Transarterial chemoembolization (TACE) is a cornerstone locoregional therapy for hepatocellular carcinoma (HCC), yet most candidates also have cirrhosis. That makes TACE a balancing act: controlling tumor progression while protecting a liver with limited functional reserve, often over multiple sessions. This narrative review synthesizes current evidence on TACE-induced liver injury (TACE-LI), with emphasis on its definitions, mechanisms, risk prediction, and prevention, and further contextualizes emerging data on the gut-liver axis and inflammasome signaling. Clinically, TACE-LI spans a spectrum from transient biochemical worsening and post-embolization syndrome (PES; fever, pain, malaise) to clinically meaningful decompensation and post-TACE liver failure (PTLF). A key challenge is that the literature uses heterogeneous definitions and thresholds for both TACE-LI and PTLF, complicating comparisons between studies and weakening clarity around retreatment decisions. Mechanistically, injury is multifactorial: arterial ischemia from embolization, ischemia-reperfusion and oxidative stress, local chemotherapeutic toxicity and material retention, biliary or microvascular injury, and a systemic inflammatory response that can drive both symptoms and laboratory derangement. Our review also highlights how cirrhosis-associated gut barrier dysfunction may prime inflammatory cascades through dysbiosis, bacterial translocation, and endotoxin signaling (e.g., LPS-TLR4), potentially shaping vulnerability after embolization. In this context, inflammasome pathways, especially NLRP3, are discussed as amplifiers that translate danger signals (DAMPs), reactive oxygen species, and microbial cues into IL-1β/IL-18 release and pyroptotic injury, linking sterile ischemic damage to immune activation. For risk stratification, baseline hepatic reserve (Child-Pugh, ALBI), tumor burden, and technical intensity remain central, and dynamic indicators such as post-TACE ALBI deterioration help capture clinically relevant trajectories. Our review also summarizes predictive tools such as nomograms and models for complications (including PES), and notes ongoing exploration of machine-learning-assisted decision support. Prevention ultimately rests on careful patient selection, liver-sparing technique (including superselective approaches when feasible), and structured peri‑procedural care to mitigate PES and reduce infectious or biliary complications.
Intestinal fibrosis is a severe complication of inflammatory bowel disease (IBD) with limited effective therapeutic interventions. Nintedanib, a multi-target kinase inhibitor, exerts well-characterized antifibrotic activity in pulmonary fibrosis and may serve as a candidate agent for IBD-related intestinal fibrosis. To compare the anti-inflammatory and antifibrotic efficacy of nintedanib with prednisolone and sulfasalazine in a DSS-induced mouse intestinal fibrosis model. Forty-eight C57BL/6 mice were randomly allocated to four DSS-treated intervention groups (12 mice per group: Group A prednisolone, Group B sulfasalazine, Group C nintedanib, Group D normal saline), plus a normal untreated control Group E (n=7). Intestinal fibrosis was induced via four cycles of intermittent 2% DSS drinking water. On Day 26 prior to drug administration, five mice from each group were randomly euthanized for baseline detection to verify successful model establishment. The remaining mice received 14 consecutive days of intragastric treatment. Measured endpoints included body weight recovery, disease activity index (DAI), colon morphological parameters, serum TGF-β and TNF-α levels, and collagen deposition quantified via Masson's trichrome staining. Group C achieved slightly higher body weight recovery (19.6±1.4%) than Group A (18.7±0.2%) and Group B (19.4±1.5%), while Group D only recovered 3.4±0.9% (P<0.001). Nintedanib treatment significantly improved colon length and reduced colon weight compared with the two conventional drugs, though colon length in Group C was still markedly shorter than that of normal mice. Serum TGF-β and TNF-α were reduced more substantially in Group C; however, cytokine concentrations remained 2-3 times higher than baseline values of healthy animals and failed to return to normal levels. Masson staining revealed that collagen deposition in Group C decreased by roughly 10% relative to Groups A and B (25±3.2% vs 35±4.2%, 34±3.8%). Currently, there is no unified gold-standard threshold for evaluating antifibrotic efficacy in preclinical intestinal fibrosis models, and relevant quantitative criteria vary widely across published studies. In this DSS-induced colitis model, nintedanib produced modest anti-inflammatory and collagen-reducing effects compared with prednisolone and sulfasalazine used in this study. These preclinical preliminary results warrant further research to evaluate nintedanib as a potential therapeutic candidate for fibrostenotic Crohn's disease.
