Gastrointestinal (GI) health is essential for maintaining systemic balance, influencing digestion, immunity, and neuroendocrine signaling. However, GI disorders such as irritable bowel syndrome, inflammatory bowel disease, gastroesophageal reflux disease, peptic ulcers, and constipation are increasingly prevalent, significantly affecting global health and healthcare economics. Although conventional pharmacological treatments offer symptomatic relief, their long-term use is often associated with adverse effects, resistance, and limited efficacy, prompting a shift toward alternative and complementary therapies. Traditional systems of medicine, such as Ayurveda, Traditional Chinese Medicine, Unani, and Siddha, emphasize holistic approaches, including herbal formulations that target underlying causes rather than just symptoms. This review provides a comprehensive analysis of the role of natural products and traditional herbals in GI health. It discusses key bioactive constituents, flavonoids, alkaloids, terpenoids, and polyphenols, known for their anti-inflammatory, antimicrobial, gastroprotective, and prebiotic properties. Widely used herbal remedies such as Triphala, licorice root, peppermint oil, turmeric, and psyllium are highlighted for their proven therapeutic actions. Additionally, the review documents more than 300 medicinal plants traditionally used in diverse cultures worldwide for managing GI conditions, based on ethnopharmacological evidence. While the therapeutic promise is substantial, challenges such as formulation standardization, herb-drug interactions, and limited clinical data remain. The review underscores the need for integrating traditional wisdom with modern scientific validation, offering a path forward for safe, effective, and personalized GI healthcare.

Parenteral nutrition (PN)-associated cholestasis (PNAC) is frequently diagnosed in premature infants; however, not all PN-exposed infants develop PNAC. We propose that, in premature infants receiving PN and varying amounts of enteral feeds, differences in the gut microbiome and fecal bile acid content are associated with PNAC development. This study aimed to examine the fecal microbiome and bile acid content of premature infants on PN to determine if there is a relationship with the development of PNAC.

Twenty-two preterm infants had serial bilirubin measurements and fecal samples collected during their neonatal intensive care unit admission. Fecal samples underwent 16S rRNA gene sequencing and bile acid analysis. Binomial regression, adjusting for postmenstrual age with feed amount as a moderator, was used to assess the impact of the fecal microbiome and bile acids on PNAC development.

Cholestatic patients (n = 11) had greater PN and antibiotic exposure (p = 0.020; p = 0.010) and longer neonatal intensive care unit stays (p = 0.0038) than non-cholestatic patients. Microbiome richness was higher in non-cholestatic infants (p < 2E-16), with no difference in β diversity (p = 1.0). Cholestatic infants had a significantly higher abundance of Proteobacteria and Fusobacteriota and a lower abundance of Bacteroidota (p < 2E-16). Akkermansia was abundant in all infants on low feeds; as feed volume increased, Akkermansia abundance significantly increased in non-cholestatic infants (p < 2E-16). Bile acid analysis demonstrated significantly lower deoxycholic acid concentrations in cholestatic infants (p < 2E-16). Metagenomic analysis revealed an increase in Proteobacteria requiring augmented stress responses in non-cholestatic infants.

This is the first study to directly explore the relationship between PNAC susceptibility, the microbiome, and fecal bile acids in preterm infants. The microbiome and bile acid patterns identified here may inform the development of targeted therapeutics for this vulnerable population.

Clove essential oil (CEO) derived from Syzygium aromaticum and miswak (Salvadora persica) contains bioactive compounds with antimicrobial properties. Due to the growing interest in alternatives to conventional antibiotics, this study aimed to evaluate the in vitro antimicrobial efficacy of CEO, miswak, and their combination against key peri-implantitis pathogens.

The antimicrobial activities of CEO, miswak, and their combinations were tested against Fusobacterium nucleatum, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia. Disc diffusion and serial dilution methods were used to measure the inhibition zones and minimum inhibitory concentrations, respectively. Doxycycline served as a standard antibiotic for comparison, while ethanol was used as a negative control. Data were analyzed using one-way analysis of variance and Tukey’s honestly significant difference test, with significance set at α = 0.05.

