Hepatocellular carcinoma (HCC) remains one of the most fatal cancers, primarily due to late diagnosis and the lack of effective early biomarkers. Recent advances in multi-omics and liquid biopsy technologies hold promise for improving early detection, prognostication, and monitoring of HCC. Understanding the immune landscape of HCC through genetic and epigenetic signatures is essential for identifying therapeutic targets and improving immunotherapy outcomes. This review aims to present current findings on immune-related biomarkers, multi-omics strategies, and biomarker validation in HCC. It also aims to evaluate the role of liquid biopsy and gene signatures in predicting treatment responses, with a specific focus on their applications in immunotherapy. The goal is to provide a comprehensive framework for integrating these emerging tools into clinical practice. The integration of multi-omics approaches has led to the identification of robust gene signatures that predict HCC prognosis and response to immune checkpoint inhibitors. Liquid biopsy technologies, including circulating tumor DNA, provide non-invasive alternatives for monitoring tumor evolution and therapeutic responses. Despite promising results, challenges remain in clinical validation, particularly in cross-platform reproducibility and the interpretation of complex multi-omics data. While genetic biomarkers are rapidly advancing, their clinical application in personalized medicine remains hindered by technical and ethical challenges, such as data privacy, informed consent, and method standardization. The integration of multi-omics data and liquid biopsies offers a promising path toward real-time, personalized treatment and the development of universal prognostic signatures for HCC. However, successful clinical adoption depends on cross-disciplinary collaboration to standardize data protocols and overcome challenges regarding accuracy, reproducibility, and patient privacy.

Synucleinopathies, including Parkinson’s disease (PD), dementia with Lewy bodies, and multiple system atrophy (MSA), are a group of neurodegenerative diseases characterized by the oligomerization of α-synuclein protein in neurons or glial cells. Various splicing isoforms of α-synuclein have been described, each with different aggregation properties. The α-synuclein gene (SNCA) has been identified as a highly significant genetic risk locus associated with various synucleinopathies across populations. This study aimed to assess the association of SNCA genetic variants with MSA and the levels of SNCA transcripts in peripheral blood mononuclear cells (PBMCs) from MSA and PD patients.

In this retrospective case–control study, 96 MSA patients, 1086 PD patients, and 485 healthy volunteers were included. PCR followed by restriction endonuclease analysis was used to detect four SNCA single-nucleotide polymorphisms (rs356219, rs3756063, rs11931074, and rs356168) in these individuals. In addition, RT-qPCR was performed to detect the levels of α-synuclein transcripts (SNCA mRNA isoforms -140, -126, and -112) in PBMCs of 24 MSA patients (including parkinsonian (MSA-P) and cerebellar (MSA-C) variants), 31 PD patients, and 32 healthy volunteers.

The frequency of the ‘T’ allele (of rs11931074) was significantly higher in MSA patients than in the healthy controls. The level of SNCA-140 mRNA was significantly decreased in MSA and PD patients compared with the controls, while the level of SNCA-112 mRNA was significantly increased in MSA-P patients than in PD patients and the controls. SNCA-112 mRNA/SNCA-140 mRNA and SNCA-112 mRNA/SNCA-126 mRNA ratios were significantly increased in MSA patients than in the controls.

The SNCA rs11931074 polymorphism is associated with MSA. There is a pronounced alteration in the expression of SNCA transcripts in PBMCs of MSA and PD patients.