Chronic pancreatitis (CP) imposes substantial clinical and economic burden, yet contemporary nationwide trends and disparities are incompletely characterized. We quantified national trends in CP hospitalizations, examined sociodemographic disparities, and evaluated clinical outcomes and resource utilization using the National Inpatient Sample (NIS) 2016-2022. We conducted a retrospective cohort study of adults (≥18 years) with chronic pancreatitis (CP) identified by ICD-10-CM codes (primary or secondary diagnosis) in the National Inpatient Sample (NIS), 2016-2022. We described patient and hospital characteristics and modeled temporal trends in CP-associated hospitalizations using survey-weighted logistic regression with year as a continuous variable. To contextualize temporal changes during the COVID-19 pandemic, we additionally calculated annual CP-associated hospitalization rates per 100,000 all-cause hospitalizations. estimated adjusted odds ratios (aORs) for hospitalization by race/ethnicity and key risk factors (alcohol use disorder [AUD], non-alcohol substance use disorder [SUD], psychiatric disorders, homelessness), adjusting for age, sex, Elixhauser comorbidity index, hospital characteristics, and region. We summarized in-hospital outcomes, complications, and resource utilization. We identified 15,732 CP hospitalizations (mean age 49.9 ± 14.0 years; 52.8% male). Most were White (63.7%), followed by Black (21.4%) and Hispanic (10.1%). Mean length of stay (LOS) was 4.5 ± 5.3 days, and mean total hospital charges were $48,068 ± 73904.35 . In adjusted models treating year as a continuous variable, the odds of CP-associated hospitalization decreased by approximately 8% annually (adjusted odds ratio [aOR] 0.92; 95% CI 0.90-0.94; p<0.001). Although absolute weighted counts transiently increased in 2020, rates normalized to all-cause hospitalizations continued to decline overall, decreasing from 41.9 per 100,000 hospitalizations in 2016 to 27.5 per 100,000 in 2022. After adjustment, Black patients had significantly higher odds of CP hospitalization than White patients (aOR 1.15; 95% CI 1.09,1.21; p < 0.001). Hispanic (aOR 0.75; 95% CI 0.70,0.80; p = 0.0195) and Asian/Pacific Islander patients (aOR 0.48; 95% CI 0.40,0.58; p < 0.001) had substantially lower odds. Behavioral and social risk factors demonstrated strong association with CP hospitalization: AUD (aOR 5.76; 95% CI 5.48,6.064; p < 0.001), non-alcohol SUD (aOR 2.67; 95% CI 2.55,2.79; p < 0.001) and psychiatric comorbidity (aOR 1.57; 95% CI 1.50,1.65; p < 0.001) were independently associated with higher hospitalization risk. Homelessness was associated with lower odds after adjustment (aOR 0.76; 95% CI 0.64,0.90; p = 0.002). Overall in-hospital mortality was low (0.3%). Complications included acute kidney injury (9.2%), venous thrombosis (2.6%), portal vein thrombosis (1.7%), and sepsis (0.7%). From 2016-2022, CP-associated hospitalization rates declined overall, although absolute hospitalization counts demonstrated a transient increase during the first pandemic year. Marked disparities persist-higher odds among Black patients and strong associations with AUD/SUD and psychiatric comorbidity. Despite low inpatient mortality, CP continues to generate significant resource use. These findings support targeted prevention (alcohol/substance use), integrated behavioral health, and equity-focused strategies to reduce avoidable hospitalizations.
To systematically characterize existing prognostic models and to evaluate and compare their discriminative performance in patients with intrahepatic cholangiocarcinoma (iCCA) after curative resection. We systematically searched Web of Science, Embase, Cochrane Library, PubMed, and MEDLINE (January 2010 to January 2026). Two reviewers independently screened studies, extracted data, and assessed risk of bias using PROBAST+AI. Tested and selected variables were summarized using frequencies. Discriminative performance estimates (C-index and area under the curve [AUC]) with 95% CI were pooled via random-effects meta-analysis after logit transformation. All analyses were performed using R, version 4.4.2. A total of 60 studies involving 82 prediction models were included. Frequencies revealed that traditional variables were consistently considered, including markers of tumor burden and invasiveness, inflammation-related and nutrition-related markers, and individual characteristics. Meta-analysis of 36 studies showed a pooled training set C-index of 0.723 (95% CI: 0.705-0.740) and AUC of 0.767 (95% CI: 0.700-0.823), while the validation set showed a pooled C-index of 0.696 (95% CI: 0.673-0.718) and AUC of 0.787 (95% CI: 0.690-0.860). These performance metrics were consistently higher than those of the AJCC staging system (7th edition), the AJCC staging system (8th edition), and the LCSGJ staging system. Subgroup analyses suggested that incorporating treatment-related variables, distinguishing resection status, and using recurrence as an endpoint tended to improve model discrimination. Considerable heterogeneity was observed. In this systematic review and meta-analysis, existing prognostic models for iCCA demonstrated good discriminative performance. These models outperformed conventional staging systems and provided predictive value for both survival and recurrence. Nevertheless, methodological shortcomings remain in most models and warrant further refinement.
