Annals of hepatology最新文献

Introduction and objectives: Living donor liver transplantation is a vital option in low- and middle-income countries with limited access to deceased donor organs. In 2017, Fundación Cardioinfantil-La Cardio established Colombia's first adult living donor liver transplantation program. This study describes donor selection, outcomes, and complication proportion over eight years.

Materials and methods: We conducted a retrospective cohort study of all adult donor candidates evaluated between February 2017 and January 2025. Donors underwent a comprehensive four-phase assessment (clinical, laboratory, psychosocial, and imaging). Eligibility criteria included age 18-50, BMI <30 kg/m² or minimal hepatic steatosis, ABO compatibility, residual liver volume >35%, and graft-to-recipient weight ratio >1% (or >0.8% for donors under 35). Graft volume estimates were validated intraoperatively using CT-based volumetry. Postoperative complications were classified using Clavien-Dindo, and bivariate analyses explored predictors of adverse outcomes and hospital stay duration.

Results: Of 137 candidates, 133 were included, and 63 (47.4%) completed donation. Donors had a mean age of 31.4 years, and 51.9% were women. Main exclusion reasons included steatosis >20%, recipient receiving a deceased donor organ, anatomical variants, and low graft volume. Among donors, 81.1% experienced no complications. Minor complications (12.7%) included biliary issues, liver dysfunction, and surgical site infections. No vascular or thrombotic events were reported. Elevated ICU liver enzymes were associated with complications and prolonged hospitalization. A learning curve was evident, with fewer severe complications observed after the 44th procedure.

Conclusions: These findings demonstrate the feasibility and safety of living donor liver transplantation in resource-constrained settings, supporting the development of similar programs in LMICs.

Chronic liver disease (CLD) remains a major global health burden, driven by persistent hepatic injury that triggers inflammation, vascular dysfunction and progressive extracellular matrix (ECM) deposition. These processes disrupt the liver architecture, leading to advanced liver fibrosis or cirrhosis and increasing the risk of severe complications such as portal hypertension, hepatocarcinoma and even death. While fibrosis and cirrhosis were historically regarded as irreversible, accumulating experimental and clinical evidence now support the potential for fibrosis and even cirrhosis regression once the etiological insult is controlled. Nevertheless, fibrosis regression is not universally observed: about 25% of patients with advanced CLD and sustained hepatitis B virus suppression and over one-third of those with metabolic dysfunction-associated steatotic liver disease after bariatric surgery fail to experience fibrosis regression. Notably, fibrosis regression is often partial and slower in advanced CLD or cirrhosis, especially in decompensated stages, highlighting the need for a better understanding of the cellular and molecular mechanisms that either facilitate or restrict hepatic tissue repair. This review summarizes current knowledge on the dynamics of liver fibrosis regression, with a particular emphasis on the liver sinusoidal endothelial cell (LSEC) as a central regulator of the microenvironment. We discuss how LSEC phenotype determines interactions with hepatic stellate cells (HSCs), immune cells, and hepatocytes, thereby shaping the balance between fibrogenesis and resolution. Mechanisms such as endothelial capillarization, macrophage-driven inflammation, HSC activation and hepatocyte regeneration are examined in the context of both disease progression and regression. Special attention is given to vascular alterations, which represent a major limiting factor for recovery in advanced CLD. We also highlight recent experimental advances, including insights from extracellular vesicle-mediated communication, microenvironmental stiffness, transcriptomic studies of LSEC plasticity during regression, and novel biomarkers of fibrosis regression. Understanding the spatiotemporal orchestration of these processes may inform novel therapeutic strategies aimed at restoring vascular and parenchymal homeostasis, ultimately enabling fibrosis reversal, portal pressure reduction, and improved clinical outcomes in patients with advanced CLD.

Chronic hepatitis C virus (HCV) infection remains a major global public health challenge. Despite the availability of highly effective therapies capable of curing the vast majority of patients, millions remain undiagnosed and often present for medical care at advanced stages of disease. This delay not only increases mortality and the burden of cirrhosis and hepatocellular carcinoma but also affects quality of life, productivity, and healthcare system costs. In this context, screening emerges as a cornerstone for achieving HCV elimination. It enables the identification of hidden cases, early treatment initiation, prevention of complications, and reduction of community transmission. At the population level, prioritizing individuals with the highest likelihood of transmitting infection produces a multiplier effect, while both universal and risk-based strategies have consistently proven cost-effective, generating medium-term savings. In Latin America, the epidemiological landscape is heterogeneous. While overall prevalence in the general population is relatively low, high endemicity persists in vulnerable groups such as people who inject drugs, incarcerated individuals, and patients undergoing hemodialysis. Major barriers include fragmented health systems, lack of clinical registries, stigma, and restricted access to diagnosis and therapy. Yet, the region also holds clear opportunities: simplified diagnostic pathways using rapid testing and reflex algorithms, micro-elimination in key populations, pooled procurement of antivirals through the Pan American Health Organization, and the integration of digital health and telemedicine. In conclusion, HCV screening constitutes both a public health necessity and an ethical obligation. Its organized and sustainable implementation is essential to translate therapeutic efficacy into collective benefit and to accelerate progress toward the elimination of hepatitis C.

