Proton pump inhibitor treatment aggravates bacterial translocation in patients with advanced cirrhosis and portal hypertension

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Abstract: Recent studies have linked proton pump inhibitor (PPI) treatment to increased complications of cirrhosis, such as bacterial infections and hepatic encephalopathy. However, the underlying pathophysiological mechanisms remain unclear. The present study investigated the hypothesis that PPI treatment may promote adverse effects in patients with advanced cirrhosis by affecting subclinical bacterial translocation (BT) from the gut into the portal venous bloodstream. Blood samples from the portal vein were obtained during implantation of a transjugular intrahepatic portosystemic shunt (TIPS) in a total of 80 cirrhosis patients with PPI treatment (PPI group, n = 57) and without PPI treatment (no-PPI group, n = 23). BT was identified using a 16S ribosomal RNA gene (V1V2 region) polymerase chain reaction. The microbiota composition in the portal venous blood samples was further analyzed by deep amplicon sequencing. Indeed, the prevalence of BT was significantly higher in the PPI group compared to the no-PPI group (86.0% vs 52.2%, P = 0.001). Importantly, this effect was not attributable to group differences in the severity of cirrhosis, parameters of portal hypertension, or medication. Microbiome analyses showed significantly increased alpha-diversity (Shannon) in the portal venous blood of the PPI group. Taxonomic analyses revealed significantly increased Streptococcus abundances in these patients. The present study reveals aggravated BT in patients with advanced cirrhosis and portal hypertension receiving PPI therapy. Increased BT could be an important pathomechanism contributing to the adverse effects of PPI treatment in patients with cirrhosis

Standort
Deutsche Nationalbibliothek Frankfurt am Main
Umfang
Online-Ressource
Sprache
Englisch
Anmerkungen
mBio. - 14, 5 (2023) , mbio.00492-23, ISSN: 2150-7511

Ereignis
Veröffentlichung
(wo)
Freiburg
(wer)
Universität
(wann)
2023
Urheber

DOI
10.1128/mbio.00492-23
URN
urn:nbn:de:bsz:25-freidok-2388518
Rechteinformation
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Letzte Aktualisierung
25.03.2025, 13:46 MEZ

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