Rare genetic liver diseases collectively affect millions of individuals worldwide and encompass a heterogeneous group of monogenic disorders including Wilson disease, alpha-1 antitrypsin deficiency, glycogen storage diseases, urea cycle disorders, progressive familial intrahepatic cholestasis, and acute hepatic porphyrias. While conventional management relies on dietary modification, pharmacotherapy, and ultimately liver transplantation, the advent of clustered regularly interspaced short palindromic repeats (CRISPR)-based gene editing has opened transformative therapeutic avenues. This review provides a comprehensive and critical appraisal of the current landscape of CRISPR-based therapies for genetic liver diseases, from preclinical proof-of-concept studies to landmark clinical trials. We examine the evolution from conventional Cas9 nuclease-mediated editing to precision tools including base editors and prime editors, which enable single-nucleotide corrections without inducing double-strand DNA breaks. The role of lipid nanoparticle delivery systems in achieving efficient hepatocyte-targeted delivery is discussed, alongside emerging challenges in pediatric dosing and immunogenicity. We highlight the paradigm shift toward personalized, patient-specific CRISPR therapies, exemplified by the first-in-human bespoke gene editing treatment delivered in 2025. Competing nucleic acid technologies, including RNA interference and antisense oligonucleotides, are compared in terms of durability, safety, and cost-effectiveness. Finally, we critically evaluate the evolving regulatory landscape and propose a priority framework for selecting genetic liver diseases most amenable to CRISPR-based correction. This review underscores that CRISPR gene editing is transitioning from experimental promise to clinical reality for genetic liver diseases, with personalized approaches poised to redefine the treatment paradigm.
Cancer mortality among individuals aged 15-45 years is a critical metric for assessing progress in cancer control. This study examined long-term mortality trends and sociodemographic disparities for the six leading causes of cancer death among individuals aged 15-45 years in the United States from 1999 to 2023. Mortality data were obtained from the Centers for Disease Control and Prevention Wide-ranging Online Data for Epidemiologic Research (CDC WONDER) database (1999-2023). Death records for individuals aged 15-45, with any of the six cancers listed as the underlying cause, were included. Age-adjusted mortality rates (AAMRs) per 100,000 population were calculated. Temporal trends were analyzed using Joinpoint regression to compute the average annual percent change (AAPC) and 95% confidence interval (CI). Future mortality through 2035 was projected using autoregressive integrated moving average (ARIMA) modeling. Between 1999 and 2023, Lung cancer mortality declined most sharply (AAPC: -4.79*; 95% CI: -5.45 to -4.13). Breast cancer mortality also exhibited a significant decrease. In contrast, colorectal cancer (CRC) mortality increased significantly (AAPC: 0.88*; 95% CI: 0.72 to 1.04), emerging as the only major cancer with a sustained upward trajectory in this age group. Mortality from leukemia, brain cancer, and cervical cancer remained stable or declined modestly. Pronounced disparities were observed across census regions, racial/ethnic groups, and sex. ARIMA projections indicated that CRC mortality among individuals aged 15-45 years is expected to increase further through 2035, whereas mortality from lung cancer and breast cancer is projected to continue declining. Substantial reductions in lung cancer mortality among individuals aged 15-45 years in the United States have been offset by a concerning rise in colorectal cancer mortality in this age group. Strategic shifts toward risk-stratified screening, equitable care, and targeted interventions are imperative.
