: Upon pathological examination, the FZHY-treated mice showed significantly reduced liver damage. The expression of α-SMA increased markedly upon treatment with CCl(4) and the increase was reversed by FZHY treatment. FZHY treatment also enhanced the activation of hepatic NK cells and the production of interferon-gamma (IFN-γ). The protective effects of FZHY were reversed in the mice that were depleted of NK cells by anti-ASGM-1 Ab treatment. CONCLUSIONS: FZHY can efficiently inhibit CCl(4)-induced liver fibrosis. Furthermore, the depletion of NK cells attenuates the protective effects of FZHY. We conclude that FZHY could be an effective drug for liver fibrosis, and its mechanism of action involves the activation of hepatic NK cells.


Assuntos
Medicamentos de Ervas Chinesas/uso terapêutico , Células Matadoras Naturais/efeitos dos fármacos , Cirrose Hepática/tratamento farmacológico , Fígado/efeitos dos fármacos , Actinas/biossíntese , Alanina Transaminase/metabolismo , Animais , Aspartato Aminotransferases/metabolismo , Autoanticorpos/imunologia , Autoanticorpos/farmacologia , Tetracloreto de Carbono , Modelos Animais de Doenças , Medicamentos de Ervas Chinesas/farmacologia , Gangliosídeo G(M1)/imunologia , Interferon gama/biossíntese , Células Matadoras Naturais/imunologia , Cirrose Hepática/sangue , Cirrose Hepática/induzido quimicamente , Masculino , Camundongos , Camundongos Endogâmicos C57BL
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