SciCombinator

Discover the most talked about and latest scientific content & concepts.

Concept: Cirrhosis

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Assessment of the severity of liver disease following infection with hepatitis C virus (HCV) is important in treatment selection and prognosis. As invasive liver biopsy procedures are regarded as the reference method to assess the stage of fibrosis, it is important to identify patient characteristics that are predictive of liver fibrosis severity. The aim of the study was to describe the distribution of liver severity scores, clinical characteristics, and physicians' assessment of fibrosis among HCV patients in 5 European countries.

Concepts: Scientific method, Cirrhosis, Hepatitis, Liver, Hepatitis C, Hepatitis B, Hepatitis A, Liver biopsy

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To assess the efficacy and safety of anticoagulant drug, danaparoid sodium, for the treatment of portal vein thrombosis (PVT) in patients with liver cirrhosis.

Concepts: Thrombosis, Cirrhosis, Liver, Hematology, Vein, Heparin, Hepatic portal vein, Anticoagulants

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Damaged, necrotic, or apoptotic hepatocytes release damage-associated molecular patterns that initiate sterile inflammation, and liver inflammation drives liver injury and fibrosis. Here we identified hepatic NF-κB-inducing kinase (NIK), a Ser/Thr kinase, as a novel trigger of fatal liver inflammation. NIK is activated by a broad spectrum of stimuli. It was upregulated in injured livers in both mice and humans. In primary mouse hepatocytes, NIK overexpression stimulated, independently of cell injury and death, release of numerous chemokines and cytokines that activated bone marrow-derived macrophages (BMDMs). BMDMs in turn secreted pro-apoptotic molecules that stimulated hepatocyte apoptosis. Hepatocyte-specific expression of the NIK transgene triggered massive liver inflammation, oxidative stress, hepatocyte apoptosis, and liver fibrosis, leading to weight loss, hypoglycemia, and death. Depletion of Kupffer cells/macrophages reversed NIK-induced liver destruction and death. Conclusion: the hepatocyte NIK-liver immune cell axis promotes liver inflammation, injury and fibrosis, thus driving liver disease progression. (Hepatology 2014;).

Concepts: Immune system, Cancer, Apoptosis, Cirrhosis, Liver, Glycogen, Bile, Hepatocyte

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Progressive liver fibrosis is the result of chronic liver injury and characterized by excessive accumulation of extracellular matrix that may result in liver failure. Activated Hepatic Stellate Cells are known to play a central role in this process and their elimination is a crucial step towards the resolution and reversion of liver fibrosis. Here we investigated the potential application of an anti-Epidermal Growth Factor receptor scFv antibody-Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (scFv425-sTRAIL) fusion protein in the targeted elimination of activated Hepatic Stellate Cells.

Concepts: Protein, Glucose, Receptor, Cirrhosis, Liver, Hepatic stellate cell, Hepatic encephalopathy, Growth factor receptor

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Based on up-to-seven criteria and Child-Pugh score, four sub-stages of Barcelona Clinic Liver Cancer (BCLC) intermediate hepatocellular carcinoma (HCC) were proposed. The purpose of this study was to validate and modify this proposal.

Concepts: Cancer, Cirrhosis, Hepatocellular carcinoma, Hepatology, Hepatitis C, Liver transplantation

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We herein report a clinical pitfall regarding the treatment of a case of pulmonary tuberculoma in a patient with chronic hepatitis C. The patient presented with both chronic hepatitis C and pulmonary tuberculoma, and we initiated treatment of the chronic hepatitis C first due to the potential for liver injury; however, the patient’s condition worsened in terms of the pulmonary tuberculosis. This case highlights the need to select the initial treatment for pulmonary tuberculoma, not chronic hepatitis C. In addition, we report that, although the administration of anti-tuberculosis chemotherapy regimens containing pyrazinamide (PZA) substantially increases the incidence of drug-induced hepatitis in patients with chronic hepatitis, we were fortunately able to use PZA without observing drug-induced hepatitis in this case because we closely monitored the patient’s liver function.

