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Histopathological impact of SARS-CoV-2 on the liver: Cellular damage and long-term complications
(Baishideng Publishing Group, 2024)
Rodríguez-Espada, Alfonso
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Salgado-de la Mora, Moisés
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Rodríguez-Paniagua, Briana Mariette
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Limón-de la Rosa, Nathaly
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Martínez-Gutiérrez, Mónica Itzel
Coronavirus disease 2019 (COVID-19), caused by the highly pathogenic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), primarily impacts the respiratory tract and can lead to severe outcomes such as acute respiratory distress syndrome, multiple organ failure, and death. Despite extensive studies on the pathogenicity of SARS-CoV-2, its impact on the hepatobiliary system remains unclear. While liver injury is commonly indicated by reduced albumin and elevated bilirubin and transaminase levels, the exact source of this damage is not fully understood. Proposed mechanisms for injury include direct cytotoxicity, collateral damage from inflammation, drug-induced liver injury, and ischemia/hypoxia. However, evidence often relies on blood tests with liver enzyme abnormalities. In this comprehensive review, we focused solely on the different histopathological manifestations of liver injury in COVID-19 patients, drawing from liver biopsies, complete autopsies, and in vitro liver analyses. We present evidence of the direct impact of SARS-CoV-2 on the liver, substantiated by in vitro observations of viral entry mechanisms and the actual presence of viral particles in liver samples resulting in a variety of cellular changes, including mitochondrial swelling, endoplasmic reticulum dilatation, and hepatocyte apoptosis. Additionally, we describe the diverse liver pathology observed during COVID-19 infection, encompassing necrosis, steatosis, cholestasis, and lobular inflammation. We also discuss the emergence of long-term complications, notably COVID-19-related secondary sclerosing cholangitis. Recognizing the histopathological liver changes occurring during COVID-19 infection is pivotal for improving patient recovery and guiding decision-making. ©
Scopus© Citations 2 26
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Galectin-3 as a Biomarker of Disease Severity in Acute-on-Chronic Liver Failure
(2020)
Cervantes-Álvarez, Eduardo
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Limón-de la Rosa, Nathaly
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Vilatoba, Mario
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Pérez-Monter, Carlos
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Hurtado-Gómez, Sahara
*Purpose: A matter of great importance is the discovery of alternative diagnostic measures that can detect liver disease at an early stage, especially when at risk of developing acute on chronic liver failure (ACLF), to optimize outcome and survival. Galectin-3 (Gal-3) is a lectin that binds to β-galactosides and can be secreted to the systemic circulation, regulating inflammation and fibrosis. Due to its direct role in inflammation and fibrosis, levels of this lectin can reflect the progression of liver damage and the possible consequent multiorgan failure, which is a distinctive characteristic of ACLF. The purpose of this study is to determine if liver Gal-3 expression is a useful biomarker of disease progression. *Methods: Liver samples from cirrhotic patients with compensated, decompensated cirrhosis and ACLF were collected at the time of liver transplant. The liver from donors was used as controls. RNA was extracted and liver Gal-3 expression was analyzed by quantitative polymerase chain reaction (qPCR). The values obtained were correlated with clinical and biochemical parameters using Pearson’s and Spearman’s correlation coefficients. A comparison among 3 different groups was performed using the Kruskal-Wallis test with Dunn’s multiple comparisons test.
51 2
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Liver transplantation is beneficial regardless of cirrhosis stage or acute-on-chronic liver failure grade: A single-center experience
(2022)
Cervantes-Álvarez, Eduardo
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Vilatoba, Mario
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Limón-de la Rosa, Nathaly
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Méndez-Guerrero, Osvely
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Kershenobich, David
Background: Liver transplantation for the most critically ill remains controversial; however, it is currently the only curative treatment option. Aim: To assess immediate posttransplant outcomes and compare the short (1 year) and long-term (6 years) posttransplant survival among cirrhotic patients stratified by disease severity. Methods: We included cirrhotic patients undergoing liver transplantation between 2015 and 2019 and categorized them into compensated cirrhosis (CC), decompensated cirrhosis (DC), and acute-on-chronic liver failure (ACLF). ACLF was further divided into severity grades. Our primary outcomes of interest were total days of intensive care unit (ICU) and hospital stay, development of complications and posttransplant survival at 1 and 6 years. ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
Scopus© Citations 5 30 2
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Galectin‐3 is overexpressed in advanced cirrhosis and predicts post‐liver transplant infectious complications
(2022)
Cervantes‐Alvarez, Eduardo
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Limón-de la Rosa, Nathaly
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Vilatoba, Mario
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Pérez Nicomedes, Carlos
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Hurtado‐Gomez, Sahara
Background & aims: Patients with advanced cirrhosis often have immune dysfunction and are more susceptible to infections. Galectin-3 is a β-galactoside-binding lectin implicated in inflammation, immune regulation and liver fibrosis. We aim to investigate galectin-3 expression in advanced cirrhosis and its ability to predict post-transplant infectious complications. Methods: We collected sera and liver samples from 129 cirrhotic patients at the time of liver transplantation and from an external cohort of 37 patients with alcoholic liver disease including alcoholic hepatitis (AH) at the time of diagnosis. Galectin-3 was assessed by ELISA, real-time PCR, immunohistochemistry and RNA-seq. Receiver operating characteristic curves and Cox proportional-hazards regression analysis were performed to assess the predictive power of galectin-3 for disease severity and post-transplant infections.
Scopus© Citations 14 23 1
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Time-Dependent Changes of Laboratory Parameters as Independent Predictors of All-Cause Mortality in COVID-19 Patients
(2022)
Limón-de la Rosa, Nathaly
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Cervantes-Álvarez, Eduardo
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Méndez-Guerrero, Osvely
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Gutiérrez-Gallardo, Miguel A.
