Clostridioides difficile infection (CDI) is associated with significant morbidity and mortality and carries a high risk of recurrence. Given the substantial healthcare burden and the evolving nature of CDI, understanding the role of emerging treatment strategies is essential. While oral vancomycin remains a mainstay of CDI treatment, the past decade has brought several notable advances in agents and practices that may be used for CDI treatment and prevention. Fidaxomicin or vancomycin are now recommended for an initial episode of CDI, with several guidelines giving preference to fidaxomicin based on its demonstrated ability to reduce recurrent CDI. Promising developments have emerged regarding the use of fecal microbiota-based therapies in the management of CDI, including conventional fecal microbiota transplantation and the approved live biotherapeutic products, Rebyota and Vowst. These therapies help restore the microbiota of the colon to treat severe CDI and prevent recurrence in select patients. Several strategies have emerged to prevent recurrent CDI, including bezlotoxumab, a single-dose, weight-based IgG1 monoclonal antibody that may be given to patients at high risk of recurrence. Additional pipeline therapies, such as vaccines, beta-lactamases, and bacteriophages, may provide future opportunities for CDI management. This narrative review aimed to summarize societal guideline recommendations for CDI management, describe the evidence for key therapies used in CDI treatment, and review recent updates on emerging treatment modalities.

Hepatic encephalopathy (HE) is a brain disorder secondary to cirrhosis, characterized by cognitive deficits, psychiatric manifestations, and motor impairments. It is associated with frequent hospitalizations, high mortality rates, and poor quality of life in cirrhotic patients. Additionally, ammonia and inflammation are key contributors to the onset of HE. Rifaximin is minimally absorbed in the intestine and is considered a locally acting, semi-synthetic antibiotic with broad-spectrum antibacterial activity. The pharmacological effects of rifaximin include reducing plasma ammonia levels, decreasing proinflammatory cytokine levels, and modulating gut microbiota and their functions. Currently, both Chinese and EASL clinical practice guidelines recommend rifaximin (800–1,200 mg/d) as a first-line treatment for HE for up to six months. However, the efficacy and safety of long-term (≥six months) use of rifaximin for HE remain debated. This review aimed to analyze the long-term (≥six months) use and dose-effect relationships of rifaximin treatment for HE. Long-term, low-dose use of rifaximin (600–800 mg/d) may offer potential benefits in terms of efficacy, safety, and cost-effectiveness.

Previous studies suggest that taurine supplementation may attenuate atherosclerosis by reducing lipid levels. However, energy drinks containing taurine have been shown to increase blood pressure, a key risk factor for atherosclerosis. Thus, the role of taurine in atherosclerosis remains controversial. This study aimed to investigate the effect of taurine on the development of atherosclerotic plaques.

Plasma taurine levels were measured in 105 patients with varying degrees of coronary heart disease and in 40 healthy individuals using 1,2-13C2-taurine-based ultra-performance liquid chromatography-tandem quadrupole mass spectrometry (UPLC-QQQ-MS/MS). Apolipoprotein E knockout (ApoE−/−) C57BL/6J mice, fed a high-fat diet and subjected to left carotid artery ligation with cannula insertion, received taurine or saline for four consecutive days. Healthy control mice were fed a normal chow diet and underwent a sham operation. Serum taurine levels, lipid indicators, and arterial histology in the individual mice were examined.

Plasma taurine levels were significantly higher in patients with acute myocardial infarction (4.04 ± 0.24 μg/mL) compared to healthy controls (3.52 ± 0.22 μg/mL). Taurine treatment significantly decreased plaque areas in the carotid artery, reduced Masson’s Trichrome staining, and lowered the ratio of anti-α-SMA to anti-CD68 staining in ApoE−/− mice. Additionally, taurine treatment increased the levels of matrix metalloproteinase 2 in the cultured vascular endothelial cells in vitro.

These findings suggest that taurine supplementation may reduce both the size and stability of atherosclerotic plaques. Therefore, dietary taurine supplements should be used with caution.

Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related death worldwide. Multiple treatment modalities are available for the management of HCC, depending on its stage as determined by the Barcelona Clinic Liver Cancer staging system. Because liver transplantation (LT) theoretically removes the cancer and replaces the organ at risk for future malignancy, LT is often considered the most definitive and one of the most efficacious treatment options for HCC. Nevertheless, the success and efficacy of liver transplantation depend on various tumor characteristics. As a result, multiple criteria have been developed to assess the appropriateness of a case of HCC for LT, with the pioneering Milan Criteria established in 1996. Over the past 20 to 30 years, these criteria have been critically evaluated, expanded, and often liberalized to make LT for patients with HCC a more universally applicable option. Furthermore, the development of other treatment modalities has enabled downstaging and bridging strategies for HCC prior to LT. In this narrative and comprehensive review, we provided an update on recent trends in the epidemiology of HCC, selection criteria for LT, implementation of LT across different regions, treatment modalities available as bridges, downstaging strategies, alternatives to LT, and, finally, post-LT surveillance.

Liver injury in Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) is a multifaceted disorder, lacking cohort homogeneity due to a variety of potential causes, including drugs, arsenic and other heavy metals, glyphosate, infections, and ultraviolet radiation. The goals of this review were (1) to analyze the role of diagnostic algorithms in assessing causality for potential culprits involved in the development of liver injury associated with immune-mediated SJS and TEN, which represent immune-based variant disorders within a continuous spectrum. Milder forms are classified as SJS or SJS/TEN overlap, while TEN is known as the most serious form; and (2) to interpret the findings that allow for the characterization of the different types of these disorders. The manuscript is based on an extensive literature search for single case reports, case cohorts, and review articles. Search terms included: Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis, and specific diagnostic algorithms such as the Roussel Uclaf Causality Assessment Method (RUCAM) and the Algorithm of Drug Causality for Epidermal Necrolysis (ALDEN). For the purpose of basic feature description, the uniform term SJS/TEN is used in the current analysis. SJS/TEN presents with five different cohort types: SJS/TEN type (1), which refers to a cohort of SJS/TEN caused by drugs, as assessed by both ALDEN and RUCAM; type (2), representing SJS/TEN due to drugs and assessed by ALDEN only, but not by RUCAM; type (3), which includes a cohort of SJS/TEN caused by drugs, assessed by non-ALDEN and non-RUCAM tools; type (4), which focuses on a cohort of SJS/TEN caused by non-drug culprits, assessed by various tools; and type (5), which considers a cohort of SJS/TEN caused by unknown culprits. Using this new SJS/TEN typology will help better characterize individual features, personalize treatment, and clarify pathogenetic specifics for each of the five disease types. This new SJS/TEN typology provides clarity by replacing issues of inhomogeneity with cohort homogeneity.

Acute liver failure (ALF) is a disorder with various etiologies. Although the causes leading to this disruptive condition are well documented in published ALF cohorts, there is significant concern among patients who experience ALF with indeterminate causes, an issue requiring thorough analysis. This review aimed to analyze cohort studies on ALF with a focus on unknown causes leading to classification as indeterminate ALF. The analysis revealed that, among 67 worldwide adult and pediatric ALF cohorts, indeterminate causes of ALF ranged from 2% to 100%, with an average of 30%. Among the 13 pediatric ALF cohorts, the corresponding range was 22% to 100%, with an average of 47%, while among the 55 adult ALF cohorts, the range was 2% to 78%, with an average of 26%. The percentage values were higher in pediatric cohorts due to the higher incidence of rare genetic causes compared to adult patients. Notably, higher rates of indeterminate causes were found in cohorts studied before the availability of diagnostic serologic screening parameters and polymerase chain reaction techniques for various hepatitis virus infections. Patients with indeterminate ALF may not have received a specific treatment that, if effective, could have helped prevent liver transplantation. It is concluded that, in future cases, all efforts must be undertaken to clearly establish the cause of severe liver injury, enabling effective therapy when available and helping reduce the risk of progression to ALF and the need for liver transplantation.