Concepts: Cirrhosis, Hepatitis, Tuberculosis, Hepatitis C, Latent tuberculosis, Tuberculosis treatment, Rifampicin, Isoniazid

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We have read with great interest the article by Petta et al. (1). In this study, the performance of combined noninvasive tools for identifying advanced fibrosis was assessed in two independent cohorts of Italian biopsy-proven nonalcoholic fatty liver disease (NAFLD) patients. In conclusion, the combination of liver stiffness measurement (LSM) with NAFLD fibrosis score (NFS) was found to be able to accurately diagnose or exclude the presence of severe liver fibrosis, also reducing of about 50-60% the number of needed diagnostic liver biopsies. However, we would like to share our thoughts and contributions with Petta and colleagues. This article is protected by copyright. All rights reserved.

Concepts: Cirrhosis, Non-alcoholic fatty liver disease, Fatty liver, Steatosis

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Liver X receptor (LXR) is an oxysterol-activated nuclear receptor involved in the control of major metabolic pathways for cholesterol homeostasis and lipogenesis. Although the role of LXR in hepatic steatosis is well known, its correlation with intrahepatic inflammation and fibrosis has not been thoroughly studied. We investigated the association between LXRα, hepatic inflammation, and fibrosis, as well as its correlation with other intrahepatic lipid transporters in patients with nonalcoholic fatty liver disease (NAFLD).

Concepts: Metabolism, Obesity, Cirrhosis, Metabolic syndrome, Metabolic pathway, Non-alcoholic fatty liver disease, Fatty liver, Steatosis

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The hepatitis C virus may lead to cirrhosis, liver cancer, liver transplant, and increased mortality. With standard treatment peginterferon-alpha and ribavirin (PR), sustained viral response (SVR) was less than 50 %. SVR rates improve greatly when PR is combined with telaprevir or boceprevir.

Concepts: Cirrhosis, Hepatitis, Liver, Hepatocellular carcinoma, Interferon, Hepatitis C, Hepatitis B, Hepatitis A

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Retrospective studies have shown that two-dimensional magnetic resonance elastography (2D-MRE), a novel MR method for assessment of liver stiffness, correlates with advanced fibrosis in patients with nonalcoholic fatty liver disease (NAFLD). Prospective data on diagnostic accuracy of 2D-MRE in the detection of advanced fibrosis in NAFLD are needed. The aim of this study is to prospectively assess the diagnostic accuracy of 2D-MRE in predicting advanced fibrosis (stage 3 or 4) in well-characterized patients with biopsy-proven NAFLD. Methods: This is a cross-sectional analysis of a prospective study including 117 consecutive patients (56% women) with biopsy-proven NAFLD who underwent a standardized research visit: history, exam, liver biopsy assessment (using the NASH CRN Histologic Scoring System), and 2D-MRE from 2011-2013. The radiologist and pathologist were blinded to clinical and pathology/imaging data, respectively. Receiver operating characteristics (ROC) were examined to assess the diagnostic test performance of 2D-MRE in predicting advanced fibrosis. Results: The mean (± standard deviation) of age and BMI was 50.1 (± 13.4) years and 32.4 (± 5.0) Kg/m(2) , respectively. The median time interval between biopsy and 2D-MRE was 45 days (IQR 50 days). The number of patients with fibrosis stages 0, 1, 2, 3, and 4 was 43, 39, 13, 12 and 10, respectively. The area under the ROC curve for 2D-MRE discriminating advanced fibrosis (stage 3-4) from stage 0-2 fibrosis was 0.924 (p-value <0.0001). A threshold of > 3.63 kPa had a sensitivity 0.86 (95% CI; 0.65-0.97), specificity 0.91 (95% CI; 0.83-0.96), PPV 0.68 (95% CI; 0.48-0.84), and NPV 0.97 (95% CI; 0.91-0.99). Conclusions: MRE is accurate in predicting advanced fibrosis and may be utilized for non-invasive diagnosis of advanced fibrosis in patients with NAFLD. (Hepatology 2014).

Concepts: Median, Cirrhosis, Hepatology, Standard deviation, Receiver operating characteristic, Non-alcoholic fatty liver disease, Fatty liver, Steatosis