Cannabinoid hyperemesis syndrome is an underrecognized cause of recurrent vomiting, weight loss, and abdominal pain in adolescents, often overlooked due to its nonspecific presentation and overlap with other gastrointestinal conditions. This case report highlights a 13-year-old female who presented with significant weight loss and postprandial bilious vomiting initially attributed to superior mesenteric artery syndrome. Persistent symptoms, despite surgical removal of an incidental ovarian dermoid cyst, prompted reevaluation after nondiagnostic imaging and lack of improvement. Further history two weeks later revealed daily cannabis use, confirmed by a positive urine toxicology screen for tetrahydrocannabinol. Following supportive care and cannabis cessation, her symptoms resolved. This case illustrates how incomplete social histories and incidental findings can delay the identification of cannabinoid hyperemesis syndrome and lead to unnecessary procedures. Early use of urine toxicology screening and validated substance use tools (CRAFFT, BSTAD, S2BI) in adolescents with persistent vomiting and abdominal pain can facilitate timely recognition, reduce hospital length of stay, and improve outcomes.

Pancreatic cystic neoplasms (PCNs) are increasingly detected in clinical practice, yet substantial variability exists in imaging interpretation and reporting, which may affect clinical decision-making. This guideline was developed to standardize diagnostic imaging evaluation and reporting for PCNs. A multidisciplinary expert panel conducted literature search and critical appraisal of domestic and international evidence, identified key clinical questions, and formulated recommendations using the Grading of Recommendations Assessment, Development and Evaluation framework. A modified Delphi consensus process and external review were performed to ensure the robustness of the recommendations. A total of 21 key questions were addressed, covering essential aspects of imaging evaluation and reporting for PCNs, including the preferred imaging modality for suspected lesions; standardized measurement of cyst size and mural nodules and their clinical significance; definitions of cyst wall and septal thickening; optimal imaging approaches for assessing the relationship between cystic lesions and the main pancreatic duct; measurement and evaluation of main pancreatic duct diameter and dilation; imaging-based classification of intraductal papillary mucinous neoplasms and serous cystic neoplasms; assessment of ductal obstruction, calcification, hemorrhage, and pancreatitis-related changes; criteria for suspicious lymph nodes; differentiation of PCNs from pancreatic pseudocysts or retention cysts; and recommended imaging modalities and follow-up intervals. This guideline provides a structured and evidence-based framework for imaging evaluation and reporting of PCNs, which may improve the consistency and clarity of imaging reports and support clinical decision-making.

Early risk stratification of severe acute liver injury (SLI), a precursor to acute liver failure (ALF), is vital for timely intervention, but no universal prognostic assessment tool covers both conditions. This study aimed to develop a simplified prognostic model for early risk assessment in SLI/ALF patients.

A retrospective cohort study consecutively enrolled SLI patients (including those progressing to ALF) from July 1, 2020 to May 31, 2025. Baseline clinical and laboratory data on admission were collected, with 90-day transplant-free survival as the primary outcome. Independent prognostic factors were screened via Cox regression to build a simplified scoring model, whose performance was compared with the Model for End-Stage Liver Disease (MELD), King’s College Criteria (KCC), and the Acute Liver Failure Study Group Prognostic Index (ALFSG-PI).

Of 302 patients, 190 (62.9%) achieved 90-day transplant-free survival. Multivariate Cox regression identified international normalized ratio (hazard ratio [HR]: 1.118, 95% confidence interval [CI]: 1.050–1.191), platelet count (HR: 0.995, 95% CI: 0.993–0.998), and hepatic encephalopathy grade ≥ 2 (HR: 5.187, 95% CI: 3.403–7.907) as independent predictors, forming the HIP (derived from the above-mentioned three predictors) model. It showed good discrimination ((area under the receiver operating characteristic curve [AUC]): 0.82), outperforming MELD (AUC: 0.76, P = 0.019) and KCC (AUC: 0.72, P = 0.002), and performing comparably to ALFSG-PI (AUC: 0.80, P = 0.429). The model also performed robustly in ALF subgroups defined by the American College of Gastroenterology and the 2024 Chinese Medical Association guidelines (AUCs: 0.80 and 0.76, respectively) and achieved an AUC of 0.85 in the validation set.

The HIP model is a simple and effective tool for prognostic risk stratification in SLI/ALF patients, suitable for emergency and primary care to facilitate timely intervention.