Inflammatory bowel disease (IBD) and primary biliary cholangitis (PBC) have been reported to coexist in some patients, but the extent of this association remains to be further clarified. Clarifying their shared genetic architecture and intercellular interaction patterns may provide insight into the biological links between these two immune-mediated diseases and inform future disease monitoring strategies. This study integrated summary statistics from genome-wide association studies (GWAS) of two independent IBD cohorts and one PBC cohort, along with spatially resolved single-cell transcriptomic data. Genetic correlations were examined using linkage disequilibrium score regression, genetic covariance estimation, and localized variant association analyses. Shared susceptibility loci were identified through conditional/joint false discovery rate (FDR) approaches and multi-trait joint analysis. Furthermore, a genetic information-guided cell-type spatial mapping strategy was applied to delineate disease-associated cellular populations at single-cell resolution. Genetic analyses revealed significant genome-wide correlations and extensive polygenic overlap between IBD, its subtypes, and PBC. Local variation analyses further identified multiple chromosomal regions exhibiting regional genetic associations shared by both diseases. Several putative shared susceptibility loci were discovered, with a subset validated using independent datasets. The genetic information-guided spatial mapping approach demonstrated comparable tissue-resident cell distribution patterns between IBD and PBC. By integrating GWAS data with single-cell transcriptomic profiling, this study provides a systematic characterization of the genetic relationships between IBD and PBC. These findings offer genetic and cellular-level insights that contribute to a deeper understanding of the molecular basis underlying their comorbidity.
Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and remains a major cause of cancer-related mortality worldwide. This study aimed to evaluate the safety and efficacy of hepatic artery infusion chemotherapy (HAIC) combined with camrelizumab and apatinib in patients with advanced HCC. A retrospective analysis was conducted on patients with advanced HCC who received either camrelizumab plus apatinib (n = 65) or HAIC combined with camrelizumab and apatinib (n = 65). Objective response rate (ORR), disease control rate (DCR), serum tumor marker levels, including alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), and carbohydrate antigen 19-9 (CA19-9), adverse events, progression-free survival (PFS), and overall survival (OS) were compared between the two groups. Baseline clinical characteristics were comparable between the two groups. Compared with camrelizumab plus apatinib alone, treatment with HAIC combined with camrelizumab and apatinib achieved significantly higher ORR and DCR and was associated with more favorable post-treatment serum AFP, CEA, and CA19-9 levels. Treatment-related adverse events were generally manageable. At the final follow-up, median PFS was 15 (2-24) months in the camrelizumab plus apatinib group and 15 (8-30) months in the HAIC plus camrelizumab plus apatinib group, respectively. Median OS of the two groups was 20 (6-27) months and 21 (10-30) months, respectively. Based on the Kaplan-Meier analysis, patients receiving the trimodality therapy demonstrated significantly prolonged PFS and OS. Together, HAIC combined with camrelizumab and apatinib demonstrated favorable efficacy and acceptable safety in patients with advanced HCC. This combination regimen may represent a promising therapeutic strategy for advanced HCC.
Bowel urgency is one of the most distressing symptoms experienced by patients with inflammatory bowel disease (IBD). The relationship between bowel urgency and multidimensional IBD-related disability has not been well characterised. We conducted a multicentre cross‑sectional study including adult patients with Crohn's disease (CD) and ulcerative colitis (UC). Patients completed self-administered questionnaires evaluating bowel urgency and IBD-related disability using the IBD-Disk questionnaire. Severe bowel urgency was defined as an IBD-disk bowel urgency subscore ≥6. A total of 2,514 patients (1,715 with CD) were included. Severe bowel urgency was observed in 17.1% of patients with UC and in 20.4% of patients with CD, compared to 3.6% and 7.6%, respectively, in those in clinical remission according to PRO-2 criteria. In multivariate analysis in patients with UC, factors associated with severe bowel urgency were general well-being subscore ≥2 and abdominal pain subscore ≥2 while treatment with advanced therapy, clinical remission according to PRO-2, fatigue subscore <5, work productivity subscore <3 and sexual life subscore <2 were negatively associated. In patients with CD, factors were rectal bleeding subscore ≥2, abdominal pain subscore ≥2 and history of intestinal resection while clinical remission, fatigue subscore <5, work productivity subscore <3 and sexual life subscore <2 were negatively associated. Severe bowel urgency is frequent in both patients with CD and UC beyond IBD activity and is strongly associated with various dimensions of IBD-related disability. These findings emphasise the importance of systematically assessing urgency in routine clinical practice.
Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) affects over half of patients with type 2 diabetes (T2DM), and advanced fibrosis is the strongest predictor of liver-related mortality. Although liver biopsy is the diagnostic gold standard, its invasiveness limits routine use. The accuracy of serum-based non-invasive tests (NITs) compared with liver stiffness measurement (LSM) in T2DM remains uncertain. The Universal Index for Cirrhosis (UIC index) is a newer fibrosis score with strong performance across mixed liver disease etiologies and has not been evaluated in MASLD in T2DM. This study assessed the diagnostic accuracy of the UIC index compared with established NITs using vibration-controlled transient elastography (VCTE) as the comparator for clinically significant and advanced fibrosis in a referral-based T2DM outpatient population. In this retrospective study, adults with T2DM evaluated across outpatient clinics between 2013 and 2024 were included. Demographic, clinical, and laboratory data were collected within 30 days of VCTE. Clinically significant fibrosis and advanced fibrosis/cirrhosis were defined as LSM >8 kPa and >12 kPa, respectively. Diagnostic performance was assessed, and the area under the receiver operating curve (AUROC) was calculated. Logistic regression identified predictors of fibrosis presence and severity. A total of 199 patients were analyzed (mean age 58.8 years; mean BMI 35 kg/m²). Fibrosis prevalence was 97.5% for LSM >8 kPa and 44% for LSM >12 kPa. Non-Caucasian race and higher serum albumin were independently associated with lower fibrosis risk, while increasing AST and declining platelet counts were associated with greater fibrosis severity. For LSM >8 kPa, FIB-4 ≥ 1.3, and UIC index ≥4.5, the diagnostic performance was similar (AUROC 0.69 vs. 0.68). For LSM >12 kPa, FIB-4 > 2.67 demonstrated the highest AUROC (0.72), while UIC index ≥8 showed balanced sensitivity (66%) and specificity (57%). The AUROC differences between FIB-4 and UIC were not statistically significant. FIB-4 and the UIC index demonstrated comparable diagnostic performance, each with distinct strengths and limitations.
To investigate the clinical characteristics, mutation spectrum of the ABCC2 gene, and genotype-phenotype correlations in Chinese pediatric patients with Dubin-Johnson syndrome (DJS). Six children diagnosed with DJS at Kunming Children's Hospital from April 2018 to August 2021 were enrolled. Clinical, biochemical, and imaging data were collected. Peripheral blood samples were obtained from the probands and their families. Targeted high-throughput sequencing of ABCC2 was performed, with identified variants validated by Sanger sequencing and segregation analysis. Pathogenicity was assessed following established guidelines. All patients presented primarily with jaundice; the proportion of serum direct bilirubin to total bilirubin ((DBIl/TBIl)) exceeded 20%. We identified 12 ABCC2 pathogenic mutant alleles, including 4 missense, 2 nonsense, 2 frameshift, 1 synonymous, 1 in-frame deletion, and 2 splice-site mutations. Among these, three were novel and previously unreported: c.4210_4212del, c.4237_4238insCT, and c.4532dupA. Exons 20, 28, and 30 emerged as mutational hotspots. Genotype-phenotype relationships were complex: carriers of in-frame deletions exhibited milder manifestations, while truncating mutations did not consistently lead to the most severe phenotypes. Comorbidities and allelic interactions together constituted a "composite pathogenicity burden" that determined phenotypic severity. This study expands the ABCC2 mutation spectrum in Chinese DJS patients, reports three novel mutations, and introduces a "composite pathogenicity burden" model that highlights the multifactorial nature of clinical presentation. These findings provide a basis for improved genetic counseling and precision management of DJS.
Vascular liver diseases (VLDs) are rare conditions affecting adults of working age, yet there are no real-world data on their impact on employment. A multicenter cross-sectional study was conducted in France and Spain, using clinical records and self-administered questionnaires. Employment outcomes in patients with a VLD and controls were compared using indirect standardisation with age- and sex-adjusted population norms. Multivariable logistic regression assessed factors associated with health-related inactivity (unable to work due to illness/disability) and health-related absenteeism from work. Of 1136 eligible patients, 595 (52.4%) responded and the data of 432 participants aged 25-64 were analysed. Health-related inactivity (13.0% of patients) and health-related absenteeism over the last year (48.5%) were higher in patients with a VLD than in the general population (Standardised Ratio (SR) = 2.61, 95%CI:1.95-3.42; SR = 1.57, 95%CI:1.33-1.87 respectively). History of gastrointestinal bleeding (adjusted Odds Ratio (aOR) = 2.64, 95%CI:1.17-5.98) and prior interventional procedures (aOR = 2.49, 95%CI:1.06-5.88) were significantly associated with inactivity. Older patients (versus 25-44 years old) and those with a low/moderate educational level (versus high) were more likely to experience inactivity (aOR = 2.23, 95%CI:1.07-4.65; aOR = 3.11, 95%CI:1.53-6.35 respectively). Absenteeism was associated with moderate/severe pain (aOR = 2.45,95%CI:1.10-5.44) and unmet needs for special illness-related leave (aOR = 2.97,95%CI:1.33-6.63). Patients with VLD face disadvantages in employment participation and absenteeism, driven by disease severity and symptom burden. These effects are most pronounced among low-educated individuals, highlighting socioeconomic disparities in work retention. This underscores the need for targeted workplace accommodations, supportive employment policies, and social care support.
