Search Results (7,040)

Background: While pediatric obesity prevalence is rising, the association between ICD-coded obesity, healthcare resource utilization, and inpatient outcomes in middle-income countries remains poorly quantified. This study examined inpatient diagnostic patterns, resource utilization, and in-hospital mortality among hospitalized pediatric patients with ICD-coded obesity in Thailand’s Universal Coverage scheme during a 9-year period. Methods: We analyzed nationwide inpatient administrative data from January 2015 to December 2023 for children aged 1 month to <18 years. ICD-coded obesity was defined using ICD-10-TM codes recorded as either a principal diagnosis or a comorbidity. Outcomes included length of stay, hospital costs, and in-hospital mortality. Univariable and multivariable regression models were used to estimate associations between ICD-coded obesity and inpatient outcomes, with adjustment for age, sex, region, hospital level, admission year, and disease categories. Results: Among 14,483,566 hospitalized children, 42,168 had ICD-coded obesity. Notably, 95.7% of children with ICD-coded obesity were recorded as a comorbidity rather than the primary reason for admission. Children with ICD-coded obesity as a comorbidity had 156.8% higher median hospital costs. Across all major categories of common acute diseases (respiratory, intestinal, digestive), children with ICD-coded obesity had significantly higher median costs and longer length of stay compared to children without ICD-coded obesity. In regression analyses, ICD-coded obesity remained associated with longer length of stay (adjusted ratio, 1.21; 95% CI, 1.16–1.26; p < 0.001) and higher hospitalization cost (adjusted cost ratio, 1.42; 95% CI, 1.32–1.53; p < 0.001). The association with in-hospital mortality was observed in the unadjusted model but was attenuated after adjustment and was not statistically significant (adjusted odds ratio, 1.14; 95% CI, 0.89–1.45; p = 0.303). Conclusions: In Thailand’s national universal coverage scheme, ICD-coded obesity was associated with greater inpatient resource utilization, especially longer length of stay and higher hospitalization costs. These findings support the need for weight-aware inpatient management and adjusted funding models for hospitals treating this higher-resource-utilization subgroup. Full article

Inflammatory bowel disease (IBD) represents a growing global health threat that markedly increases colorectal cancer risk, yet conventional immunosuppressive agents achieve mucosal healing in only a limited subset of patients. M2-polarized macrophages have been recognized as crucial regulators of mucosal repair through their ability to maintain intestinal microenvironment homeostasis. Here, we investigated the potential effects and mechanisms of macrophage-derived exosomes (Exos) on epithelial barrier function in a murine model of IBD. Murine colitis was induced by intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS), followed by treatment with Exos isolated from IL-33-treated macrophages (IL-33-Exos) or untreated macrophages (PBS-Exos). Our findings showed that IL-33-Exos markedly ameliorated inflammatory intestinal mucosal injury and improved intestinal barrier dysfunction. Concurrently, IL-33-Exos mitigated intestinal epithelial cell damage, thereby preserving intestinal mucosal integrity. Mechanistic studies revealed that the beneficial effects of IL-33-Exos were implicated in upregulation of Wnt/β-catenin signaling in intestinal epithelial cells. Translationally, these findings suggest that IL-33-Exos may promote epithelial repair in experimental colitis, offering a novel therapeutic avenue for clinical management of inflammatory bowel disease. Full article

