Prophylactic Antibiotics in Cirrhosis: Are They Promoting or Preventing Infections?

García–Tsao, Guadalupe

doi:10.1002/cld.819

Cited by 13 publications

(24 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Targeting gut-bacterial translocation using antibiotic prophylaxis to reduce LPS-induced monocyte PGE2 production may improve monocyte dysfunction. Indeed, persistent gut translocation of bacterial products causes immune exhaustion (9), however concerns over antimicrobial resistance limit use of this approach (40). Non-antibiotic therapies to reduce gut-bacterial translocation may also improve PGE2-induced monocyte dysfunction (41).…”

Section: Discussionmentioning

confidence: 99%

Monocyte dysfunction in decompensated cirrhosis is mediated by the prostaglandin E2-EP4 pathway

et al. 2021

View full text Add to dashboard Cite

This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

show abstract

Section: Discussionmentioning

confidence: 99%

Monocyte dysfunction in decompensated cirrhosis is mediated by the prostaglandin E2-EP4 pathway

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Because bacterial translocation from the gut lumen to extraintestinal sites causes infections, prevention of infections is http://www.e-cmh.org https://doi.org/10.3350/cmh.2020.0086 mostly based on the use of orally administered, poorly absorbed antibiotics (known as selective intestinal decontamination). 33,34 Several antibiotics were tested and/or used for this purpose, such as polymyxin, neomycin, gentamycin, colistin, paromomycin, and trimethoprim/sulfamethoxazole. 35,36 Currently, norfloxacin and rifaximin are the forms of selective intestinal decontamination for which there is the most evidence in cirrhosis.…”

Section: Intestinal Dysbiosismentioning

confidence: 99%

From intestinal dysbiosis to alcohol-associated liver disease

Mendes

Schnabl

2020

Clin Mol Hepatol

View full text Add to dashboard Cite

Alcohol-associated intestinal dysbiosis and bacterial overgrowth can lead to a dysregulation of tryptophan metabolism and lower production of indoles. Several of these indole derivatives are aryl hydrocarbon receptor ligands that, in turn, are involved in antimicrobial defense via induction of interleukin-22 (IL-22). IL-22 increases the expression of intestinal regenerating islet-derived 3 (Reg3) lectins, which maintain low bacterial colonization of the inner mucus layer and reduce bacterial translocation to the liver. Chronic alcohol consumption is associated with reduced intestinal expression of Reg3β and Reg3γ, increased numbers of mucosa-associated bacteria and bacterial translocation. Translocated microbial products and viable bacteria reach the liver and activate the innate immune system. Release of inflammatory molecules promotes inflammation, contributes to hepatocyte death and results in a fibrotic response. This review summarizes the mechanisms by which chronic alcohol intake changes the gut microbiota and contributes to alcohol-associated liver disease by changing microbial-derived metabolites.

show abstract

“…Therefore, clinicians should pay significant attention to the prevention of infections, which could avoid secondary complications (further development of decompensation, recurrent infections, ACLF and death) of cirrhosis. 37 Basophils may induce and expand inflammation by producing specific cytokines and proteases and are Open access related to T helper 2 immune responses. 38 39 However, their role in decompensated liver cirrhosis has rarely been reported.…”

Section: Discussionmentioning

confidence: 99%

Recompensation factors for patients with decompensated cirrhosis: a multicentre retrospective case–control study

Wang

Zhao

et al. 2021

BMJ Open

View full text Add to dashboard Cite

ObjectivesWe aimed to evaluate recompensation factors among patients with decompensated cirrhosis.DesignA multicentre retrospective case–control study was conducted. Data were collected from and compared between groups of patients with recompensated and acute decompensated cirrhosis. Univariable and multivariable logistic regressions were used to select indicators associated with recompensation among patients with decompensated cirrhosis with different complications. A decision tree with 10-fold cross-validation was used to develop the model to identify patients with recompensation. We followed the transparent reporting of a multivariable prediction model for individual prognosis or diagnosis (TRIPOD) guideline for development and reporting of the new model.SettingThe study was conducted in six tertiary public hospitals in Chongqing, China.ParticipantsThis study included 3953 patients with decompensated cirrhosis.ResultsIn the total sample of included patients, there were 553 patients with recompensation and 3400 patients with acute decompensation, including 1158 patients with gastrointestinal bleeding, 1715 patients with a bacterial infection, 104 patients with hepatic encephalopathy and 423 patients with ascites. The most relevant indicator of recompensation selected by the decision tree model was albumin, with a threshold of 40 g/L. Total protein, haemoglobin, basophil percentage, alanine aminotransferase, neutrophil-to-lymphocyte ratio and diabetes were also selected to subsequently distinguish patients. The terminal nodes with a probability of recompensation was 0.89. The overall accuracy rate of the model was 0.92 (0.91–0.93), and it exhibited high specificity (86.9%) and sensitivity (92.6%).ConclusionsThe occurrence of recompensated cirrhosis could be identified by albumin, total protein, haemoglobin, basophil percentage, alanine aminotransferase, neutrophil-to-lymphocyte ratio and diabetes. These simple variables may help clinicians develop a treatment plan to encourage patients with decompensated cirrhosis to recompensate.

show abstract

Prophylactic Antibiotics in Cirrhosis: Are They Promoting or Preventing Infections?

Abstract: http://aasldpubs.onlinelibrary.wiley.com/hub/journal/10.1002/(ISSN)2046-2484/video/14-3-reading-garcia-tsao a video presentation of this article https://www.wileyhealthlearning.com/Activity/6904685/disclaimerspopup.aspx questions and earn CME

Cited by 13 publications

References 18 publications

Monocyte dysfunction in decompensated cirrhosis is mediated by the prostaglandin E2-EP4 pathway

Monocyte dysfunction in decompensated cirrhosis is mediated by the prostaglandin E2-EP4 pathway

From intestinal dysbiosis to alcohol-associated liver disease

Recompensation factors for patients with decompensated cirrhosis: a multicentre retrospective case–control study

Contact Info

Product

Resources

About