Jie XH, Xi DY, Zhang SS, Yan XB. Acute liver injury after transcatheter arterial chemoembolization in patients with hepatitis B virus-related intermediate or advanced hepatocellular carcinoma stages. World J Gastroenterol 2026; 32(24): 118709 [DOI: 10.3748/wjg.118709]
Corresponding Author of This Article
Xue-Bing Yan, PhD, Professor, Department of Infectious Diseases, The Affiliated Hospital of Xuzhou Medical University, No. 99 Huaihai West Road, Xuzhou 221132, Jiangsu Province, China. yxbxuzhou@126.com
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Gastroenterology & Hepatology
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Jie XH, Xi DY, Zhang SS, Yan XB. Acute liver injury after transcatheter arterial chemoembolization in patients with hepatitis B virus-related intermediate or advanced hepatocellular carcinoma stages. World J Gastroenterol 2026; 32(24): 118709 [DOI: 10.3748/wjg.118709]
World J Gastroenterol. Jun 28, 2026; 32(24): 118709 Published online Jun 28, 2026. doi: 10.3748/wjg.118709
Acute liver injury after transcatheter arterial chemoembolization in patients with hepatitis B virus-related intermediate or advanced hepatocellular carcinoma stages
Author contributions: Jie XH and Xi DY share co-first authorship based on their equivalent substantive contributions to experimental execution and analytical rigor throughout this collaborative research; Jie XH contribute to data acquisition, literature screening, literature mining, and manuscript drafting; Xi DY contribute to the study design and statistical analyses; Zhang SS conducted quality assessment; Yan XB provided conceptual guidance and secured funding; all authors have reviewed and approved the final manuscript.
Institutional review board statement: The study was reviewed and approved by the Medical Ethics Committee of The Affiliated Hospital of Xuzhou Medical University, No. XYFY2025-KL533-01.
Informed consent statement: Given the retrospective nature of the study without active interventions, the institutional review board waived the requirement for informed consent from patients.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Data sharing statement: Technical appendix, statistical code, and dataset available from the corresponding author. Consent was not obtained but the presented data are anonymized and risk of identification is low.
Corresponding author: Xue-Bing Yan, PhD, Professor, Department of Infectious Diseases, The Affiliated Hospital of Xuzhou Medical University, No. 99 Huaihai West Road, Xuzhou 221132, Jiangsu Province, China. yxbxuzhou@126.com
Received: January 15, 2026 Revised: February 11, 2026 Accepted: March 10, 2026 Published online: June 28, 2026 Processing time: 148 Days and 20.8 Hours
Abstract
BACKGROUND
Acute liver injury (ALI) is a prevalent complication following transcatheter arterial chemoembolization (TACE), a procedure frequently used in patients with hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). This complication may break the treatment schedule and have a negative influence on the clinical outcomes.
AIM
To determine the risk factors for post-TACE ALI and establish nomogram for personalized prediction in patients with HBV-related intermediate-to-advanced HCC.
METHODS
This retrospective study encompassed 172 patients with HBV-related intermediate to advanced HCC who underwent TACE from January 2019 to December 2024. Patients were categorized into ALI and non-ALI groups. Clinical data were collected within one week before and after TACE. A predictive nomogram was constructed based on independent risk factors identified by multivariate logistic regression. The discriminative ability, calibration, and clinical net benefit of this model were validated using receiver operating characteristic curves (area under the curve), calibration curves, and decision curve analysis.
RESULTS
The retrospective study was based on clinical and laboratory data from 172 patients with a clinical diagnosis of HBV-related HCC and who received TACE treatment. Of these, 62 patients (36.0%) developed ALI. Multivariate analysis revealed Child-Pugh stage (A vs B/C), number of TACE treatments, and HBV DNA levels (≥ 20 IU/mL) as independent predictors of ALI (P < 0.05). A nomogram incorporating these variables was developed to facilitate individualized risk assessment.
CONCLUSION
Child-Pugh stage, number of TACE treatments, and HBV DNA load are significant predictors of ALI following TACE in patients with HBV-related intermediate or advanced HCC. By integrating these variables, the proposed nomogram provides a practical tool for individualized risk assessment and may assist in perioperative management and treatment planning. External validation through multicenter prospective studies is warranted.