Necrotising enterocolitis (NEC) remains an important disease for neonatologists, with diagnostic and management challenges and impacts on mortality and neurodisability. NEC can present in a non-specific way, and differentiating from late-onset sepsis (LOS), focal perforation (FIP) and feed intolerance can be difficult. Biomarkers have been extensively explored as a way to help more definitively identify NEC or rule it out. Many biomarkers that have been studied are blood biomarkers, and several other extensive reviews of biomarkers in NEC exist. In this narrative review, we focus on non-invasive samples, namely stool, urine and saliva, and on tests that are already available as point-of-care tests (POCTs) or are likely to be available as POCTs soon given current technologies. Faecal calprotectin and urinary intestinal fatty acid-binding protein (IFABP) have the most data to currently support their use in larger multi-centre studies and appear most likely to achieve translation into clinical practice. Saliva appears the most under-researched potential source of a non-invasive POCT for a biomarker for NEC. For faecal calprotectin and urinary IFABP, data that are most lacking relate to specificity, particularly the performance of these tests to differentiate NEC from FIP or LOS (occurring in the absence of NEC). We suggest a study design to facilitate moving towards the clinical use of non-invasive biomarkers in NEC. Full article

Alcohol-related liver disease (ALD) poses a significant global health burden, driven by complex mechanisms including oxidative stress, inflammation, and gut–liver axis disruption. While the individual roles of gut microbiota dysbiosis and ageing in ALD pathogenesis are increasingly recognized, their synergistic interaction remains poorly understood. This review synthesizes current evidence to argue that there is an interaction between ageing and the gut microbiota that collectively amplifies progression of ALD. Specifically, ageing promotes gut dysbiosis through immunosenescence (e.g., reduced IgA diversification and antimicrobial peptide decline), intestinal barrier failure, and altered microbial metabolite profiles (e.g., decreased short-chain fatty acids and dysregulated bile acid metabolism). Conversely, dysbiosis-derived metabolites and endotoxins modulate ageing-related signaling pathways, including SIRT1, FOXO, and Nrf2, thereby accelerating hepatic cellular senescence, inflammation, and fibrogenesis. Furthermore, we also discussed the typical microbial changes in ALD. These include an increase in the Proteobacteria, a decrease in the Bacteroidetes, as well as imbalances in fungi and viruses. In ageing, similar but distinct shifts occur, such as reduced microbial diversity, decreased short-chain fatty acid producers, and increased intestinal permeability. Therapeutic strategies targeting the gut microbiota (probiotics, fecal microbiota transplantation) or ageing-related pathways (SIRT1 activators) hold promise. Future research priorities include validating ageing-associated microbial signatures as predictors of ALD progression and testing microbiota-targeted interventions in aged preclinical models. Collectively, this review identifies the microbiota–ageing axis as a tractable therapeutic target for ALD and provides a framework for future mechanistic and translational studies. Full article

The gut microbiome of rainbow trout (Oncorhynchus mykiss) and Atlantic salmon (Salmo salar) is increasingly recognized as a functional interface linking dietary inputs, epithelial barrier integrity, mucosal immunity, environmental stress, disease susceptibility, and antimicrobial-resistance risk in intensive aquaculture. Based on available salmonid studies and relevant evidence from broader fish and aquaculture systems, this review synthesizes current knowledge on salmonid gut microbial composition, nutritional modulation, microbiome–mucosal immune interactions, aquaculture stressors, antibiotic exposure, antibiotic resistance genes (ARGs), mobile genetic elements (MGEs), metagenomics, multi-omics, and emerging microbiome-informed decision-support tools. Current evidence does not support a universally stable single-core microbiota in these species. Instead, community structure is shaped by developmental stage, freshwater–seawater transition, intestinal segment, digesta versus mucosa sampling, diet, temperature, stress, health status, and methodological workflow. Feed substitution and functional additives can remodel the gut microbiota, but these shifts should be interpreted alongside histology, barrier function, metabolic profiles, immune indicators, and disease-resistance phenotypes. Antibiotic exposure may reduce acute bacterial disease pressure while disturbing community structure and potentially enriching ARGs or ARG–MGE associations. Risk assessment should therefore move beyond ARG abundance toward host–ARG–MGE linkage using shotgun metagenomics, metagenome-assembled genomes, long-read sequencing, Hi-C, and externally validated multi-omics models. Machine learning and artificial intelligence approaches may support feature screening, risk stratification, and decision support, but their application in salmonid gut-health management remains at an early stage and requires external validation across sites, production stages, diets, and seasons. Full article