Pancreatic cancer encompasses a heterogeneous group of malignancies, primarily divided into endocrine and exocrine types, with pancreatic ductal adenocarcinoma representing approximately 90% of cases. While the incidence of pancreatic cancer is relatively low, accounting for about 3% of all cancers in the United States, it has a disproportionately high mortality rate, responsible for around 7% of cancer-related deaths. In 2024, it is estimated that there will be 66,440 new diagnoses and 51,750 fatalities associated with this disease. The overall five-year survival rate remains alarmingly low at just 13%, primarily due to late-stage diagnosis; over 80% of pancreatic ductal adenocarcinoma patients present with unresectable tumors and metastases at the time of diagnosis. This review aims to highlight recent advancements in imaging and laboratory tests that are paving the way for innovative screening and diagnostic approaches. Some of the modalities discussed in detail include endoscopic ultrasound (EUS) and its modifications, such as EUS elastography, EUS contrast-enhanced, and EUS Fine Needle Aspiration, as well as multi-detector computed tomography scans, magnetic resonance imaging, and positron emission tomography scans. Furthermore, laboratory tests, such as multi-marker analysis and circulating tumor DNA, alongside traditional markers like carcinoembryonic antigen, carbohydrate antigen 19-9, and carbohydrate antigen 125, are explored. The role of radiomics and proteomics in the early detection of pancreatic cancer is also discussed. These developments hold the promise of improving early detection, which is crucial for enhancing patient outcomes in pancreatic cancer. On the treatment front, conventional therapies, including platinum-based therapies and monoclonal antibodies, are reviewed, alongside innovative therapies such as immunotherapies, chimeric antigen receptor T-cell therapy, and cancer vaccines. It has been increasingly recognized that the intricate patho-mechanisms underlying tumorigenesis in pancreatic cancers necessitate a deeper understanding to facilitate targeted therapeutic strategies. We also explore various newer therapies currently in clinical trials, assessing their practicality and effectiveness in real-world settings.

Early detection of hepatocellular carcinoma (HCC) is crucial for improving survival in patients with chronic hepatitis. The GALAD algorithm combines gender (biological sex), age, α-fetoprotein (AFP), Lens culinaris agglutinin-reactive fraction of AFP (AFP-L3), and protein induced by vitamin K absence or antagonist-II (PIVKA-II) for HCC detection. Similarly, the GAAD algorithm incorporates gender (biological sex), age, AFP, and PIVKA-II. This study aimed to assess the clinical utility of AFP-L3 in the GALAD algorithm and its potential synergies with ultrasound. We compared the clinical performance of GALAD with GAAD; AFP; AFP-L3; and PIVKA-II, with or without ultrasound, in Taiwanese adults.

A total of 439 serum samples were analyzed using a Cobas® e 601 analyzer (healthy controls, n = 200; chronic liver disease controls, n = 177; HCC cases, n = 62). Performance was assessed through receiver operating characteristic curve analyses to calculate the area under the curve.

The area under the curve for differentiating early-stage HCC from patients with chronic liver disease was optimal for PIVKA-II (84.9%), GAAD (79.8%), and GALAD (79.4%), with slightly improved performance for detecting all-stage HCC. Clinical performance was unaffected by disease stage or etiology. Sensitivity for early-stage HCC was highest for GAAD (57.6%) and GALAD (57.6%). Sensitivity for each strategy was further enhanced when combined with ultrasound, regardless of disease stage or etiology (P < 0.01).

These findings indicate that the role of AFP-L3 in the GALAD algorithm is minimal, supporting the use of GAAD for HCC detection. A combination of GAAD, GALAD, or PIVKA-II with ultrasound may improve diagnostic efficiency compared with recommended strategies.

Solute carrier (SLC) family transporters are crucial transmembrane proteins responsible for transporting various molecules, including amino acids, electrolytes, fatty acids, and nucleotides. To date, more than fifty SLC transporter subfamilies have been identified, many of which are linked to the progression of hepatic steatosis and fibrosis. These conditions are often caused by factors such as non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, which are major contributors to the global liver disease burden. The activity of SLC members regulates the transport of substrates across biological membranes, playing key roles in lipid synthesis and metabolism, mitochondrial function, and ferroptosis. These processes, in turn, influence the function of hepatocytes, hepatic stellate cells, and macrophages, thereby contributing to the development of hepatic steatosis and fibrosis. Additionally, some SLC transporters are involved in drug transport, acting as critical regulators of drug-induced hepatic steatosis. Beyond substrate transport, certain SLC members also exhibit additional functions. Given the pivotal role of the SLC family in hepatic steatosis and fibrosis, this review aimed to summarize the molecular mechanisms through which SLC transporters influence these conditions.