Carbohydrate antigen 72-4 (CA72-4) is a serum tumor marker linked to tumor-associated glycoprotein 72 (TAG-72), a high-molecular-weight mucin-like antigen identified during the monoclonal-antibody era. Although developed later than CA19-9 and most closely associated with gastric cancer, CA72-4 has since attracted broader interest across gastrointestinal oncology, peritoneal disease, malignant effusions, cytology, benign false-positive states and TAG-72-directed translational research. This review examines the history, biology, clinical utility, diagnostic limitations and future applications of CA72-4 and TAG-72, using gastric cancer as the principal clinical anchor while considering wider esophagogastric, colorectal, appendiceal, pancreaticobiliary, peritoneal and fluid-based applications. Current evidence supports CA72-4 as an adjunctive biomarker rather than a population screening test or stand-alone diagnostic tool. Its most defensible clinical roles are in gastric cancer risk stratification, peritoneal disease assessment, selected multimarker panels and malignant effusion work-up. Looking ahead, TAG-72 may ultimately prove more clinically consequential than serum CA72-4 itself if imaging, cytology-based diagnostics and targeted therapeutic platforms continue to mature.
Geriatric syndromes such as frailty and sarcopenia are multidomain indicators of functional status in relation to the chronic disease burden of an aging adult. The human microbiota has gained increasing spotlight in regulating key aspects inherent of aging. In this review, we survey the current literature exploring the pathophysiological intersections of the gut microbiome and the aging process and associated geriatric syndromes that ultimately influence health span and lifespan. We discuss how intrinsic and extrinsic factors can influence age-related gut dysbiosis and propose areas of future directions for further research for identifying therapeutic targets to promote healthy aging.
The transcriptomic changes in the jejunum involved in Linghu’s obesity-diarrhea syndrome (ODS) are revealed in the previous study. In the present study, we performed a reanalysis of differentially expressed genes related to nutrient absorption from this dataset and found that gene sets involved in the digestion and absorption of three major nutrients - fats, carbohydrates, and proteins - were predominantly upregulated in the jejunal epithelium of patients with ODS. These changes specifically pertain to fat digestion and absorption, carbohydrate uptake and transport, and protein catabolism. These findings suggest that the jejunum of patients with ODS may exhibit a unique state of “diarrhea-hyperabsorption”. In this article, we provide an in-depth discussion of this phenomenon and propose hypotheses, aiming to offer insights for the study of the pathological mechanisms underlying ODS and its clinical management.
Microplastics and nanoplastics (MNPs) are increasingly recognized as ubiquitous environmental contaminants with unavoidable human exposure through ingestion and inhalation. The gastrointestinal tract is an important interface between MNPs and the intestinal microbiota, epithelium and immune system. Interest in the effects of MNPs on human health has been increasing particularly in inflammatory bowel disease (IBD), a chronic immune-mediated disease in which environmental factors are thought to contribute to disease pathogenesis. Experimental studies have suggested that intestinal MNP exposure may promote several pathways relevant in IBD including dysbiosis, mucus disruption, impaired epithelial integrity, intestinal permeability and activation of immune pathways. Current evidence is largely translational and is dominated by experimental models that do not reflect real world human exposures. Human studies in IBD are currently limited to a small number of observational studies with data vulnerable to confounding and reverse causation. Despite increasing mechanistic plausibility, there is still no direct evidence that MNPs cause IBD or alter the disease course. In this narrative review we summaries the current knowledge on human MNPs exposures, we examine experimental evidence for biologically plausible pathways through which MNPs may influence intestinal inflammation and the emerging human evidence in IBD. We also explore the major analytical and methodological limitations in the field.