Bacillus subtilis has been widely investigated as a probiotic feed additive for weanling piglets due to its potential to improve growth performance, gut health, and disease resilience during the post-weaning period. This systematic review evaluated the effects of Bacillus subtilis supplementation in pigs following PRISMA guidelines and the PICOS framework. A total of 619 records published between 2000 and 2025 were identified through PubMed, Scopus, and AGRICOLA databases, of which 29 studies met the inclusion criteria for qualitative synthesis. Overall, Bacillus subtilis supplementation frequently improved average daily gain, body weight, feed efficiency, and reduced diarrhea incidence, particularly under enteric challenge conditions. Many studies also reported beneficial effects on intestinal morphology, immune regulation, intestinal barrier-related gene expression, nutrient digestibility, and modulation of gut microbiota toward bacterial communities associated with intestinal health. However, responses varied depending on Bacillus subtilis strain, dosage, diet composition, and experimental design. In contrast, effects on biochemical and oxidative stress indicators were less consistent across studies. Collectively, the findings support the potential role of Bacillus subtilis as a functional probiotic in swine nutrition while highlighting the need for standardized long-term studies to better define optimal strains, supplementation strategies, and mechanisms of action. Full article

Background/Objectives: Ferroptosis, an iron-dependent cell death driven by lipid peroxidation, is implicated in the pathogenesis of ulcerative colitis (UC). Tryptophan metabolism and its interaction with the aryl hydrocarbon receptor (AhR) and nuclear factor erythroid 2–related factor 2 (Nrf2) axis represent a crucial regulatory network in intestinal homeostasis. This study aimed to investigate whether the probiotic fermentation product postbiotic Nagqu4580 alleviates UC by modulating this network to inhibit intestinal epithelial ferroptosis. Methods: An acute UC model was induced in mice using 4% dextran sodium sulfate (DSS). The therapeutic effects of postbiotic Nagqu4580 were evaluated through disease activity index (DAI), colon length, histopathology, inflammatory cytokines, and intestinal barrier function. Ferroptosis was assessed by measuring lipid peroxidation (MDA, 4-HNE), antioxidant capacity (GSH/GSSG), and expression levels of GPX4 and ACSL4. Serum tryptophan metabolites were profiled using targeted metabolomics, the activation of the AhR/Nrf2 pathway was examined by Western blot, immunofluorescence, and qPCR, and gut microbiota composition was analyzed by 16S rRNA sequencing. Results: Postbiotic Nagqu4580 dose-dependently ameliorated DSS-induced UC in mice, as evidenced by reduced DAI scores, mitigated colon shortening and histological damage, decreased inflammatory cytokines (TNF-α, IL-1β, IL-6), and restored intestinal barrier function by upregulating tight junction proteins (Claudin-1, ZO-1, Occludin). Mechanistically, postbiotic Nagqu4580 inhibited intestinal epithelial ferroptosis by reducing MDA and 4-HNE levels, restoring the GSH/GSSG balance, downregulating ACSL4, and upregulating GPX4. Serum metabolomics revealed that postbiotic Nagqu4580 reshaped tryptophan metabolism, increasing beneficial metabolites such as 5-hydroxyindoleacetic acid (5-HIAA) and decreasing potentially harmful metabolites such as 3-indoxyl sulfate (3-IS). 16S rRNA sequencing further revealed that the postbiotic Nagqu4580 partially reversed DSS-induced gut microbiota dysbiosis, with a slight increase in the abundance of beneficial genera and a significant reduction in the abundance of pro-inflammatory genera. Furthermore, postbiotic Nagqu4580 significantly activated the AhR/Nrf2 signaling pathway, enhancing the expression of AhR, Nrf2, and their downstream antioxidant genes HO-1 and GPX4. Conclusions: Postbiotic Nagqu4580 alleviates UC by inhibiting intestinal epithelial ferroptosis. Our data suggest that this protective effect is associated with the remodeling of gut microbiota-related tryptophan metabolism and subsequent activation of the AhR/Nrf2 antioxidant axis. Our findings highlight the therapeutic potential of postbiotic Nagqu4580 as a postbiotic agent for UC. Full article