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Kershenobich, David
Independent predictors of mortality for COVID-19 patients have been identified upon hospital admission; however, how they behave after hospitalization remains unknown. The aim of this study is to identify clinical and laboratory parameters from admission to discharge or death that distinguish survivors and non-survivors of COVID-19, including those with independent ability to predict mortality. In a cohort of 266 adult patients, clinical and laboratory data were analyzed from admission and throughout hospital stay until discharge or death. Upon admission, non-survivors had significantly increased C reactive protein (CRP), neutrophil count, neutrophil to lymphocyte ratio (NLR) (p < 0.0001, each), ferritin (p < 0.001), and AST (aspartate transaminase) (p = 0.009) compared to survivors. During the hospital stay, deceased patients maintained elevated CRP (21.7 mg/dL [admission] vs. 19.3 [hospitalization], p = 0.060), ferritin, neutrophil count and NLR. Conversely, survivors showed significant reductions in CRP (15.8 mg/dL [admission] vs. 9.3 [hospitalization], p < 0.0001], ferritin, neutrophil count and NLR during hospital stay. Upon admission, elevated CRP, ferritin, and diabetes were independent predictors of mortality, as were persistently high CRP, neutrophilia, and the requirement of invasive mechanical ventilation during hospital stay. Inflammatory and clinical parameters distinguishing survivors from non-survivors upon admission changed significantly during hospital stay. These markers warrant close evaluation to monitor and predict patients’ outcome once hospitalized.
Scopus© Citations 4 9 1
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Galectin-3 as a potential prognostic biomarker of severe COVID-19 in SARS-CoV-2 infected patients
(2022)
Cervantes-Álvarez, Eduardo
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Limón-de la Rosa, Nathaly
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Salgado-de la Mora, Moisés
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Valdez-Sandoval, Paola
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Palacios-Jiménez, Mildred
Severe COVID-19 is associated with a systemic hyperinflammatory response leading to acute respiratory distress syndrome (ARDS), multi-organ failure, and death. Galectin-3 is a ß-galactoside binding lectin known to drive neutrophil infiltration and the release of pro-inflammatory cytokines contributing to airway inflammation. Thus, we aimed to investigate the potential of galectin-3 as a biomarker of severe COVID-19 outcomes. We prospectively included 156 patients with RT-PCR confirmed COVID-19. A severe outcome was defined as the requirement of invasive mechanical ventilation (IMV) and/or in-hospital death. A non-severe outcome was defined as discharge without IMV requirement. We used receiver operating characteristic (ROC) and multivariable logistic regression analysis to determine the prognostic ability of serum galectin-3 for a severe outcome. Galectin-3 levels discriminated well between severe and non-severe outcomes and correlated with markers of COVID-19 severity, (CRP, NLR, D-dimer, and neutrophil count). Using a forward-stepwise logistic regression analysis we identified galectin-3 [odds ratio (OR) 3.68 (95% CI 1.47–9.20), < 0.01] to be an independent predictor of severe outcome. Furthermore, galectin-3 in combination with CRP, albumin and CT pulmonary affection > 50%, had significantly improved ability to predict severe outcomes [AUC 0.85 (95% CI 0.79–0.91, < 0.0001)]. Based on the evidence presented here, we recommend clinicians measure galectin-3 levels upon admission to facilitate allocation of appropriate resources in a timely manner to COVID-19 patients at highest risk of severe outcome.
Scopus© Citations 43 44 1
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Increased Hepatic Expression of SARS-CoV-2 Entry Points and Proinflammatory Cytokines in Cirrhosis
(2022)
Limón-de la Rosa, Nathaly
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Cervantes-Álvarez, Eduardo
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Navarro Álvarez, Nalu
It has been recently reported that patients with cirrhosis have significantly higher mortality following severe acute respiratory syndrome coronavrisu 2 (SARS-CoV-2) infection compared with those without.1,2 Specifically, it was demonstrated that mortality was greater in those with advanced cirrhosis (Child-Pugh B and C), and that from cirrhotic patients experiencing SARS-CoV-2 infection, close to half suffer acute decompensation including acute-on-chronic liver failure (ACLF).2 Unfortunately, the presence of hepatic decompensation at baseline has been shown to be an independent predictor of all-cause mortality in patients with coronavirus disease 2019 (COVID-19).1 Patients with decompensated cirrhosis contracting COVID-19 have a poor outcome, with an overall reported mortality of over 30%.1. Copyright © 2022 AGA Institute. Published by Elsevier Inc. All rights reserved.
Scopus© Citations 5 15 2
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Direct or collateral liver damage in SARS-CoV-2-infected patients
(2020)
Lizardo-Thiebaud, María José
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Cervantes-Álvarez, Eduardo
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Limón-de la Rosa, Nathaly
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Palacios-Jiménez, Mildred
Liver injury can result from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection with more than one-third of COVID-19 patients exhibiting elevated liver enzymes. Microvesicular steatosis, inflammation, vascular congestion, and thrombosis in the liver have been described in autopsy samples from COVID-19 patients. Several factors, including direct cytopathic effect of the virus, immune-mediated collateral damage, or an exacerbation of preexisting liver disease may contribute to liver pathology in COVID-19. Due to its immunological functions, the liver is an organ likely to participate in the viral response against SARS-CoV-2 and this may predispose it to injury. A better understanding of the mechanism contributing to liver injury is needed to develop and implement early measures to prevent serious liver damage in patients suffering from COVID-19. This review summarizes current reports of SARS-CoV-2 with an emphasis on how direct infection and subsequent severe inflammatory response may contribute to liver injury in patients with and without preexisting liver disease. © 2020 American Institute of Physics Inc.. All rights reserved.
Scopus© Citations 24 29 2

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