Hypoalbuminemia is common in severe acute pancreatitis (SAP) and is associated with poor outcomes. Early administration of human albumin has been proposed to improve outcomes by expanding the intravascular volume and correcting hypoalbuminemia. We performed a systematic review to evaluate whether early albumin infusion in patients with moderate SAP reduces the incidence of sepsis and improves clinical outcomes. We searched the MEDLINE, EMBASE, and Cochrane CENTRAL databases from inception to January 15, 2026, for studies of albumin infusion in adult patients with moderate or SAP. Eligible studies included randomized controlled trials (RCTs) and cohort studies that compared early albumin infusion with no albumin or crystalloid-only therapy. The primary outcome was sepsis incidence. The secondary outcomes included in-hospital mortality, and A.P.-related complications. Six studies (one RCT and five retrospective cohorts studies) met the inclusion criteria. Albumin infusion protocols varied (5% albumin 30 g/day for 2-3 days in the RCT). Early albumin administration was associated with a significantly lower risk of sepsis in patients with SAP. However, their effects on mortality were inconsistent. One cohort study of patients with hypoalbuminemic SAP reported significantly lower in-hospital mortality with albumin therapy. However, the RCT showed no difference in the 60-day mortality between the albumin and control groups. None of the included studies reported a clear reduction in pancreatitis-specific complications attributable to albumin. Early albumin infusion in moderate to SAP was associated with a lower risk of sepsis across studies but yielded no clear improvement in overall mortality.
Diagnosing Covert Hepatic Encephalopathy (CHE) in alcohol-related cirrhosis is complicated by potential overlap with alcohol-related cognitive impairment (ARCI), whose effect on recommended CHE tests remains poorly characterized. We aimed to assess the performance of PHES, MoCA and the Simplified Animal Naming Test (sANT) in patients with chronic alcohol exposure, with and without cirrhosis. In this prospective single-center cohort, patients admitted for alcohol withdrawal or pre-liver-transplant workup were assessed with PHES (CHE if <-4), MoCA (impairment if <26) and sANT. Correlations and factors associated with CHE were analyzed by univariate and multivariate analysis; sANT diagnostic performance for CHE detection was evaluated by ROC analysis against PHES as the reference standard. 236 patients were included, 137(58%) with cirrhosis (age 61 [54-64], MELD 14 [9-19]; 13% clinical HE) and 99 without (age 48 [42-55]). PHES<-4 occurred in 34(33%) non-cirrhotic versus 52(38%) cirrhotic patients; sANT was below the CHE cut-off in 27% and 27% respectively. sANT AUROC for CHE in cirrhosis was 0.77(0.69-0.85). sANT correlated significantly with PHES and MoCA in both groups (rho 0.44-0.56). In multivariate analysis, PHES was associated with sANT, MoCA, creatinine and albumin; MoCA with sANT, PHES and education. A comparable proportion of patients crossed the PHES and sANT cut-offs whether or not they had cirrhosis, suggesting failure to distinguish ARCI from CHE in alcohol-related cirrhosis. Clinicians should interpret abnormal CHE tests with caution in this population. Further research is required to better disentangle ARCI from CHE. Magnetic resonance imaging and spectroscopy, therapeutic tests, or more accurate biomarkers, are promising opportunities.