Background/Objectives: Insulin resistance is increasingly recognized as a cause of colorectal neoplasms, but its measurement requires fasting insulin, which is not routinely available in clinical settings. The triglyceride–glucose (TyG) index, derived from fasting triglyceride and glucose, has emerged as a simple surrogate of insulin resistance. We aimed to evaluate the association of the TyG index with colorectal adenoma, identify a clinically usable cut-off, and examine whether the association is preserved across major subgroups. Methods: We conducted a cross-sectional analysis of 7251 asymptomatic adults who underwent screening colonoscopy and same-day biochemistry at university hospital health care centers in Daejeon and Chungcheong province of South Korea between November 2019 and June 2022. The TyG index was calculated as ln[fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2]. Multivariable logistic regression was used to estimate odds ratios (ORs) for adenoma; discrimination was evaluated by area under the receiver-operating-characteristic curve (AUC), and the optimal cut-off was identified by Youden’s J. Large adenoma (≥10 mm) was analyzed as a secondary outcome. Results: Among 7251 participants (mean age 54.1 ± 11.2 years; 59.7% male; mean BMI 24.7 ± 3.4 kg/m²), 2402 (33.1%) had at least one colorectal adenoma. Adenoma prevalence rose monotonically across TyG quartiles (Q) (Q1, 26.3%; Q2, 32.0%; Q3, 35.5%; Q4, 38.7%; p for trend <0.001). A 1-standard deviation (SD) increase in TyG index was associated with adenoma prevalence in the fully adjusted model (OR 1.13, 95% confidence interval (CI) 1.06–1.20), and the Q4-versus-Q1 OR was 1.29 (1.09–1.53). The optimal cut-off for adenoma was TyG index = 8.55 (AUC 0.564, sensitivity 59.1%, specificity 50.8%); the association was modestly stronger for large adenoma (AUC 0.585; adjusted OR per 1-SD 1.25, 1.09–1.43). Subgroup analyses showed consistent effects across sex, age, body mass index, hypertension, diabetes, and metabolic-syndrome strata (all p for interaction >0.17). Conclusions: In a large screening cohort, an elevated TyG index was associated with the presence of colorectal adenoma, with a graded dose–response relationship and a modestly more pronounced association for large adenoma. Although discrimination by TyG index alone is too modest to support its use as a stand-alone screening tool, the index may serve as a low-cost adjunct within a multifactorial risk-stratification framework. Full article

Acute diarrheal disease (ADD) caused by parasites and Tuberculosis (TB) remain major public health concerns in vulnerable indigenous communities with limited access to sanitation, safe water, and healthcare, and where humans, animals and the environment interact closely. Using a One Health framework, this study investigated TB and Intestinal parasites in human, animal and environmental samples from 15 Wayuu indigenous communities in Manaure, La Guajira. A total of 190 samples, including human sputum and feces, animal milk and feces, soil and drinking water, were analyzed according to sample type, preservation suitability, and availability using parasitological concentration techniques, qPCR for helminth detection, metatranscriptomic sequencing, Xpert ^® MTB/RIF assay, and mycobacterial culture. Mycobacterium tuberculosis was detected in 8.3% of human sputum samples, with no evidence of rifampicin resistance, whereas Mycobacterium bovis was not detected in animal milk. Human fecal samples analyzed by microscopy showed Blastocystis sp. and the Entamoeba histolytica/Entamoeba dispar complex (38.8% each), followed by Giardia (19.4%), Hymenolepis nana and Trichuris trichiura (5.1% each) and Hymenolepis diminuta (1%). Commensal parasites were also identified, with Entamoeba coli (46.9%) being the most frequent species, indicating inadequate sanitary conditions and poor hygiene practices. Co-infections were common in humans (60.2%). In animal fecal samples, strongylids (66.7%), amoebas (16.7%) and Giardia (8.3%) were observed. Giardia sp. was detected in 2.38% of soil samples by microscopy, supporting environmental circulation, whereas no parasites were detected in water sediments. Multiplex qPCR detected Trichuris trichiura DNA in human feces and Trichuris spp. DNA in soil and sheep fecal samples. Metatranscriptomic analysis of 22 human fecal samples revealed a high diversity and frequency of parasitic protozoa (90.9%), with Blastocystis spp. being the most frequent (81.8%). Additionally, reads of free-living amoebae, including Acanthamoeba spp. (10%) and Naegleria spp. (5%) were detected in community drinking water sources. These findings suggest active transmission of TB and parasitic-associated ADD in Wayuu communities and highlight the need for integrated surveillance and culturally appropriate interventions focused on sanitation, hygiene, veterinary services and community health education to improve the living and health conditions of these vulnerable populations. Full article