Gastric varices (GV) are a distinct and clinically challenging manifestation of portal hypertension characterized by complex vascular anatomy and unique hemodynamic behavior. Unlike esophageal varices (EV), GVs arise from interactions between afferent portal inflow, large variceal reservoirs, and spontaneous portosystemic shunts, resulting in a low-pressure, high-flow system that often responds poorly to conventional pressure-reducing therapies. Consequently, management strategies extrapolated from EV are frequently inadequate. Advances in endoscopic ultrasound (EUS), cross-sectional imaging, and interventional radiology have facilitated a paradigm shift toward a pathophysiology-driven approach. Contemporary evaluation integrates endoscopic classification based on anatomical location (Sarin), EUS for assessment of feeding vessels and flow dynamics, and computed tomography/magnetic resonance imaging for mapping afferent and efferent pathways using Kiyosue and Saad-Caldwell classifications. These frameworks enable hemodynamic triage into shunt-dominant, pressure-dominant, and complex patterns, which directly inform therapeutic selection. Endoscopic therapies, including cyanoacrylate injection and EUS-guided coil ± glue embolization, target the variceal reservoir and inflow, providing effective local control. Radiologic interventions address systemic hemodynamics, with retrograde transvenous obliteration (Balloon-occluded retrograde transvenous obliteration/plug-assisted retrograde transvenous obliteration/coil-assisted retrograde transvenous obliteration) preferred for shunt-dominant varices and transjugular intrahepatic portosystemic shunt for pressure-driven disease. Surgical options remain relevant in selected conditions such as left-sided portal hypertension. Clinical modifiers, including hepatic reserve, encephalopathy, ascites, and portal vein patency, further refine treatment decisions. A multidisciplinary, mechanism-based strategy is essential to optimize outcomes. Future research should focus on integrated classification systems and prospective comparative studies to establish standardized, individualized management algorithms.
BACKGROUND Liver fibrosis is a key determinant of prognosis and management in chronic liver diseases. Although liver biopsy is considered the gold standard for fibrosis assessment, its invasiveness, sampling variability, and associated risks have prompted increasing reliance on non-invasive tests. This systematic review evaluates the diagnostic accuracy and clinical applicability of non-invasive modalities for diagnosing liver fibrosis in adult patients with chronic liver diseases. AIM To systematically evaluate the diagnostic accuracy, clinical utility, and applicability of non-invasive tests for detecting and staging liver fibrosis in adult patients with chronic liver diseases, using liver biopsy as the reference standard. METHODS A systematic literature search was conducted using predefined search terms combining liver fibrosis, chronic liver disease, non-invasive diagnostic tests, and diagnostic accuracy measures, with liver biopsy as the reference standard. Studies were selected based on a PICO (Population, Intervention, Comparison, Outcome) framework including adults (≥ 18 years) with chronic liver diseases such as hepatitis B, hepatitis C, non-alcoholic fatty liver disease, and alcohol-related liver disease. Eligible interventions included serum biomarkers (e.g. , aspartate aminotransferase-to-platelet ratio index, fibrosis-4 index, enhanced liver fibrosis), imaging-based techniques (e.g. , transient elastography, acoustic radiation force impulse, magnetic resonance imaging elastography), and combined diagnostic algorithms. Diagnostic accuracy outcomes including sensitivity, specificity, positive predictive value, and negative predictive value were extracted. Two independent reviewers performed abstract and full-text screening according to predefined inclusion and exclusion criteria, with disagreements resolved by consensus or a third reviewer. RESULTS The included studies comprised prospective and retrospective cohort studies, randomized controlled trials, and cross-sectional studies. Elastography-based techniques consistently demonstrated high diagnostic accuracy for detecting significant and advanced fibrosis across multiple chronic liver disease etiologies. Serum biomarker panels showed variable performance but were effective as first-line screening tools due to their accessibility and cost-effectiveness. Heterogeneity was observed in study design, fibrosis staging systems, and cut-off values. CONCLUSION Non-invasive tests represent reliable and clinically applicable alternatives to liver biopsy for fibrosis assessment in chronic liver diseases. Elastography-based modalities, particularly transient elastography and two-dimensional shear wave elastography, demonstrated consistently high diagnostic accuracy for advanced fibrosis across included studies. Serum biomarker panels such as fibrosis-4 index and enhanced liver fibrosis showed variable performance but are effective as first-line screening tools due to their accessibility and cost-effectiveness. A sequential diagnostic approach integrating serum biomarkers followed by imaging modalities improves overall diagnostic accuracy and reduces the need for invasive procedures. However, significant heterogeneity in study design, patient populations, and cut-off values limits standardization and highlights the need for larger multicentric validation studies.
