World Journal of Hepatology最新文献

Background: Posterior reversible encephalopathy syndrome (PRES), characterized by acute neurological deterioration and extensive white matter lesions on T2-fluid attenuated inversion recovery magnetic resonance imaging (MRI), is increasingly associated with calcineurin inhibitors (CNI)-related neurotoxicity. Prompt diagnosis is crucial, as early intervention, including the modification or discontinuation of CNI therapy, strict blood pressure management, corticosteroid treatment, and supportive care can significantly improve patient outcomes and prognosis. The growing clinical recognition of CNI-related PRES underscores the importance of identifying and managing this condition in patients presenting with acute neurological symptoms.

Case summary: This report describes three cases of liver transplant recipients who developed PRES. The first case involves a 60-year-old woman who experienced seizures, aphasia, and hemiplegia on postoperative day (POD) 9, with MRI revealing ischemic foci followed by extensive white matter lesions. After replacing tacrolimus, her symptoms improved, and no significant MRI abnormalities were observed after three years of follow-up. The second case concerns a 54-year-old woman with autoimmune hepatitis who developed headaches, seizures, and extensive white matter demyelination on MRI on POD24. Following the switch to rapamycin and the initiation of corticosteroids, her symptoms resolved, and she was discharged on POD95. The third case details a 60-year-old woman with hepatocellular carcinoma who developed PRES, evidenced by brain MRI abnormalities on POD11. Transitioning to rapamycin and corticosteroid therapy led to her full recovery, and she was discharged on POD22. These cases highlight the critical importance of early diagnosis, CNI modification, and stringent management in improving outcomes for liver transplant recipients with CNI-related PRES.

Conclusion: Clinical manifestations, combined with characteristic MRI findings, are crucial in diagnosing PRES among organ transplant recipients. However, when standard treatments are ineffective or MRI results are atypical, alternative diagnoses should be taken into considered.

Background: C23, an oligo-peptide derived from cold-inducible RNA-binding protein (CIRP), has been reported to inhibit tissue inflammation, apoptosis and fibrosis by binding to the CIRP receptor; however, there are few reports on its role in liver fibrosis and the underlying mechanism is unknown.

Aim: To explore whether C23 plays a significant role in carbon tetrachloride (CCl4)-induced liver fibrosis.

Methods: CCl4 was injected for 6 weeks to induce liver fibrosis and C23 was used beginning in the second week. Masson and Sirius red staining were used to examine changes in fiber levels. Inflammatory factors in the liver were detected and changes in α-smooth muscle actin (α-SMA) and collagen I expression were detected via immunohistochemical staining to evaluate the activation of hematopoietic stellate cells (HSCs). Western blotting was used to detect the activation status of the transforming growth factor-beta (TGF-β)/Smad3 axis after C23 treatment.

Results: CCl4 successfully induced liver fibrosis in mice, while tumor necrosis factor-alpha (TNF-α), IL (interleukin)-1β, and IL-6 levels increased significantly and the IL-10 level decreased significantly. Interestingly, C23 inhibited this process. On the other hand, C23 significantly inhibited the activation of HSCs induced by CCl4, which inhibited the expression of α-SMA and the synthesis of collagen I. In terms of mechanism, C23 can block Smad3 phosphorylation significantly and inhibits TGF-β/Smad3 pathway activation, thereby improving liver injury caused by CCl4.

Conclusion: C23 may block TGF-β/Smad3 axis activation, inhibit the expression of inflammatory factors, and inhibit the activation of HSCs induced by CCl4, alleviating liver fibrosis.

The albumin-bilirubin (ALBI) score is a useful prognostic marker that predicts mortality in patients suffering from terminal diseases. Recently, it has been reported that ALBI score is a predictor of non-malignant liver diseases. The cutoff point of the ALBI score that distinguishes hepatocellular carcinoma from non-malignant liver disease is still not identified. Therefore, the ALBI score is a sensitive rather than a specific predictor of the poor outcomes of liver diseases. There are many hematological indices and ratios that are utilized as prognostic biomarkers. Among these biomarkers are the neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio (PLR), and platelet-hemoglobin ratio (PHR), which are useful discriminating prognostic biomarkers for liver diseases, e.g., hepatocellular carcinoma, hepatitis, liver fibrosis, etc. There is evidence that PLR and PHR are prognostic biomarkers that predict the poor outcomes of diseases. Therefore, concomitant measurements of ALBI score and PHR or ALBI score and PLR will improve the predictive value that can differentiate hepatocellular carcinoma from non-malignant diseases.

It is not complicated for the clinician to diagnose a patient with advanced fibrosis or liver cirrhosis when he has already presented some decompensation of his liver disease. However, it is in the earliest stages when the patient's prognosis can be modified the most. Since liver disease is generally asymptomatic, not invasive markers are of great relevance. In the era of omics, it is time for metabolomics to accompany genomics and proteomics, which are more established in the diagnostics and prognostics clinical toolbox. Metabolomics, understood as the comprehensive evaluation of the metabolites present in the organism in a specific physiological situation, has undoubted advantages in the study and identification of serum markers relevant to a specific pathology. Last year, I read with interest two articles published in this journal: "Baseline metabolites could predict responders with hepatitis B virus-related liver fibrosis for entecavir or combined with FuzhengHuayu tablet" by Dai et al and "Metabolomics in chronic hepatitis C: Decoding fibrosis grading and underlying pathways" by Ferrasi et al. Both papers illuminate the power of metabolomics to provide us with new tools in the management of liver disease. In this editorial, I comment on these studies and others, and note how they can contribute to our understanding of liver disease in more than one way.