Core Tip: This study identifies Child-Pugh stage, number of transcatheter arterial chemoembolization (TACE), and hepatitis B virus (HBV) DNA load as independent risk factors for acute liver injury following TACE in patients with HBV-related intermediate to advanced hepatocellular carcinoma. We constructed a practical nomogram that integrates these variables, providing a validated tool for individualized preoperative risk stratification to optimize perioperative management and treatment planning for this specific population.
Citation: Jie XH, Xi DY, Zhang SS, Yan XB. Acute liver injury after transcatheter arterial chemoembolization in patients with hepatitis B virus-related intermediate or advanced hepatocellular carcinoma stages. World J Gastroenterol 2026; 32(24): 118709
According to global cancer statistics from 2022, hepatocellular carcinoma (HCC) is the third most common malignant tumor around the world[1]. It holds the position of the sixth most frequently diagnosed cancer and the second most common cause of cancer death in the Chinese population[2]. By contrast with Western countries, where HCC is commonly associated with alcoholic hepatitis or hepatitis C virus infection, hepatitis B virus (HBV) infection is still the major cause of HCC in the area of Asia (excluding Japan)[3,4]. Because of its insidious onset and atypical early symptoms, the majority of patients with HCC are diagnosed at an intermediate or advanced stage. Consequently, many patients miss the optimal window for curative treatments such as surgery or local ablation[5]. Transcatheter arterial chemoembolization (TACE) has therefore become one of the most important therapies for treating unresectable intermediate to advanced HCC[6,7]. TACE induces tumor ischemic necrosis and local cytotoxicity through selective embolization of tumor-feeding arteries and infusion of concentrated chemotherapeutic agents. Numerous studies have demonstrated that TACE can effectively control tumor progression and prolong survival[8,9]. However, as an invasive interventional procedure, TACE compromises the blood supply of non-tumorous liver tissue, frequently resulting in acute liver injury (ALI). In severe cases, ALI may progress to liver failure[10]. The occurrence of serious adverse events after TACE is clinically significant, as it may prevent some patients from receiving further TACE sessions, prolong treatment intervals, increase the chance of relapse, and worsen prognosis[11].
The pathophysiological mechanisms underlying post-TACE ALI are complex and multifactorial[12]. These mechanisms include direct liver toxicity from chemical therapy agents[13], ischemic and hypoxic injury to liver cells[14,15], oxidative stress, and a cascade of inflammatory reactions produced during ischemia reperfusion[16]. It is important to note that hepatic function in patients with HBV-related HCC differs from that of healthy individuals. High HBV DNA load represents active HBV replication, which can lead to persistent intrahepatic inflammation and immune activation. Previous studies suggests that a high viral load may increase the adverse effects of TACE. A high viral load impairs liver repair and exacerbates immune damage through defined pathways, thereby substantially increasing the susceptibility to post-TACE decompensation[17,18]. Besides, hepatic functional reserve (typically assessed by Child-Pugh stage), tumor burden, and prior treatment history are recognized determinants of liver injury risk following TACE. Yet, the risk profile in this specific population remains to be elucidated, as current evidence is inconsistent and lacks systematic evaluation.
Therefore, accurately identifying high risk factors for post-TACE ALI in this specific population and establishing an individualized prediction model are of substantial clinical importance. Our study aimed to systematically explore the independent risk factors affecting ALI after TACE in HBV related intermediate or advanced HCC patients through a single center retrospective analysis. Furthermore, we integrated key variables to construct a practical nomogram to help making decision in clinical situation.
MATERIALS AND METHODS
Study population
Of 172 hospitalized patients with HBV related intermediate to advanced HCC treated at the Affiliated Hospital of Xuzhou Medical University from January 2019 to December 2024 were enrolled. All patients underwent TACE treatment. TACE was performed by experienced interventional radiologists at the hospital. Patients were embolized with iodized oil. The determination of the amount of lipiodol use is based on tumor size, number, and richness of arterial blood supply. All protocols were authorized by the Affiliated Hospital of Xuzhou Medical University institutional review board (approval No. XYFY2025-KL533-01). The retrospective design of this study precluded the need for obtaining informed consent.
Case inclusion and exclusion criteria
Inclusion criteria: (1) Age ≥ 18 years of age and male or female gender; (2) Clinical diagnosis of primary liver cancer and assessed as requiring TACE; (3) Barcelona clinic liver cancer stage intermediate or advanced (stage B/C); (4) Serum positive for HBV DNA or hepatitis B surface antigens (HBsAg), or have history of chronic HBV infection; and (5) ALI was defined as an increase in serum alanine aminotransferase (ALT) or aspartate aminotransferase (AST) to ≥ 3 times the upper limit of normal (ULN), or total bilirubin (TBIL) ≥ 2 × ULN, within one week after TACE, in accordance with common criteria for drug-induced and ischemic liver injury.
