Chronic liver cirrhosis (LC) and acute-on-chronic liver failure (ACLF) are interconnected hepatic disorders associated with substantial morbidity and mortality. Despite their distinct clinical characteristics, both conditions share common pathogenic pathways that remain inadequately understood. This study aimed to identify shared gene signatures and elucidate underlying molecular mechanisms.

In this study, we employed Weighted Gene Co-Expression Network Analysis to explore transcriptomic data from the Gene Expression Omnibus for LC and ACLF.

Key co-expression modules enriched with genes involved in glycolysis and gluconeogenesis pathways were identified, implicating metabolic dysfunction as a central feature in both conditions. Furthermore, microRNA analysis revealed that hsa-miR-122 and hsa-miR-194 play pivotal roles in regulating these metabolic pathways, potentially contributing to immune dysregulation.

Our findings indicate that these shared molecular mechanisms are critical in the progression from LC to ACLF, providing novel insights into potential therapeutic targets for mitigating disease severity and improving clinical outcomes.

Chronic liver disease (CLD) is a major global health challenge, characterized by chronic inflammation that can progress to liver fibrosis, cirrhosis, and ultimately hepatocellular carcinoma. Early identification of biomarkers is crucial for effective intervention. Traditional Chinese medicine (TCM) has shown potential in improving CLD symptoms and protecting the liver, although its mechanisms remain unclear. Metabolomics, the comprehensive study of metabolites, offers a promising approach to understanding CLD pathogenesis and identifying biomarkers. Notably, metabolomics aligns with TCM’s holistic approach and may help reveal its therapeutic mechanisms. This review summarizes key metabolites associated with CLD diagnosis and progression and discusses how TCM may modulate metabolic pathways to alleviate CLD symptoms. These insights could lead to improved diagnostic and therapeutic strategies for CLD.

Lung metastasis is common in hepatocellular carcinoma (HCC) and is typically associated with a poor prognosis. In this report, we present a case of advanced HCC in a 46-year-old Chinese male with lung metastases. The patient received two cycles of sequential hepatic arterial infusion chemotherapy and transarterial embolization in combination with lenvatinib (a tyrosine kinase inhibitor) and tislelizumab (a programmed cell death protein 1 immune checkpoint inhibitor). After three months of treatment, the intrahepatic tumors showed a partial response, while the bilateral lung metastases exhibited a complete response. Concurrently, levels of alpha-fetoprotein and protein induced by vitamin K absence or antagonist-II decreased to normal levels. Systemic treatment with lenvatinib and tislelizumab was continued for 10 months. This case underscores the potential of combination therapies for advanced HCC with lung metastases and provides a novel perspective on a therapeutic approach involving sequential hepatic arterial infusion chemotherapy and transarterial embolization with immune checkpoint and tyrosine kinase inhibitors.

Patients with cirrhosis are at an increased risk of bacterial infection (BI), which is the most common precondition for acute-on-chronic liver failure (ACLF). In this study, we aimed to evaluate the ability of mitochondria-related indicators (mitochondrial mass and mitochondrial membrane potential (MMP)) of T cells in peripheral blood to predict BI and ACLF within 90 days in cirrhotic patients.

We prospectively studied mitochondria-related indicators in various T cells from 235 cirrhotic patients at the Second Hospital of Nanjing. The outcomes of interest were BI and ACLF.

The restricted cubic spline analysis showed that the MMP of CD8+ T cells had a linear relationship with the risk of BI and ACLF (both P < 0.001). Multivariable Cox regression analysis demonstrated that the MMP of CD8+ T cells was an independent risk factor for both BI and ACLF (BI: hazard ratio 0.96, 95% confidence interval 0.94–0.98; P < 0.001; ACLF: hazard ratio 0.94, 95% confidence interval 0.90–0.97; P < 0.001). The MMP of CD8+ T cells exhibited better diagnostic efficacy than traditional indices in predicting BI (C index: 0.75). The MMP of CD8+ T cells, when combined with traditional models (Child-Turcotte-Pugh and model for end-stage liver disease score), improved their diagnostic efficiency in predicting both BI and ACLF. Additionally, the MMP of CD8+ T cells showed a significant negative correlation with inflammation-related markers (P < 0.05). Mitochondrial damage and abnormally activated mitochondrial autophagy were observed in CD8+ T cells from cirrhotic patients with low MMP.

The MMP of CD8+ T cells could serve as a valuable predictor of BI and ACLF within 90 days in cirrhotic patients.

Therapy-related B-lymphoblastic leukemia (B-ALL) following treatment for multiple myeloma is a rare occurrence. Despite its rarity and the lack of recognition by the World Health Organization as a distinct disease entity, previous publications indicate its possible emergence following myeloma treatment.

The patient is a 65-year-old gentleman with a history of IgG kappa multiple myeloma, status post multiple lines of therapy. The patient presented with a fever, and a complete blood count showed cytopenia. Bone marrow morphologic evaluation revealed numerous blasts. Immunophenotypic analysis demonstrated that these blasts were B lymphoblasts, despite MYC and unusual surface kappa light chain expression. A diagnosis of B-ALL with surface kappa light chain expression post-myeloma treatment was made. Ancillary studies indicated that the B-ALL and the previous myeloma were clonally unrelated. Next-generation gene sequencing revealed pathogenic mutations in KDM6A and KRAS.

