Introduction: Nonalcoholic fatty liver disease (NAFLD) patients can progress to cirrhosis. In these, there is a compensated stage in which esophageal varices can exist. However, no more than 20% of these patients have varices needing treatment (VNT).
Objective: Evaluate the accuracy of non-invasive models to predict esophageal varices, as well as their performance to avoid esophagogastroduodenoscopy (EGD) with a risk of missing VNT of less than 5%, in Brazilian patients with compensated advanced chronic liver disease (cACLD) secondary to NAFLD.
Methods: Twenty-one patients with biopsy-proven cACLD secondary to NAFLD were submitted to liver stiffness measurement (LSM) by transient elastography (TE), and data were collected to measure platelet count/spleen diameter ratio (PSR), LSM-spleen diameter to platelet ratio score (LSPS), varices risk score (VRS), Baveno VI, Expanded Baveno VI and NAFLD cirrhosis criteria.
Results: The mean age was 61 (±6.6) years, and 81% were female; 14% presented VNT. For detection of VNT, LSPS and VRS performed excellently, with an area under receiver operating characteristic (AUROC) of 0.961 for both. LSM presented an AUROC of 0.889 and a cutoff point of 21.8 kPa. LSPS and VRS enabled sparing 75-80% of EGDs for VNT, with no risk of missing varices. Expanded Baveno VI enabled sparing 71% of EGDs, with 4.8% risk of missing VNT.
Conclusion: LSPS and VRS performed excellently in both predicting VNT and sparing EGD, and Expanded Baveno VI showed good performance in sparing EGDs, with acceptable risk of missing VNT. An LSM cutoff point was established and had good performance.
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http://dx.doi.org/10.1016/j.aohep.2020.07.003 | DOI Listing |
JHEP Rep
February 2025
Department of Gastroenterology and Hepatology, Hospital Universitario Ramón y Cajal, Instituto Ramon y Cajal de Investigación Sanitaria (IRYCIS), Universidad de Alcalá, Madrid, Spain.
Background & Aims: Systemic inflammation is a driver of decompensation in cirrhosis with unclear relevance in the compensated stage. We evaluated inflammation and bacterial translocation markers in compensated cirrhosis and their dynamics in relation to the first decompensation.
Methods: This study is nested within the PREDESCI trial, which investigated non-selective beta-blockers for preventing decompensation in compensated cirrhosis and clinically significant portal hypertension (CSPH: hepatic venous pressure gradient ≥10 mmHg).
J Ultrason
December 2024
Department of General and Pediatric Radiology, Wrocław Medical University, Wrocław, Poland.
Aim: Chronic hepatitis C virus infections can lead to liver fibrosis. Appropriate treatment of chronic hepatitis C may result in significant fibrosis reversal. The best method to assess liver fibrosis is an invasive hepatic biopsy.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of General Surgery, First Affiliated Hospital of Anhui Medical University, Hefei, China.
Background: Adenocarcinoma of the esophagogastric junction (AEGJ) is a highly aggressive tumor that frequently metastasizes to the liver. Understanding the cellular and molecular mechanisms that drive this process is essential for developing effective therapies.
Methods: We employed single-cell RNA sequencing to analyze the tumor heterogeneity and microenvironmental landscape in patients with AEGJ liver metastases.
Front Immunol
January 2025
Department of Otolaryngology, Changhai Hospital, Naval Medical University, Shanghai, China.
Background: There is no consensus regarding the optimal regimen for metastatic nasopharyngeal carcinoma (dmNPC). Locoregional intensity modulated radiotherapy (LRRT) following palliative chemotherapy (PCT) has been shown to prolong the overall survival (OS) and improve the progression-free survival (PFS) of patients with dmNPC, compared with PCT alone. However, patients with a high tumor burden do not benefit from additional LRRT, which inevitably results in toxicity.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, China.
CCL2, a pivotal cytokine within the chemokine family, functions by binding to its receptor CCR2. The CCL2/CCR2 signaling pathway plays a crucial role in the development of fibrosis across multiple organ systems by modulating the recruitment and activation of immune cells, which in turn influences the progression of fibrotic diseases in the liver, intestines, pancreas, heart, lungs, kidneys, and other organs. This paper introduces the biological functions of CCL2 and CCR2, highlighting their similarities and differences concerning fibrotic disorders in various organ systems, and reviews recent progress in the diagnosis and treatment of clinical fibrotic diseases linked to the CCL2/CCR2 signaling pathway.
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