Exclusion criteria: (1) Concurrent other primary malignancies; (2) Incomplete clinical data; (3) Coinfection with other viruses (hepatitis C virus, human immunodeficiency virus, etc.); (4) Presence of autoimmune diseases; and (5) Presence of liver injury at baseline.
Data collection
The electronic medical record system of the Affiliated Hospital of Xuzhou Medical University was used to collect clinical data of patients. Collected indicators included: Total cholesterol, alpha fetoprotein, HBsAg, hepatitis B e antigens, HBV DNA, ALT, AST, gamma-glutamyl transpeptidase (GGT), TBIL, albumin (ALB), prothrombin time, white blood cell count, neutrophil count, lymphocyte count, platelet count, etc., along with imaging data. Based on the laboratory and imaging indicators within one week after TACE and referring to the liver injury grading standards as above, the liver injury occurring during treatment was graded.
Statistical analysis
This retrospective study uses R 4.2.2 for analysis of data and construction of the model. For normally distributed continuous variables, data are expressed as means and compared using the Student’s t-test. For non-normally distributed data are presented as medians and analyzed with the non-parametric rank-sum test. As for categorical variables, they were summarized as frequencies, and using the χ2 test to perform group comparisons. Statistically significant variables from the univariate analysis were entered into a multivariate logistic regression model to identify independent risk factors. The nomogram was developed and subsequently assessed through receiver operating characteristic (ROC), calibration, and decision curve analysis (DCA). P < 0.05 was considered statistically significant in all tests.
RESULTS
Comparison ALI and non-ALI patient profiles
A total of 172 patients with HBV-related intermediate to advanced HCC were included. Patients were separated into two groups on account of whether liver injury occurred after TACE: ALI group (n = 62) and non-ALI group (n = 110). Variables that reached statistical significance between both groups included Child-Pugh stages, the number of TACE treatments, tumor diameter, prognostic nutritional index, HBV DNA level, ALB, prothrombin time, and international normalized ratio (P < 0.05) (Table 1).
Table 1 Comparison of baseline data of 172 cases of hepatitis B virus-related intermediate to advanced hepatocellular carcinoma, mean ± SD/n (%).
Identification of risk factors for post-TACE ALI in patients with HCC
To screen independent risk factors, univariate analysis was performed on Table 2. The results showed significant differences between the two groups in Child-Pugh stages, number of TACE treatments, and HBV DNA level (P < 0.05). Variables with P < 0.05 in the univariate analysis were included in the multivariate logistic regression model for adjustment and it demonstrated that Child-Pugh stage, number of TACE treatments, and HBV DNA level were independent influencing factors for post-TACE ALI (Table 2).
Table 2 Risk factors for post-transcatheter arterial chemoembolization acute liver injury in patients with hepatitis B virus-related hepatocellular carcinoma.
The final model incorporated three independent predictors from the multivariate analysis: Child-Pugh stage, number of TACE treatments, and HBV DNA level. These were integrated into a nomogram, assigning weights based on regression coefficients, to provide a prediction model to estimate the individual risk of ALI after TACE (Figure 1).
To check on the accuracy of this prediction model, a comprehensive validation was performed. The ROC curve was used to evaluate the discrimination of the model. As shown in Figure 2, the nomogram achieved an area under the curve (AUC) of 0.706, which was superior to the predictive performance of Child-Pugh stage alone (AUC = 0.584), number of TACE treatments alone (AUC = 0.598), or HBV DNA alone (AUC = 0.625) (Figure 2). Calibration curve analysis demonstrated a good degree of concordance between predicted and observed probabilities (Figure 3A). DCA validated the utility of this nomogram, showing it provides greater net benefits in clinical decision-making for the prediction of post-TACE ALI in patients with HBV-related intermediate or advanced HCC (Figure 3B).
Figure 2 Receiver operating characteristic curve analysis of the model.
TACE: Transcatheter arterial chemoembolization; HBV: Hepatitis B virus; AUC: Area under the curve.
Figure 3 Calibration and clinical net benefit of the model.
A: Calibration curve of the column line nomogram model; B: Decision curve analysis of the column nomogram model. TACE: Transcatheter arterial chemoembolization; HBV: Hepatitis B virus.