Inflammatory Bowel Disease (IBD) negatively impacts quality of life, increasing the risk of psychological disorders. Acceptance and Commitment Therapy (ACT) is a form of psychotherapy that has shown promise for individuals living with chronic illnesses. This meta-analysis aims to explore the efficacy of ACT in managing psychological symptoms in patients with IBD, compared to usual care. A systematic search was conducted across PubMed, Web of Science, SCOPUS, CENTRAL, and Google Scholar from inception to August 2025. Eligible studies comprised randomized controlled trials and quasi-experimental studies that compared ACT with usual or other interventions in IBD patients. Standardized Mean Differences (SMDs) with 95% confidence intervals (CIs) were calculated for assessed continuous outcomes. CRD420251153446. Nine studies involving 459 patients were included. ACT significantly reduced anxiety scores compared to non-ACT (SMD = -0.34; 95% CI: [-0.56 to -0.12]; P < 0.01). Still, the improvements in depression (P = 0.08), stress (P = 0.08), Crohn's disease activity (P = 0.06), and ulcerative colitis activity (P = 0.59) were not statistically significant compared to non-ACT. Subgroup analysis indicated significant improvements in anxiety (SMD = -0.34; 95% CI: -0.64 to -0.03; P = 0.03, I² = 0%), depression (SMD = -0.44; 95% CI: [-0.80 to -0.08]; P = 0.02) and stress (SMD = -0.55; 95% CI: [-0.92 to -0.19]; P < 0.01) scores when ACT was compared with treatment-as-usual. In contrast, no significant differences in depression, anxiety, or stress were found between ACT and other active psychoeducational interventions. Anxiety score was significantly improved post-intervention (SMD = -0.37; 95% CI: [-0.70 to -0.04]; P = 0.03) and at 1-2 months (SMD = -0.33; 95% CI: [-0.63 to -0.03]; P = 0.03), while stress score was significantly improved at 1-2 months (SMD = -0.41; 95% CI: [-0.74 to -0.07]; P = 0.02). ACT reduced anxiety, depression, and stress versus treatment-as-usual. Additionally, ACT reduced anxiety and stress scores at 1-2 months versus the control group. However, no improvement was observed in CD or UC activity. ACT was not superior to other active controls, such as CBT. Larger, longer follow-up periods and randomized trials are needed to confirm effects on psychological outcomes and disease activity.
Due to the lack of uniform diagnostic criteria and the exclusive use of computed tomography as an indicator, the prevalence of sarcopenia in patients with stomach cancer varies considerably. Currently, limited data are available from comprehensive studies utilizing bioelectrical impedance analysis (BIA) for muscle mass, combined with handgrip strength and gait speed, to assess sarcopenia in treatment-naïve gastric cancer patients. Therefore, this study aims to investigate this condition among treatment-naïve gastric cancer patients in China. This study aimed to assess the prevalence of Chinese sarcopenia in treatment‑naïve gastric cancer patients by using BIA with handgrip strength and gait speed, in line with the standard Chinese Guidelines for the Diagnosis and Treatment of Sarcopenia. Employing a single-center cross-sectional design, this study assessed the prevalence of sarcopenia in treatment-naïve gastric cancer patients using BIA and standard Chinese diagnostic criteria. Additionally, comparative analyses of body composition and laboratory parameters were conducted to discern significant differences between patients with and without sarcopenia. Using Chinese diagnostic criteria and BIA, we identified a sarcopenia prevalence of 17.49% in treatment-naïve gastric cancer patients. This cohort demonstrated significant muscle and fat depletion alongside a 62.68% prevalence of GLIM-defined malnutrition. Additionally, sarcopenia was associated with a higher risk of anemia and significantly reduced serum albumin and total protein levels relative to patients without the condition. Sarcopenia imposes a significant clinical burden on Chinese patients recently diagnosed with gastric cancer, and is frequently associated with severe malnutrition and anaemia.
Colorectal cancer (CRC), the second leading cause of cancer-related death worldwide, has declined in the United States over the past two decades due to expanded screening and improved systemic therapies. Although mortality has decreased in older adults, recent data suggest an increasing trend in younger populations. The concurrent rise in metabolic comorbidities may be contributing; however, no national multi-decade study has evaluated trends, disparities, and trajectories in CRC mortality with co-existing metabolic comorbidity. Using the CDC WONDER Multiple Cause-of-Death database (1999-2024), we identified decedents aged ≥25 years with CRC as the underlying cause and ≥1 metabolic condition (obesity, Type-2 DM, hypertension, dyslipidemia) listed in any death-certificate field, representing co-documented metabolic comorbidity. Age-adjusted mortality rates (AAMRs) were calculated by direct standardization. Joinpoint regression assessed temporal trends, and ARIMA modeling projected mortality through 2031. From 1999 to 2024, overall CRC AAMR declined by ∼40% (32.06 to 19.38 per 100,000; AAPC -2.04%), whereas CRC with metabolic comorbidity AAMR nearly doubled (1.37 to 2.47 per 100,000; AAPC +2.01%). The proportion of CRC deaths with co-documented metabolic comorbidity tripled, from 4.27% to 13.03%. Steepest increases occurred for dyslipidemia (+7.65%), adults aged 25-44 years (+6.70%), males (+2.80%), Hispanic (+4.16%) and White (+2.22%) individuals, Southern region (+3.92%), and noncore rural areas (+2.48%). ARIMA projections estimate growth to 2.81 per 100,000 by 2031 (+13.8% increase). CRC mortality with co-documented metabolic comorbidity is rising despite an overall decline in CRC mortality, highlighting an increasing metabolic burden among CRC decedents. Persistent demographic and geographic disparities underscore the need for integrated metabolic-oncologic care and targeted prevention strategies.
