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Risk factors for autoimmune liver disease recurrence after liver transplantation
(Baishideng Publishing Group Inc., 2025)
Salgado-de la Mora, Moisés
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Mendez-Guerrero, Osvely
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Torre, Aldo
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Vilatoba, Mario
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Castro Narro, Graciela E
Background: Autoimmune liver disease (AILD) recurrence is common after liver transplantation (LT). While several risk factors for recurrence have been identified, their combined predictive value has yet to be thoroughly investigated. Aim: To evaluate the combined predictive value of clinical and laboratory risk factors for AILD recurrence after LT. Methods: This retrospective cohort study included 79 patients with AILD who underwent LT at a single liver transplant center. We compared clinical and laboratory variables between patients with and without recurrent disease and assessed the predictive performance of these factors using four logistic regression models and their corresponding area under the receiver operating characteristic curve (AUC). Results: Recurrent AILD occurred in 26.58% of patients (95%CI: 17-38), the median time to recurrence was 28 months (interquartile range: 16-38). Patients with recurrent AILD had significantly higher pre-transplant Child-Pugh scores [11.61 ± 1.16 vs 10.58 ± 1.96 points; odds ratio (OR) = 1.43, 95%CI: 1.03-2.00; P = 0.032] and model for end-stage liver disease score (MELD) (22.76 ± 5.47 vs 18.81 ± 7.24 points; OR = 1.08, 95%CI: 1.01-1.16; P = 0.032), compared to those without recurrence. Additionally, baseline alanine aminotransferase (ALT) > 2 times the upper limit of normal (ULN) was significantly associated with recurrence (31% vs 57.1%; OR = 2.96, 95%CI: 1.06-8.28; P = 0.038). Our models, incorporating several risk variables, demonstrated moderate predictive ability for AILD recurrence. The AUCs were as follows: (1) Model 1 (AUC = 0.75, 95%CI: 0.58-0.87); (2) Model 2 (AUC = 0.74, 95%CI: 0.59-0.90); (3) Model 3 (AUC = 0.72, 95%CI: 0.58-0.88); and (4) Model 4 (AUC = 0.63, 95%CI: 0.40-0.76), with no statistically significant difference between the models (P = 0.488). Conclusion: Higher pre-transplant Child-Pugh and MELD scores, as well as ALT > 2 ULN, were associated with an increased risk of AILD recurrence. ©The authors ©Baishideng Publishing Group Inc.
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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 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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