CEO exhibited inhibition zones of 10–16 mm, comparable to that of doxycycline (13–16 mm), whereas miswak (6–13 mm vs. 1–14 mm) and the CEO–miswak combination (8–14 mm vs. 0–14 mm) showed lower activity. Mean minimum inhibitory concentration values were lowest for doxycycline (1.73 ± 0.46 µg/mL), followed by CEO (2.37 ± 0.24 µg/mL) and CEO–miswak combination (2.92 ± 0.12 µg/mL). Statistical analysis showed that the CEO–miswak combination was less effective than CEO (p = 0.0326) and doxycycline (p = 0.0001), but not different from miswak (p = 0.9836). CEO showed slightly greater activity than miswak (p = 0.0605).

Among the natural extracts tested, CEO exhibited superior antimicrobial efficacy, whereas miswak was less effective. The combination of CEO with miswak did not enhance antimicrobial efficacy, suggesting antagonistic interactions between their bioactive compounds.

Familial hypobetalipoproteinemia (FHBL), caused by apolipoprotein B (APOB) variants, disrupts APOB-containing lipoprotein synthesis, leading to reduced serum total cholesterol, low-density lipoprotein cholesterol, and APOB. Heterozygous carriers are often asymptomatic, while homozygotes exhibit severe manifestations like malabsorption, vitamin deficiencies, and hepatic steatosis. In recent years, FHBL has attracted increasing attention due to its association with liver disease and its role as a unique monogenic model of steatotic liver disease independent of cardiometabolic risk factors. Mechanistically, lipid overload, endoplasmic reticulum stress, oxidative damage, and impaired autophagy may drive hepatocellular injury and fibrosis. Challenges include insufficient diagnosis, sparse epidemiological data, and unclear disease progression. Enhanced genetic testing, mechanistic research, and longitudinal studies are critical to improving diagnosis, risk assessment, and therapies for FHBL-associated liver disease.

Characteristic signs of alopecia are gradual thinning, disruption of structural features, and the hair development cycle (anagen, catagen, telogen) against the background of miniaturization of hair follicles, which leads to baldness and psychological stress in patients. Despite the rapid development and clinical application of synthetic pharmacological, cellular/acellular, and molecular drugs, no effective therapeutic agent against alopecia has yet been developed. Great hopes are pinned on the improvement of therapeutic strategies with the introduction of exosomes into practical application, which contain a wide array of active substances for the targeted stimulation of hair follicle activity (anagen inducers) through the regulation of intracellular signaling cascades, growth factors, and microRNAs. The review discusses in detail the microRNAs and their intracellular targets that control hair follicle morphogenesis. It also focuses on the prospects of using stem cell exosomes from various sources for the treatment of alopecia, providing a clinical rationale for potential benefits and risks.

Hepatocellular carcinoma (HCC) is the most common subtype of primary liver cancer and continues to be a major cause of cancer-related mortality, particularly in regions of China with a high hepatitis B virus prevalence. Early-stage diagnosis remains challenging due to its asymptomatic onset and the limited sensitivity of conventional biomarkers, which together contribute to delayed detection, suboptimal therapeutic outcomes, and poor prognosis. These limitations underscore the urgent need for reliable, sensitive, and specific biomarkers to enable timely detection and targeted intervention. Protein induced by vitamin K absence or antagonist-II, an abnormal prothrombin variant generated under vitamin K deficiency or antagonism, has emerged as a promising candidate with diagnostic and therapeutic relevance in HCC. This review critically examines the molecular and biological characteristics of protein induced by vitamin K absence or antagonist-II, evaluates its clinical utility in HCC diagnosis and management, and delineates the current limitations hindering its broader application. Furthermore, future perspectives are proposed to guide translational research and clinical implementation. Collectively, this review aims to provide a comprehensive theoretical framework to advance precision diagnosis and individualized treatment strategies for HCC.

Myosteatosis is associated with poor outcomes in various liver diseases. However, standardized methods for assessing, defining, and diagnosing myosteatosis in the context of liver diseases remain unclear. Furthermore, the underlying mechanisms by which myosteatosis leads to pathophysiological progression and adverse health outcomes remain elusive. Therefore, in this review, we elaborate on the currently available measures, definitions, and diagnostic criteria of myosteatosis in the existing literature. We thoroughly clarify the recent evidence and data regarding the possible involvement of myosteatosis in the progression and deterioration of various liver diseases and resulting complications, including liver cirrhosis, chronic viral hepatitis, non-alcoholic/metabolic-associated fatty liver disease, primary sclerosing cholangitis, liver transplantation, and hepatocellular carcinoma. Additionally, it synthesizes insights from basic research on the pathogenesis of myosteatosis, which involves multifactorial mechanisms, including insulin resistance, mitochondrial dysfunction, and chronic inflammation. Finally, from an operational and pragmatic perspective, several regimens, including physical, nutritional, and pharmacological therapies, have been discussed as potential treatments for myosteatosis.