Model robustness assessment
To assess the robustness of the findings, three statistical models with different adjustment strategies were constructed (Table 3). In the unadjusted model 1, HBV DNA level (20-2000 IU/mL and > 2000 IU/mL) and TACE treatment were identified as significant risk factors for ALI [odds ratio (OR) = 2.566, 2.982, and 2.245, respectively], whereas Child-Pugh stage was a protective factor (OR = 0.409). In model 2, after adjusting for demographic variables, the OR values and significance of each factor remained largely unchanged. In model 3, after adjusting liver function related indicators (ALT, AST, GGT, TBIL, ALB), the OR for high HBV DNA level (> 2000 IU/mL) increased from 2.987 to 3.610 and remained statistically significant (P = 0.007). The OR for TACE increased slightly (from 2.180 to 2.321), with P value remaining significant. The OR for Child-Pugh stage decreased slightly in model 3 but remained statistically significant. Overall, the associations of HBV DNA load, number of TACE treatments, and Child-Pugh stage with ALI remained stable across different levels of multivariable adjustment, supporting the robustness of this model.
HCC is a malignant tumor that originates from hepatocytes and is the most common type of primary liver cancer[19,20]. It typically arises in the setting of underlying chronic liver disease, with hepatitis virus infection being one of its major risk factors. With a steadily rising global incidence, HCC has become a leading worldwide health concern and ranks as the second most common cause of cancer death after lung cancer. It has no specific symptoms at the early stage and is easily misdiagnosed as chronic liver disease. The tumor has often progressed to an intermediate or advanced stage when typical symptoms appear, missing the best timing or opportunity for surgery. Therefore, TACE serves as a mainstay in the local treatment and clinical management of intermediate to advanced HCC. It works by slowing tumor progression and alleviating tumor burden, thereby improving patients’ quality of life and extending overall survival. However, ALI is observed in a proportion of cases following TACE. The underlying mechanisms include the toxicity of the delivered chemotherapy and the inflammatory reaction triggered by ischemia-reperfusion after embolization. As a result, the normal liver microenvironment was disrupted, which in turn stimulates liver fibrosis and angiogenesis, this may be related to poor TACE efficacy and unfavorable HCC prognosis[21,22]. This study confirmed that better Child-Pugh stage, number of TACE, and high HBV DNA level are independent risk factors for post-TACE ALI.
The Child-Pugh stage is an extensively employed scoring system for evaluating residual hepatic function and reserve. Higher Child-Pugh stages (B/C) correlate with severely compromised liver synthesis, metabolism, and excretion. The inadequate liver compensatory reserve post-procedure makes this classification a strong predictor for liver failure following TACE[23]. However, a seemingly paradoxical phenomenon exists in clinical observation: Some patients with good Child-Pugh stage (A) also developed ALI postoperatively. The underlying mechanism may be that a better liver function is always accompanied by a richer hepatic arterial blood supply. During TACE, this rich blood supply could result in more chemotherapy drug retention, therefore promoting a more significant localized inflammatory reaction. Recent studies have suggested that the mesenchymal-epithelial transition factor (MET) signaling may play a key role within hepatocytes of such patients. The pathway is essential for sustaining hepatocyte viability and inhibiting mitochondrial apoptosis. When ischemia hypoxia stress induced by TACE activates c-Jun N-terminal kinase (JNK), normal MET signaling can inhibit JNK by activating protein kinase B. If MET signaling in hepatocytes is relatively insufficient or suppressed, even if overall liver function is acceptable, it may not effectively restrain JNK activation and its translocation to mitochondria, leading to excessive mitochondrial oxidative damage and hepatocyte death, ultimately manifesting as ALI[24]. This provides a molecular perspective for understanding this paradox, but the exact mechanism still requires more basic research for verification.
