Increased Endotoxin Activity Is Associated with the Risk of Developing Acute-on-Chronic Liver Failure.

acute-on-chronic liver failure endotoxin activity rifaximin

Journal

Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588

Informations de publication

Date de publication:
14 May 2020
Historique:
received: 17 04 2020
revised: 06 05 2020
accepted: 12 05 2020
entrez: 20 5 2020
pubmed: 20 5 2020
medline: 20 5 2020
Statut: epublish

Résumé

Acute-on-chronic liver failure (ACLF) leads to systematic inflammatory response syndrome and multiple organ failure. This study investigated the relationship between endotoxin (Et) and ACLF with the aim of determining whether Et activity (EA) is useful as a predictive biomarker of ACLF development and whether rifaximin treatment decreased the risk of ACLF development. Two hundred forty-nine patients with liver cirrhosis were enrolled in this study. Et concentration was determined in the whole blood by a semiquantitative EA assay. Predictive factors of ACLF development and the risk of ACLF development with and without rifaximin treatment were identified by univariate and multivariate analysis using Fine and Gray's proportional subhazards model. EA level was higher in Child-Pugh class B than in class A patients, and class B patients had an increased risk of ACLF development compared with class A patients. Multivariate analysis showed that EA level was a predictive factor independently associated with ACLF development. Rifaximin decreased EA level and the risk of ACLF development in Child-Pugh class B patients. Et levels were associated with functional liver capacity and were predictive of ACLF development in cirrhotic patients. Rifaximin decreased Et level and the risk of ACLF development in advanced cirrhotic patients.

Identifiants

pubmed: 32422875
pii: jcm9051467
doi: 10.3390/jcm9051467
pmc: PMC7290888
pii:
doi:

Types de publication

Journal Article

Langues

eng

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Auteurs

Hiroaki Takaya (H)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Tadashi Namisaki (T)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Shinya Sato (S)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Kosuke Kaji (K)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Yuki Tsuji (Y)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Daisuke Kaya (D)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Yukihisa Fujinaga (Y)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Yasuhiko Sawada (Y)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Naotaka Shimozato (N)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Hideto Kawaratani (H)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Kei Moriya (K)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Takemi Akahane (T)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Akira Mitoro (A)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Hitoshi Yoshiji (H)

Department of Gastroenterology, Nara Medical University, Kashihara, Nara 634-8522, Japan.

Classifications MeSH