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Personalized Medicine for Liver Disease
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Personalized Medicine for Liver Disease

A special issue of Journal of Personalized Medicine (ISSN 2075-4426).

Deadline for manuscript submissions: closed (15 May 2022) | Viewed by 2297

Special Issue Editor

Dr. Giuseppe Marrone

E-Mail Website
Guest Editor
Internal Medicine and Gastroenterology Area, Fondazione Policlinico Universitario A. Gemelli, Catholic University of Rome, 00168 Rome, Italy
Interests: liver diseases; fatty liver; hepatology; liver transplantation; hepatocellular carcinoma; liver cirrhosis

Special Issue Information

Dear Colleagues,

Hepatology has been facing revolutionary changes in recent years. Starting from the end of 2013, the advent of IFN-free antiviral treatments has dramatically changed the management and prognosis of HCV infection, at all stages of liver disease. The easier eradication of HCV infections on one hand and the epidemic of metabolic syndrome and non-alcoholic fatty liver disease (NAFLD) on the other are drastically modifying the epidemiology of liver disease worldwide. Genetic profiling has allowed a better understanding of pathogenetic mechanisms of NAFLD, thus allowing the development of various molecules for the treatment of the disease that are being tested in global clinical trials. Clinicians will deal with new complexity in the treatment of NAFLD because of poly-pathology and comorbidities. From this perspective, polytherapy will inevitably involve drug–drug interaction and the risk of drug-induced liver injury (DILI). Lastly, new pharmacological treatments are emerging for hepatocellular carcinoma (HCC) with the introduction of new tyrosine kinase inhibitors (TKI) and immunotherapy, which can significantly modify the prognosis of advanced hepatocellular carcinoma.

In this scenario, the need for personalized diagnostic and therapeutic approaches is dramatically growing. Considering the increasing complexity of the management of chronic liver disease and the potential use of new and expensive treatments, genetics and biomarkers will allow to offer the right treatment to the right patient, thus reducing the risk of adverse events. 

In this Special Issue, the advances in personalized medicine in liver diseases will be presented. Papers focusing on the individualization of diagnosis and treatment of chronic liver disease, cirrhosis, and its complications will be evaluated for publication.

Dr. Giuseppe Marrone
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Personalized Medicine is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • liver diseases
  • hepatology
  • HCV
  • non-alcoholic fatty liver disease (NAFLD)
  • liver injury (DILI)
  • hepatocellular carcinoma (HCC)
  • prognosis
  • chronic liver disease
  • transplant hepatology

Published Papers (1 paper)

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Research

12 pages, 6859 KiB  
Article
Long-Term Outcome of HBV-Infected Patients with Clinically Significant Portal Hypertension Achieving Viral Suppression
by Mathias Jachs, Lukas Hartl, David Bauer, Benedikt Simbrunner, Albert Friedrich Stättermayer, Robert Strassl, Michael Trauner, Mattias Mandorfer and Thomas Reiberger
J. Pers. Med. 2022, 12(2), 239; https://doi.org/10.3390/jpm12020239 - 08 Feb 2022
Cited by 7 | Viewed by 1953
Abstract
Background: Nucleos(t)ide analog (NA) treatment for hepatitis B virus (HBV) infection may improve clinically significant portal hypertension (CSPH). Data on hepatic venous pressure gradient (HVPG) and non-invasive tests (NITs) for risk re-stratification in virally suppressed HBV-infected patients with pre-treatment CSPH are limited. Methods: [...] Read more.
Background: Nucleos(t)ide analog (NA) treatment for hepatitis B virus (HBV) infection may improve clinically significant portal hypertension (CSPH). Data on hepatic venous pressure gradient (HVPG) and non-invasive tests (NITs) for risk re-stratification in virally suppressed HBV-infected patients with pre-treatment CSPH are limited. Methods: We retrospectively included patients with long-term (>12 months) suppression of HBV replication and pre-treatment CSPH (i.e., varices, collaterals on cross-sectional imaging, or ascites). Patients were monitored by on-treatment liver stiffness measurement (LSM) and HVPG assessment. The primary outcome was (further) hepatic decompensation (including liver-related mortality). Results: Forty-two patients (n = 12 (28.6%) with previous decompensation, HBeAg-negative: n = 36 (85.7%)) were included and followed for 2.1 (0.6; 5.3) years. The median HVPG (available in n = 17) was 15 (10; 22) mmHg and the median LSM 22.5 (12.5; 41.0) kPa. LSM correlated strongly with HVPG (Spearman’s ρ: 0.725, p < 0.001) and moderately with the model for end-stage liver disease (MELD) score (ρ: 0.459, p = 0.002). LSM, MELD and albumin levels had good prognostic value for decompensation (area under the receiver operated characteristics curve (AUROC) >0.850 for all). LSM predicted (further) decompensation in competing risk regression (subdistribution hazard ratio (SHR): 1.05 (95% confidence interval(CI) 1.03–1.06); p < 0.001), even after adjusting for other factors. An LSM cut-off at 25kPa accurately stratified patients into a low-risk (n = 23, zero events during follow-up) and a high-risk (n = 19; n = 12 (63.2%) developed events during follow-up) group. Conclusions: Patients with HBV-induced CSPH who achieved long-term viral suppression were protected from decompensation, if LSM was <25 kPa. LSM ≥ 25 kPa indicates a persisting risk for decompensation, despite long-term HBV suppression. Full article
(This article belongs to the Special Issue Personalized Medicine for Liver Disease)
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