TACE involves injecting a mixture of chemotherapy drugs (doxorubicin or cisplatin) and lipiodol to selectively block tumor feeding arteries, thereby causing ischemic necrosis of the target tumor through cytotoxic effects and ischemic effects[25]. Research by Hiraoka and his team showed that repeated TACE treatments lead to continuous deterioration of liver function[26]. Repeated embolization procedures not only directly cause intrahepatic vascular endothelial injury and microcirculation disorders, leading to local ischemia reperfusion injury, but also indirectly amplify liver inflammation by inducing alterations in the gut microbiota. The latest research indicates that TACE can cause gut microbiota disturbance, particularly a reduction in Limosilactobacillus reuteri and its metabolite indole-3-lactic acid (ILA). By weakening its inhibition on the heat shock protein-90/NLRP3 inflammasome axis in hepatocytes, reduced ILA permits inflammasome activation. This, in turn, promotes the maturation and release of pro-inflammatory factors [e.g., interleukin (IL)-1β, IL-6], ultimately exacerbating both systemic and local hepatic inflammation[27]. This vicious cycle of ischemic injury and inflammatory reaction ultimately leads to progressive liver function decompensation. Previous studies have indicated that high HBV DNA load, indicative of active viral replication, has been associated with poor prognosis following locoregional or systemic therapies for HCC. In particular, it represents an independent risk factor for post-TACE ALI[28,29]. While TACE acts by elevating intratumoral drug concentration and occluding tumor blood supply to induce ischemic necrosis, the procedure itself creates an ischemic and hypoxic microenvironment that may interact synergistically with ongoing HBV replication through several interrelated pathways[30]. Viral components such as HBV DNA or the HBV X protein can engage pattern recognition receptors, including Toll-like receptor 9 and the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes axis, triggering type I interferon production and downstream inflammatory signaling (e.g., nuclear factor kappa-B, signal transducer and activator of transcription 1), which may sensitize hepatocytes to TACE-induced ischemia-reperfusion injury[31,32]. Besides, the persistent nuclear reservoir of HBV covalently closed circular DNA sustains chronic intrahepatic inflammation and viral protein expression, potentially impairing post-TACE hepatocyte repair[33]. Additionally, active HBV replication may suppress the expression of major histocompatibility complex class I on hepatocytes to cause aberrant activation of cytotoxic natural killer (NK) cells. These activated NK cells facilitate hepatocyte pyroptosis through the perforin/granzyme-gasdermin D/caspase-8 axis, releasing damage-associated molecular patterns that further activate neutrophils and induce neutrophil extracellular trap formation, thereby amplifying sterile inflammation and liver injury[34,35]. These mechanisms foster a pro-inflammatory and pro-oxidative microenvironment that likely lowers the threshold for TACE-related hepatocyte death. The detailed biochemical interplay warrants further exploration. Future studies integrating virological, transcriptomic, and proteomic data are needed to delineate these pathways in clinical samples.
The nomogram constructed in this study contains above factors and possesses good performance in discrimination and calibration. This model has the potential to help clinical workers assess the risk of liver injury in patients before an operation and to aid in individualized treatment decisions. The extensive validation results of the calibration curve and DCA confirm the reliability of our designed model from different aspects: Prediction accuracy and clinical net benefit, respectively. This means that the model can not only better distinguish between high-risk and low-risk patients, but its predicted probability is also close to the true incidence. More importantly, using this model to guide clinical decisions (such as strengthening perioperative monitoring for high-risk patients, optimizing antiviral therapy, or choosing alternative treatments) can bring greater actual benefit to patients. Admittedly, this study has several limitations inherent to its retrospective, single-center design. Although the sample size is sufficient for preliminary model development, it may compromise the stability of effect estimates for specific risk factors and restrict the generalizability of the nomogram for the reason of the lack of external validation. An important limitation is the lack of systematic data on antiviral therapy (including agent, duration, and response). This may introduce confounding in the HBV DNA-ALI association, as effective viral suppression could alter hepatocyte vulnerability to TACE-related injury. Besides, the analysis did not incorporate key mechanistic biomarkers such as inflammatory cytokines (e.g., tumor necrosis factor-α, IL-1β, IL-6) or oxidative stress indicators (e.g., malondialdehyde, superoxide dismutase, glutathione), which limit the insight into the underlying pathophysiology. A further limitation is that ALI was assessed at only one postoperative time point. Serial monitoring of liver enzymes and HBV DNA would help differentiate early ischemic injury from later events related to inflammation or viral reactivation. Therefore, external validation through multicenter, prospective cohorts is essential to validate the generalizability and clinical applicability of this nomogram.
CONCLUSION
In summary, this finding confirmed that patients who are diagnosed with HBV-related intermediate or advanced HCC with good Child-Pugh stage, repeated TACE treatments, and high HBV DNA load have a higher risk of post-TACE ALI. These variables were integrated into a nomogram, which showed acceptable discrimination, good calibration, and positive net clinical benefit, supporting its use for individualized preoperative risk stratification. However, external validation in prospective, multicenter cohorts with serial biomarker assessment is needed to confirm generalizability and to clarify the mechanisms linking HBV activity to TACE-related liver injury.
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