The disease burden of gastric cancer (GC) in China remains heavy. This study analyzed GC disease burden trends in China over recent years and projected future epidemiological patterns to inform targeted national public health prevention strategies. The prevalence, incidence, mortality, and disability-adjusted life years (DALYs) of GC in China were extracted from the Global Burden of Disease (GBD) 2023 database. The epidemiological characteristics and temporal trends were described and analyzed. The main risk factors associated with GC were analyzed, and the ARIMA model was used to predict the changing trends from 2024 to 2035. The above epidemiological indicators of GC decreased from 1990 to 2023, and exhibited a modest rebound between 2020 and 2023. The prevalence showed a downward trend in most age groups, but there was a significant upward trend in the 15-19 and 85-89 age groups. Moreover, the burden on males was significantly higher than females. The main modifiable risk factors included smoking, excessive alcohol consumption, and a high-sodium diet. Projections indicate a continued overall decline in GC burden from 2024 to 2035. Precise prevention and control measures should be implemented according to gender and age groups, and screening should be strengthened to improve the early diagnosis rate, ultimately alleviating the burden of GC in China.
Stimulant-associated gastrointestinal ischemia is rare, and isolated gastric involvement without small bowel injury has not been previously described in association with amphetamine-class drugs. Markedly elevated lipase can further obscure the diagnosis by raising clinical suspicion for acute pancreatitis. A 59-year-old male with polysubstance use disorder was found unresponsive and later reported acute epigastric pain. CT demonstrated diffuse gastric pneumatosis and intrahepatic portal venous gas. Markedly elevated lipase (5190 U/L) without radiographic pancreatitis initially prompted consideration of acute pancreatitis; however, CT imaging findings redirected the diagnostic workup. Urine toxicology was positive for amphetamines. CT angiography confirmed gastric mucosal necrosis without vascular occlusion. Endoscopy demonstrated confluent gastric mucosal necrosis with sparing of the antrum and normal duodenum. The patient recovered with supportive care. Serial lipase levels trended down from 5190 U/L at presentation to 2840 U/L on day 2 and 1120 U/L on day 3, paralleling clinical improvement and consistent with a non-pancreatic source. This case expands the spectrum of stimulant-related GI ischemia to include isolated gastric involvement. While an elevated lipase raised initial concern for pancreatitis, it was CT imaging rather than the lipase alone that correctly guided the diagnostic pathway. GI ischemia is an important but underrecognised cause of non-pancreatic hyperlipasaemia. Clinicians should be aware that GI ischemia can cause marked hyperlipasaemia. CT imaging findings rather than lipase levels alone should guide clinical decision-making in patients with stimulant use and acute abdominal pain.
Reduced urinary sodium excretion reflects disease severity in patients with cirrhosis, but routine use outside clinical settings is not feasible. Urinary chloride, reabsorbed alongside sodium, can be easily measured using a dipstick. This study examines the correlation between dipstick-measured urine chloride and urinary sodium/chloride concentrations and explores its potential to predict future acute decompensation (AD) in cirrhosis. In this prospective multicenter pilot study, hospitalized patients with cirrhosis were enrolled from four Dutch hospitals. Single urine samples were collected for dipstick chloride measurement and laboratory analysis of urinary sodium/chloride. The primary outcome measure was the correlation between dipstick and lab-based urine electrolytes and the secondary outcome was the predictive value of dipstick chloride for new-onset AD development within 90-days. A total of 100 patients (62% male) were included, with a median age of 64 years [IQR 53-70]. Dipstick urinary chloride strongly correlated with laboratory urinary chloride (r = 0.801) and urinary sodium concentrations (r = 0.757). Within 90-days, the cumulative incidence of AD was higher in patients with low urinary chloride concentration (≤38 mmol/L) compared with those with high urinary chloride (44%vs 22%, p = 0.014). Multivariate regression models showed that three variables were independently associated with an increased risk of developing new AD: low urinary chloride, diuretic use, and AD at inclusion. Dipstick-measured urinary chloride concentration correlates strongly with laboratory urinary sodium and -chloride concentration in patients with cirrhosis. Given its simplicity and low-cost, urine chloride dipstick testing may serve as a practical tool for monitoring disease course in clinical and outpatient settings.