Potential celiac disease (PCD) is defined as elevated celiac serology with a preserved small intestinal mucosa. This study aimed to identify baseline characteristics and the outcomes of children with PCD consuming a gluten-containing diet.

This was a retrospective cohort study of pediatric PCD patients diagnosed between 12/2018 and 10/2024. Baseline data included demographics, anthropometrics, clinical symptoms and signs, celiac serology, and biopsy results. Follow-up data included repeat serology and biopsy results when performed.

PCD was diagnosed in 75/517 (14.5%) children undergoing upper endoscopy for suspected celiac disease (CeD). Baseline anti-transglutaminase IgA (TTG) was above 10× the upper limit of normal (ULN) in 18 (24%), between 3–10× ULN in 52 (69.3%), and <3× ULN in five (6.6%). Anti-endomysial antibody was positive in 57 (76%). Among 48 children (64%) with at least one year of follow-up, TTG normalized in 26 (54.1%), decreased to <3× ULN in 13 (27.1%), was between 3–10× ULN in six (12.5%), and was above 10× ULN in three (6.3%). Nine children had a repeat endoscopy, and six (66.7%) were diagnosed with CeD, while three remained PCD. Among the 11 children with TTG >10× ULN and at least one year of follow-up, TTG normalized in three, declined in five, and increased or remained above 10× ULN in three.

PCD is common and may be found in children with TTG above 10× ULN; approximately half will normalize TTG. The omission of biopsies may result in an erroneous diagnosis of CeD.

The gut microbiota is crucial in maintaining host health and liver function. Fecal microbiota transplantation (FMT) has shown promising potential in treating chronic liver diseases. To help clinicians quickly master and standardize the clinical application of FMT for chronic liver disease, the Liver Related Digestive Diseases Group of the Chinese Society of Hepatology of the Chinese Medical Association has developed the “Expert Consensus on the Clinical Application of FMT for Chronic Liver Disease.” This consensus addresses the key aspects of FMT, including the indications, contraindications, efficacy, safety, donor selection, transplantation routes, precautions, and the prevention and management of adverse reactions for chronic liver conditions, such as chronic hepatitis, cirrhosis, and liver cancer, thereby offering reference and guidance to clinicians implementing FMT in the treatment of chronic liver disease.

Bacterial infections (BIs) are common and severe complications in patients with liver cirrhosis, but global data are limited. Here, we aimed to evaluate the global prevalence, temporal changes, and associated mortality risk of BIs in liver cirrhosis.

We systematically searched PubMed, Embase, Web of Science, and the Cochrane Library for eligible studies published without language restrictions until 11 August 2025. A random-effects model was used for meta-analyses, meta-regression by study year, and pooling adjusted hazard ratios.

Fifty-nine studies, including 1,191,421 patients with cirrhosis, were analyzed. The pooled prevalence of BIs (33 studies) was 35.1% (95% confidence interval (CI): 29.2–41.4). The prevalence of Escherichia coli and Streptococcus spp. was 3.8% (95% CI: 2.5–5.2) and 1.5% (95% CI: 0.8–2.6), respectively. The pooled prevalence of multidrug-resistant bacteria was 6.8% (95% CI: 4.0–11.3). The most common BI sites were the gastrointestinal tract, ascites fluid, and urinary tract. The highest prevalence of BIs was reported in Europe (38.2%; 95% CI: 24.8–53.6), followed by South America (37.5%; 95% CI: 29.7–46.1) and Asia (22.8%; 95% CI: 16.3–30.9). Patients with acute-on-chronic liver failure showed the highest prevalence of BIs (44.2%; 95% CI: 29.7–59.8). A modest increasing trend in BIs prevalence was observed over time. BIs were associated with an increased risk of mortality in patients with cirrhosis (adjusted hazard ratios 2.22, 95% CI 1.33–3.71).

BIs are prevalent in cirrhosis, especially in acute-on-chronic liver failure, with a modest upward trend and increased mortality risk.