Background/Objectives: Urinary tract infections (UTIs) represent the most common infectious complication following kidney transplantation. An increasing number of UTIs are caused by multidrug-resistant organisms (MDROs). The role of intestinal MDRO colonisation in complicated urinary tract infections (cUTIs) among kidney transplant recipients is not fully understood. Methods: We conducted a retrospective, single-centre study of kidney or kidney–pancreas transplant recipients hospitalised for infectious diseases. Each hospitalisation was analysed as a separate event. Routine rectal screening targeted carbapenem-resistant Enterobacterales and vancomycin-resistant/vancomycin-variable enterococci. Results: The study included 65 hospitalisations from 52 kidney transplant recipients, with some patients contributing multiple admissions. cUTIs accounted for 63.1% of admissions, and 22.0% of cUTIs were associated with concomitant bloodstream infection (BSI). The most frequently isolated pathogens were Klebsiella pneumoniae (58.8%) and Escherichia coli (41.2%). Extended-spectrum β-lactamase (ESBL) production was detected in 50% of E. coli isolates, while carbapenemase production was identified in 60% of K. pneumoniae isolates. MDRO rectal carriage was detected in 43.1% of cases and was more frequent in cUTI than in other infections (53.7% vs. 25.0%, p = 0.024). Carbapenemase-producing K. pneumoniae (CP-KP) rectal carriage was also more frequent in cUTI (31.7% vs. 4.2%, p = 0.011), but did not remain statistically significant after adjustment for urinary stent presence (odds ratio 7.1, 95% CI 0.7–66.2; p = 0.087). Nevertheless, CP-KP rectal carriage was associated with CP-KP cUTI aetiology (PPV 75.0%; NPV 86.4%). The median length of hospital stay (LoS) was 15 days. In multivariable analysis, a longer median LoS was associated with BSI (12.2 days; 95% CI: 0.8–23.6; p = 0.037), urinary stent presence (6.8 days; 95% CI: 1.5–12.2; p = 0.014), and older age (2.3 days; 95% CI: 0.7–4.0; p = 0.007). Conclusions: Rectal CP-KP colonisation may represent a potential marker of cUTI risk, although its independent association was not confirmed after adjustment. These findings should be interpreted with caution, given the study design and sample size and require confirmation in larger prospective studies. Rectal screening may contribute to early risk stratification, whereas its role in guiding empirical therapy remains to be prospectively evaluated. Full article