For cirrhotic refractory ascites, diuretics combined with albumin and vasoactive drugs are the first-line choice for ascites management. However, their therapeutic effects are limited, and most refractory ascites do not respond to medication treatment, necessitating consideration of drainage or surgical interventions. Consequently, numerous drainage methods for cirrhotic ascites have emerged, including large-volume paracentesis, transjugular intrahepatic portosystemic shunt, peritoneovenous shunt, automated low-flow ascites pump, cell-free and concentrated ascites reinfusion therapy, and peritoneal catheter drainage. This review introduces the advantages and disadvantages of these methods in different aspects, as well as indications and contraindications for this disease.

Chronic hepatitis B constitutes a substantial disease burden worldwide. The steps advocated by the World Health Organization in 2016 to eradicate hepatitis B by 2030 has failed to achieve significant progress, especially with respect to immunization coverage and linkage to care. The lack of governmental and public awareness regarding the long-term implications of hepatitis B burden cause underfunding of developmental projects. The presently approved treatment modalities have limited efficacy in complete viral eradication, hence the need for newer molecules to achieve functional cure (sustained undetectable hepatitis B surface antigen (HBsAg) and hepatitis B virus DNA in peripheral blood after a finite period of therapy). However, preliminary results from trials of novel therapies show their inadequacy to achieve this end by themselves but better performance with a low baseline serum HBsAg with nucleos(t)ide analogues (NA) treatment which need to be combined with/without pegylated interferon as an immunomodulator. Such therapy is limited by cost and adverse events and need to show incremental benefit over the standard of care (long-term NA therapy) with respect to efficacy and drug toxicities, making the development process tenuous. Thus, while such therapies continue to be tested, strategies should still focus on prevention of transmission by non-pharmaceutical measures, vaccination and increasing linkage to care.

Hematological abnormalities are common in cirrhosis and are associated with various pathophysiological mechanisms. Studies have documented a prevalence of thrombocytopenia, leukopenia, and anemia in patients with compensated cirrhosis of 77.9%, 23.5%, and 21.1%, respectively. These abnormalities carry significant clinical implications, including considerations for invasive procedures, infection risk, bleeding risk, and prognosis. Previously, cirrhosis was believed to predispose patients to bleeding due to alterations observed in classical coagulation tests such as prothrombin time, partial thromboplastin time, international normalized ratio, and thrombocytopenia. However, this understanding has evolved, and cirrhosis patients are now also acknowledged as being at a high risk for thrombotic events. Hemostasis in cirrhosis patients presents a complex phenotype, with procoagulant and anticoagulant abnormalities offsetting each other. This multifactorial phenomenon is inadequately reflected by routine laboratory tests. Thrombotic complications are more prevalent in decompensated cirrhosis and may correlate with disease severity. Bleeding is primarily associated with portal hypertension, endothelial dysfunction, mechanical vessel injury, disseminated intravascular coagulation, endotoxemia, and renal injury. This review comprehensively outlines hematologic index abnormalities, mechanisms of hemostasis, coagulation, and fibrinolysis abnormalities, limitations of laboratory testing, and clinical manifestations of bleeding and thrombosis in patients with liver cirrhosis.

Background: Primary abdominal pregnancy is an extremely rare form of ectopic pregnancy. Ectopic pregnancies that occur in the liver and diaphragm are even rarer, limited case reports are available in the literature.

Case summary: A woman of childbearing age was transferred to the emergency department due to lumbar and abdominal pain radiating to the back toward the lower right. After a series of physical and auxiliary examinations, she was clinically diagnosed with hepatic ectopic pregnancy. Laparoscopic surgery was performed to remove the pregnancy tissue and achieve hemostasis. After a period of follow-up, the patient was successfully cured.

Conclusion: Paying attention to the patient's signs and utilizing imaging examination methods can help avoid missed diagnoses of liver pregnancy.

Extracellular vesicles (EVs) are small particles released by many cell types in different tissues, including the liver, and transfer specific cargo molecules from originating cells to receptor cells. This process generally culminates in activation of distant cells and inflammation and progression of certain diseases. The global chronic liver disease (CLD) epidemic is estimated at 1.5 billion patients worldwide. Cirrhosis and liver cancer are the most common risk factors for CLD. However, hepatitis C and B virus infection and obesity are also highly associated with CLD. Nonetheless, the etiology of many CLD pathophysiological, cellular, and molecular events are unclear. Changes in hepatic lipid metabolism can lead to lipotoxicity events that induce EV release. Here, we aimed to present an overview of EV features, from definition to types and biogenesis, with particular focus on the molecules related to steatosis-related liver disease, diagnosis, and therapy.

Inherited metabolic liver diseases arise from genetic mutations that lead to disruptions in liver metabolic pathways and are predominantly observed in pediatric populations. The spectrum of genetic metabolic liver disorders is diverse, encompassing a range of conditions associated with aberrations in iron, copper, carbohydrate, lipid, protein, and amino acid metabolism. Historically, research in the domain of genetic metabolic liver diseases has predominantly concentrated on hepatic parenchymal cell alterations. Nevertheless, emerging studies suggest that inherited metabolic liver diseases exert significant influences on the immune microenvironment, both within the liver and systemically. This review endeavors to encapsulate the immunological features of genetic metabolic liver diseases, aiming to expand the horizons of researchers in this discipline, and to elucidate the underlying pathophysiological mechanisms pertinent to hereditary metabolic liver diseases and to propose innovative therapeutic approaches.