This case highlights the potential for therapy-related B-ALL following myeloma treatment, a phenomenon deserving further investigation. The expression of surface light chain in blasts can present a diagnostic pitfall.

In recent years, it has been found that Lycium barbarum can repair liver damage and promote liver regeneration. Additionally, the polysaccharides contained in Lycium barbarum have anticancer properties and can induce apoptosis in cancer cells. Molecular docking, a mature computer-aided method, is widely used in drug discovery. This study aimed to verify the efficacy of active ingredients of Lycium barbarum in the treatment of liver cancer by molecular docking.

The effect of the active ingredients of Lycium barbarum in the treatment of liver cancer was verified by molecular docking, based on a previous study that examined the impact of Lycium barbarum on liver cancer using network pharmacology.

The binding energies of the key active ingredients and core targets were all less than −5.0 kcal/mol (1 kcal = 4.184 J), with most of them being less than −7.0 kcal/mol. This indicates that the key active ingredients and core targets have good binding ability, with most demonstrating strong binding affinity.

Most of the active ingredients in wolfberry can spontaneously bind to the core target protein, thereby playing a therapeutic role in liver cancer.

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by distinct histological subtypes and a poor prognosis. Among these, the micropapillary pattern, typically observed focally, has been associated with worse outcomes in various cancers. This study aimed to evaluate the prognostic significance of the micropapillary pattern in PDAC, focusing on its percentage within the tumor and its impact on overall survival.

A retrospective analysis was conducted on 71 patients with surgically resected PDAC. Micropapillary patterns were categorized based on their percentage within the tumor (≥20%) and compared to non-micropapillary cases. Demographic, clinical, and histological data, including tumor nodule metastasis stage, tumor grade, peripancreatic fat tissue invasion, and resection margin status, were analyzed. Survival data were assessed using Kaplan-Meier and Cox proportional hazards models. A p-value < 0.05 was considered statistically significant.

The cohort included 28 female and 43 male patients, with a mean age of 63.25 years. Of the 71 cases, 23.9% (n = 17) exhibited a micropapillary pattern. The median overall survival for the micropapillary group was eight months, compared to 18 months for the non-micropapillary group (p = 0.017). Multivariate analysis revealed that the micropapillary group had an increased risk of mortality (hazard ratio = 1.892, p = 0.042), independent of tumor nodule metastasis stage.

Our findings indicate that the micropapillary pattern, even when present in as little as 20% of the tumor, serves as an independent prognostic factor for decreased survival in PDAC. Incorporating the percentage of the micropapillary pattern into pathology reports could provide valuable insights into the tumor’s biological behavior, potentially enhancing patient management strategies.

The importance of putative folate-biopterin metabolic interactions lies in the role they may play in the expression of several clinically relevant phenotypes. However, to date, clinical studies on folate-biopterin interactions have been limited. The purpose of this article was to highlight the close relationship between these two cofactors, which share structural similarities and exhibit overlapping metabolic pathways. This folate-biopterin crosstalk has generated several ideas and hypotheses that are critical to advancing the biochemical understanding of several important and seemingly disparate clinical and/or biologically important phenotypes. These phenotypes include melanization/pigmentation, phenylketonuria, autism, neural tube defects, affective disorders, and vascular disease. This review provides a timely, integrated overview of this important area of biochemistry, which is under-represented in the literature and would benefit from further scientific and clinical investigation using improved metabolite-specific analytical methodologies applied to clinically relevant questions.

Actively identifying the risk factors and predictive indicators associated with portal vein thrombosis (PVT) in liver cirrhosis (LC) can enable early diagnosis and treatment, which is of great significance for prolonging the survival of patients with LC. Hemodynamic disturbances, advanced LC, vascular endothelial injury, and mutations in thrombophilic genetic factors are established risk factors for PVT-LC. Venous dilatation and decreased blood flow velocity contribute to hemodynamic disturbances. The severity of LC can be assessed by the degree of portal hypertension, liver metabolic function biomarkers, and validated liver scoring systems. Iatrogenic interventions, endotoxemia, and metabolic syndrome may induce vascular endothelial injury and hypercoagulability, the latter of which can be quantified via coagulation-anticoagulation-fibrinolysis biomarkers. Mutations in thrombophilic genetic factors, such as Factor V Leiden, MTHFR C667T, and JAK2 V617F, disrupt coagulation-anticoagulation homeostasis and predispose patients to PVT-LC. This review specifically focuses on comprehensively delineating established risk factors and predictive indicators for PVT-LC, thereby providing a theoretical foundation for the construction of clinically applicable PVT predictive models to guide early interventions and improve the prognosis. Future research should further validate the associations between recently proposed risk factors and PVT-LC, while simultaneously establishing cutoff values for indicators with robust predictive value to construct a clinically applicable PVT prediction framework.