Inflammatory bowel disease is an inflammatory disorder associated with systemic immune activation, contributing to neuroinflammation, behavioral impairments and disruption of the gut–brain axis. The present study investigated the effects of p-Coumaric acid derivatives: Artepillin C (ART-C), Baccharin (BAC), and Drupanin (DRU) on colonic damage, behavioral alterations, and oxidative stress in a dextran sulfate sodium (DSS)-induced colitis by administration of 3% DSS. Mice were treated with p-Coumaric acid derivatives (0.3, 1, or 3 mg/kg, p.o.), and disease activity index and colon length were evaluated as clinical parameters. Behavioral assessments included the open field test, novel object recognition test, elevated plus maze, and tail suspension test. Oxidative stress and inflammatory markers were quantified in colon, serum, cortex, and hippocampus, alongside histological analysis of colonic tissue. DSS administration induced clinical and histopathological alterations, increased oxidative stress, and impaired recognition memory, as well as anxiety- and depressive-like behaviors. p-Coumaric acid derivatives attenuated colonic damage, preserved tissue architecture, improved recognition memory, and reduced anxiety- and depressive-like behaviors, particularly at higher doses. These effects were associated with modulation of antioxidant defenses and reduction of lipid peroxidation and inflammatory markers. p-Coumaric acid derivatives exert protective effects in DSS-induced colitis, highlighting their potential as therapeutic agents for intestinal and neurobehavioral alterations associated with IBD. Full article

Background/Objectives: Chronic intestinal failure (IF) necessitating home parenteral support (HPS) represents an end-stage condition for many gastrointestinal diseases. While long-term outcomes have been reported in HPS-dependent patients, there are limited generalisable data on survival and nutritional autonomy rates in large contemporary cohorts. The primary objective of this study was to examine the evidence on mortality and nutritional autonomy rates for HPS published to 2025. Methods: This is a systematic review and meta-analysis (PROSPERO Registration number: CRD42025645325). A database search was conducted up to 3 February 2025. Studies assessing survival and nutritional autonomy in adults with benign chronic IF receiving HPS were included. For clinical outcomes, crude proportions were calculated and a meta-analysis was performed to calculate the proportion affected per year of follow-up, with survival probabilities additionally presented on Kaplan–Meier curves. Results: Overall, 3411 records were screened and 57 studies were included. The overall mortality was 8.0% per year of follow-up (95% CI 6.0 to 10.0%), or 33.5% over a mean of 49.02 months. The summary of survival curves estimated the pooled five- and ten-year survival rates from HPS initiation as 68.71% and 52.46%, respectively. Nutritional autonomy was achieved in 35.3% of patients, at a rate of 10.0% per year of follow-up (95% CI 7.0% to 14.0%). Age, gastrointestinal anatomy, and underlying disease leading to IF were identified as potential factors associated with mortality and nutritional autonomy. Conclusions: This is the first systematic review and meta-analysis summarising the current literature on survival and nutritional autonomy in adults with chronic IF. These findings increase our understanding of this complex condition, providing baseline data to support clinical decision-making and patient counselling. Full article

Background/Objectives: Non-motor symptoms (NMS) are highly prevalent in advanced Parkinson’s disease (PD) and substantially affect quality of life. Continuous infusion therapies are established treatment options for motor fluctuations not controlled by oral medication, but their effects on NMS remain incompletely characterized. We aimed to evaluate the effects of continuous infusion therapies on NMS in advanced PD. Methods: A systematic review was conducted according to PRISMA guidelines. PubMed, Embase, and Cochrane were searched for English-language original studies published between January 2005 and 1 March 2026. Eligible studies included patients with PD treated with levodopa–carbidopa intestinal gel (LCIG), continuous subcutaneous apomorphine infusion (CSAI), subcutaneous levodopa formulations, or levodopa–entacapone–carbidopa intestinal gel (LECIG) and reported quantitative NMS outcomes. Due to methodological heterogeneity, results were synthesized qualitatively. Results: Fifty-four studies were included. Most evaluated LCIG (n = 38), followed by CSAI (n = 14), subcutaneous levodopa formulations (n = 6), and LECIG (n = 2). Overall, 4157 patients were assessed at baseline and 2919 at follow-up. Global non-motor burden improved in 33/45 (73.3%) baseline-to-follow-up comparisons. NMSS total score decreased from 84.4 ± 35.2 to 54.9 ± 17.6. The most consistent benefits were observed for sleep/fatigue and gastrointestinal symptoms. Sleep/fatigue outcomes improved in 26/31 (83.9%) baseline-to-follow-up comparisons. Cognitive outcomes were mostly stable, while cardiovascular, urinary, sexual, and mood-specific outcomes showed less consistent benefit. Conclusions: Continuous infusion therapies may be associated with reduced global non-motor burden in advanced PD, particularly sleep/fatigue and gastrointestinal symptoms. Evidence is strongest for LCIG, while data for CSAI, LECIG, and subcutaneous levodopa formulations remain limited. Full article