Alpha-1 antitrypsin deficiency (AATD) is an autosomal codominant genetic disorder caused by mutations in the SERPINA1 gene. It results in reduced circulating levels of alpha-1 antitrypsin (AAT), a serine proteinase inhibitor (PI) primarily produced by hepatocytes. The most common deficient alleles are PI*S and PI*Z, with PI*ZZ homozygotes having the most severe deficiency and highest risk for lung and liver disease. While AATD is well established as a cause of early-onset emphysema and liver cirrhosis, emerging evidence suggests a potential association with the formation of arterial aneurysms. The pathophysiological rationale for this association centers on protease-antiprotease imbalance and potential extracellular matrix degradation of elastin in arterial vessel walls. Several studies have reported increased frequencies of AATD alleles in patients with abdominal aortic aneurysms and intracranial aneurysms compared to the general population, with some demonstrating statistically significant associations. Additionally, patients with the PI*ZZ genotype have been shown to have larger aortic diameters, greater aortic stiffness, and reduced distensibility compared to controls. However, the evidence is inconsistent, as several large studies have failed to demonstrate significant associations between AATD and aneurysm formation. Overall, current evidence suggests an association of AATD with the development of arterial aneurysms. However, it is also clear that the presence of AATD alone is not sufficient to increase the risk of developing new-onset arterial aneurysms.

Amatoxin-containing mushroom poisoning causes fatal acute liver failure with >50% mortality despite maximal medical therapy. Interrupting the enterohepatic recirculation of amatoxins is a mechanistically rational but unproven therapeutic strategy. This study aimed to evaluate the efficacy and safety of biliary drainage (BD) in patients with pre-liver failure caused by amatoxin-containing mushroom poisoning.

In this prospective cohort study (ChiCTR2300073442), consecutive adults with amatoxin-induced pre-acute liver failure received standardized care (silibinin, N-acetylcysteine, dehydration). Patients undergoing percutaneous or endoscopic BD were compared to non-BD controls. The primary outcome was survival to hospital discharge.

Nine patients were enrolled (mean age: 63.3 ± 15.6 years; 44.4% female). All five patients who underwent BD (performed at a median of three days after ingestion) survived (100%), whereas only one of the four non-BD patients survived (25%; P = 0.048). BD initiated a rapid biochemical recovery: within 48 h, mean alanine and aspartate transaminase levels decreased by 67.6% and 91.6%, respectively, from their peak levels (P < 0.001), and the international normalized ratio decreased from 1.99 to 1.27 (P = 0.008). Non-survivors in the non-BD group progressed to multiorgan failure. Procedure-related complications (transient pancreatitis/amylasemia) occurred in three of the five BD patients but resolved with conservative management.

Timely BD was associated with 100% survival after amatoxin-induced pre-acute liver failure, contrasting sharply with 75% mortality in non-BD controls. The dramatic biochemical improvement after BD supports enterohepatic recirculation interruption as a mechanistic intervention. BD represents a potentially definitive, life-saving intervention for this lethal poisoning as a preliminary finding; larger, multicenter studies are required to confirm the observed association between BD and survival.

Primary liver cancer is one of the most common malignant tumors in China, which seriously threatens people’s lives and health. In recent years, with the advancement of basic and clinical research, the diagnosis and treatment methods for primary liver cancer have been continually enriched. Traditional Chinese medicine (TCM) has played an important role in the diagnosis and treatment of primary liver cancer, but there is no unified standard for differentiation and treatment, and efficacy evaluation. In order to further standardize the TCM diagnosis and treatment of primary liver cancer, according to the requirements of TCM standardization and related technical guidance documents, the drafting team compiled this guideline through literature research, expert interviews, questionnaire surveys, consensus meetings, etc., for reference by clinicians. This guideline is approved and issued by the China Association of Chinese Medicine, standard number: T/CACM 1575-2024.