Αρχειοθήκη ιστολογίου

Τετάρτη 10 Ιανουαρίου 2018

A high portal venous pressure gradient increases gut-related bacteremia and consequent early mortality after living donor liver transplantation

AbstractBackgroundPortal hypertension (PHT) is defined as a portal venous pressure gradient (PVPG) exceeding 5 mmHg, which results in severe clinical manifestations. However, the validity of intraoperative PVPG monitoring and the association between PHT and bacterial translocation (BT) after liver transplantation remain unclear.MethodsIn this retrospective study, 223 patients who underwent primary adult-to-adult living donor liver transplantation (ALDLT) from 2008 to 2015 were divided into 2 groups based on the PVPG at the end of the operation: high PVPG (>5 mmHg, n=69) and low PVPG (≤5 mmHg, n=154). The clinical factors were compared between the groups, and the association between a high PVPG and posttransplant bacteremia/bacterial infections was investigated.ResultsThe high PVPG group had a significantly higher incidence of bacteremia (46% vs. 24%, p<.001 higher mortality rate vs. p=".002)," and poorer survival the high pvpg group had a particularly incidence of bacteremia caused by bacteria including enterobacteriaceae bacteroides spp. enterococcus multivariate analysis showed that>5 mmHg (odds ratio, 2.55; 95% confidence interval, 1.18–5.55; p=.017) was an independent predictor of bacteremia due to gut bacteria.ConclusionsMonitoring of the PVPG is clinically meaningful for predicting patients' prognosis. In particular, a high PVPG with a threshold of 5 mmHg at the end of ALDLT may increase gut-related bacteremia through the mechanism of BT, resulting in early mortality. Background Portal hypertension (PHT) is defined as a portal venous pressure gradient (PVPG) exceeding 5 mmHg, which results in severe clinical manifestations. However, the validity of intraoperative PVPG monitoring and the association between PHT and bacterial translocation (BT) after liver transplantation remain unclear. Methods In this retrospective study, 223 patients who underwent primary adult-to-adult living donor liver transplantation (ALDLT) from 2008 to 2015 were divided into 2 groups based on the PVPG at the end of the operation: high PVPG (>5 mmHg, n=69) and low PVPG (≤5 mmHg, n=154). The clinical factors were compared between the groups, and the association between a high PVPG and posttransplant bacteremia/bacterial infections was investigated. Results The high PVPG group had a significantly higher incidence of bacteremia (46% vs. 24%, p<.001 higher mortality rate vs. p=".002)," and poorer survival the high pvpg group had a particularly incidence of bacteremia caused by bacteria including enterobacteriaceae bacteroides spp. enterococcus multivariate analysis showed that>5 mmHg (odds ratio, 2.55; 95% confidence interval, 1.18–5.55; p=.017) was an independent predictor of bacteremia due to gut bacteria. Conclusions Monitoring of the PVPG is clinically meaningful for predicting patients' prognosis. In particular, a high PVPG with a threshold of 5 mmHg at the end of ALDLT may increase gut-related bacteremia through the mechanism of BT, resulting in early mortality. Corresponding author: Shintaro Yagi, Ph.D., Department of Surgery, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan. Telephone: +81-75-751-3242; FAX: +81-75-751-4263; E-mail: shintaro@kuhp.kyoto-u.ac.jp Authorship S.Yao and S.Yagi designed the study and wrote the draft. S.Yao, T.Iida, and Y.Okamura acquired the data. M.Nagao analyzed the data as a specialist of infection prevention. R.Uozumi analyzed the data as a specialist of medical statistician. S. Yagi, T. Iida, Y.Okamura, T.Anazawa, H.Okajima, T.Kaido and S.Uemoto performed living-donor liver transplantations, followed up the patients. M.Nagao, T.Anazawa, H.Okajima, T.Kaido, S.Uemoto contributed to editing the manuscript. S.Uemoto supervised the study design and revised the manuscript. Disclosures The authors have no conflicts of interest or financial ties to disclose. Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

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