The etiology of inflammatory bowel disease (IBD) is not precisely defined. However, it involves environmental factors, genetic predisposition, the involvement of gut microbiota, and abnormal immune response. Angiogenesis seems to be an integral part of IBD. Impairment of the intestinal barrier may represent an initiating or early feature of the disease. Disruption of the epithelial barrier leads to the translocation of microbiota and other antigens into the mucosa, resulting in an enhanced immune response, whereas damage to the vascular barrier is related to endothelial activation and pathologic angiogenesis, both of which promote inflammation. Angiogenesis during IBD is a very complex phenomenon that includes endothelial and immune cells, growth factors, cytokines, adhesion molecules, intestinal microbiota, and signal transduction. It seems that intestinal microvascular hemostasis shifts toward a prothrombotic state, and microthrombi formation exacerbates ischemia. The angiogenic process in IBD is regulated, at least in part, by the intestinal microbiota. Antiangiogenic therapy represents a novel and significant approach to the treatment of IBD. Biologic anti-inflammatory therapy for IBD simultaneously attenuates angiogenesis to a similar degree. However, the expression of VEGF and other growth factors may have dual and opposing effects, probably depending on the stage of the disease. Thus, anti-angiogenic treatment in patients with IBD remains controversial, and clinical trials of anti-angiogenic agents are warranted. Full article

Background: Phosphatidylcholine (PC) is a major phospholipid that contributes to intestinal barrier protection and is essential for hepatic secretion of lipids and bile acids. Because inflammatory bowel disease (IBD) and primary sclerosing cholangitis (PSC) are closely linked, we hypothesized that individual serum PC species would reflect disease activity. We therefore investigated whether serum PC profiling could identify clinically useful biomarkers across the gut–liver axis. Methods: Serum concentrations of 21 PC species were quantified by direct flow injection high-resolution mass spectrometry in 16 healthy controls, 57 patients with IBD, and 20 patients with PSC. Results: In IBD, multiple serum PC species were inversely associated with inflammatory activity, showing negative correlations with serum C-reactive protein and fecal calprotectin. Patients with fecal calprotectin concentrations above the diagnostic cut-off of 120 µg/g had lower levels of PC 34:3, 36:1, 36:2, 36:3, 36:4, 36:5, 38:3, 38:4, 38:5, 38:7, 40:5, and 40:6, as well as lower total PC. In contrast, in PSC, PC 30:0, 32:0, 32:1, and 34:1 were increased compared with IBD and correlated positively with gamma-glutamyltransferase and alkaline phosphatase. Furthermore, these shorter-chain PC species as well as PC 36:1 were markedly elevated in PSC with advanced liver fibrosis compared with PSC without fibrosis. Conclusions: Serum PC species show a reciprocal disease-associated pattern in IBD and PSC. In IBD, lower concentrations of predominantly unsaturated PC species are associated with active intestinal inflammation, whereas in PSC, higher concentrations of shorter-chain PC species are associated with cholestatic injury and advanced liver fibrosis. IBD and PSC exhibit opposing serum PC signatures, suggesting that dysregulated PC metabolism is a pathophysiological feature of intestinal inflammation and PSC-associated liver fibrosis. Full article