The gut and the liver are the main organs in the regulation and distribution of zinc. Therefore, gut and liver disease impact zinc functions in other organs. Many of the phenomenological observations made in the past century concerning the role of zinc in growth and development and the role of zinc deficiency in many diseases are now better understood on the basis of zinc's remarkable catalytic, structural, and regulatory functions in over 3200 human proteins and its functions as an ionic messenger similar to calcium in intra- and extracellular communication, regulation of metabolism, and gene expression. Zinc has key roles in carbohydrate and lipid metabolism, nitrogen balance, pH control, and the synthesis and degradation of proteins. Its classification as a trace element distracts from its global significance in the proliferation and differentiation of all cells. Zinc is at least as important as iron, if not even more so. Its intricate cellular regulation by 24 membrane zinc transporters, a dozen metallothioneins and other zinc homeostatic proteins supports this tenet. This review will summarize the role of zinc in the integrity of the intestinal barrier, in maintaining a healthy gut, and, through the gut-liver axis, a healthy liver. Zinc is critical for a proper immune response to support and control inflammation, in fighting off insults and repairing tissues, but also in avoiding chronic inflammation. About 75% of patients with decompensated liver cirrhosis are zinc deficient. Zinc deficiency, a prooxidant and proinflammatory condition, needs clinical attention in liver disease, should include attention to gut health, and involve pharmacological treatment with supplemental zinc. Monotherapy with zinc alone, however, is not the answer. Along with zinc, additional therapeutics are required to restore intestinal and hepatic functions.

Introduction and objectives: Hepatic encephalopathy (HE) is a major complication after transjugular intrahepatic portal shunt (TIPS), affecting patients' quality of life. This study evaluated the efficacy of Clostridium butyricum combined with lactulose in preventing HE after TIPS.

Patients and methods: Patients were randomly divided into two groups: Clostridium butyricum plus lactulose group (trial group) and lactulose group (control group). Prophylaxis started within 24 hours post-TIPS and lasted 3 months. The primary endpoint was the occurrence of HE at 1 and 3 months after TIPS. The study also analyzed the impact on gut microbiota.

Results: No significant difference in minimal hepatic encephalopathy (MHE) incidence between the two groups. However, the trial group had a significantly lower overt hepatic encephalopathy (OHE) incidence than the control group at both one month (8.2 % vs. 26.5 %, P = 0.016) and three months (10.2 % vs. 34.7 %, P = 0.004) (HR=3.867, P = 0.008; aHR=4.819, P = 0.004). The trial group showed a higher skeletal muscle index at the third lumbar vertebra at 3 months after TIPS (42.85 ± 10.66 vs. 38.38 ± 8.61 cm²/m², P = 0.024). Combining treatment can reduce the occurrence of OHE in patients with sarcopenia (48.3 % vs. 15 %, P = 0.016). The abundance of butyrate-producing bacteria and the level of butyric acid in the trial group at 3 months after TIPS was significantly increased compared to the baseline. The levels of TNF-α and D-LDH in the trial group were significantly lower than those in the control group at 3 months after TIPS.

Conclusions: Clostridium butyricum plus lactulose can significantly reduce the incidence of OHE after TIPS and improve nutritional status. In addition, combined therapy can also increase the abundance of beneficial bacteria in stool, increase the level of butyric acid in stool, and improve the inflammatory state in patients undergoing TIPS.

Introduction and objectives: Hepatocellular carcinoma (HCC) and portal hypertension (PHT) are two common complications of cirrhosis that often co-exist and significantly affect patient prognosis, yet global management varies widely. This study evaluated Chinese physicians' perspectives on PHT screening and management in HCC.

Materials and methods: An online questionnaire survey was distributed to hepatologists, gastroenterologists, gastrointestinal oncologists, and hepatobiliary surgeons across 132 hospitals in 16 provinces throughout China from March 1, 2024, to June 30, 2024. The questionnaire comprised 57 items across four sections. This study was approved by Union Hospital, Tongji Medical College, Huazhong University of Science and Technology (No. 2024-0365) and registered at the Chinese Clinical Trial Registry (ChiCTR2400084630).

Results: Overall, 1,584 participants responded to the questionnaire. The reported PHT screening rate in HCC patients was 82.6%. Imaging was the most common modality (50.5%), followed by endoscopy (30.8%). However, adherence to the Baveno VI/VII consensus was only 28%. Complications of PHT, including gastrointestinal bleeding and ascites, significantly affected physicians' screening practices. The primary and secondary prophylaxis strategies for PHT generally comply with the Baveno VII consensus. A history of acute variceal bleeding within 6 months significantly reduced the preference for atezolizumab and bevacizumab therapy (19.6% vs. 32.9%, P<0.001). In cases of acute variceal bleeding during atezolizumab-bevacizumab therapy, 79.5% of the physicians recommended permanent discontinuation of bevacizumab, whereas 20.5% advocated continuation upon achieving hemostasis.

Conclusions: Substantial heterogeneity exists in the management of PHT among HCC patients in China, highlighting the need for targeted multidisciplinary education to standardize care and improve patient outcomes.