Eosinophilic esophagitis (EoE) is a chronic immune-mediated disease characterized by inflammation in the esophagus, occurring in genetically predisposed individuals as a consequence of food antigen sensitization. EoE prevalence has increased exponentially in the last three decades to 40 per 100000 people worldwide, making it a common cause of dysphagia and food impaction in both children and adults. Diagnosis is made by esophageal biopsy showing eosinophilia (≥ 15 eosinophils per high-power field on biopsy). In children the presentation may be feeding intolerance, in adults a form of chronic solid food dysphagia. In EoE, in the absence of treatment, active inflammation inevitably progresses to fibrostenotic remodeling, highlighting the importance of early recognition and therapy. This review outlines the clinical criteria and pathophysiological mechanisms of EoE, biomarkers for the diagnosis of EoE, and the therapeutic strategies for EoE. EoE is characterized by epithelial barrier dysfunction, Th2 inflammation and eosinophil recruitment, with microbiome influences. Diagnosis is made by standard endoscopic biopsy, or by non-intrusive esophageal string test, Cytosponge, or by impedance planimetry. Treatment includes proton pump inhibitors, topical corticosteroids, dietary elimination therapy, endoscopic dilation, and the Food and Drug Administration approved biologic dupilumab. Emerging therapies such as precision medicine and artificial intelligence are also identified as areas for attention.
Overweight is recognized as a worldwide healthcare problem. Obesity has increased in recent decades and has been considered a risk factor for many gastrointestinal (GI) disorders. Recent scientific evidence has documented the association between being overweight and GI manifestations. Body mass index (BMI) is a simple, globally used anthropometric measure, but its role in GI inflammation remains incompletely elucidated and can be challenging to study. Current knowledge suggests that higher BMI is linked to a chronic low-grade pro-inflammatory state (“metainflammation”) and several GI-relevant processes. Obesity-related dietary patterns and “fat quality” can alter mucosal immune triggering and local inflammatory cell profiles. Increased BMI is often associated with functional GI symptoms, especially gastroesophageal reflux, likely supported by delayed oesophageal clearance, altered motility, and increased intragastric pressure. Furthermore, intestinal barrier dysfunction with dysbiosis can increase permeability and facilitate the translocation of microbial products. Metabolic endotoxemia and inflammatory pathways are triggered, including TLR4/NF-κB and the NLRP3 inflammasome. Accordingly, systemic and intestinal inflammation are developed and maintained. These mechanisms also interact with adipose tissue immune-endocrine dysregulation (increased tumor necrosis factor alpha, interleukin-6, leptin, and reduced adiponectin) and macrophage cytokine amplification, potentially affecting multiple digestive organs. Although BMI does not record fat distribution or cardiometabolic status, it can still provide clinically useful risk stratification data when interpreted alongside metabolic and functional markers. This mini-review summarizes evidence on BMI and GI inflammatory vulnerability, focusing on biomolecular pathophysiology and the main mechanisms that could explain this association.
BACKGROUND The gastrointestinal tract plays an important role in host defence during critical illness. Disruption of epithelial integrity, microbiome imbalance, and immune dysregulation have all been linked to the translocation of multidrug-resistant (MDR) organisms from intestinal colonization to invasive infection. However, whether these associations reflect true causal mechanisms remains uncertain, and available human evidence has not been comprehensively synthesized using current methodological standards. AIM To systematically evaluate human evidence examining the relationship between intestinal barrier dysfunction, microbial colonization, and subsequent MDR infection in adult critical illness, with particular attention to study quality, heterogeneity, and potential confounding factors. METHODS This systematic review was conducted in accordance with PRISMA guidelines. A structured literature search was performed in PubMed, EMBASE, and the Cochrane Library (2000-2025) using predefined Boolean combinations and Medical Subject Headings. Prospective and retrospective cohort studies involving intensive care units (ICU) adults were included if they evaluated intestinal colonization, biomarkers of barrier dysfunction (citrulline and intestinal fatty acid-binding protein), microbiome alterations, or endotoxemia. Study selection and data extraction were undertaken independently by two reviewers, with disagreements resolved through discussion. Risk of bias was assessed using the Newcastle-Ottawa Scale and ROBINS-I tool. Owing to methodological and clinical heterogeneity, findings were synthesized using a structured narrative approach rather than meta-analysis. RESULTS Across the included studies, intestinal colonization with carbapenem-resistant Enterobacteriaceae , carbapenem-resistant Klebsiella pneumoniae , Acinetobacter baumannii , and vancomycin-resistant Enterococcus was consistently associated with an increased risk of subsequent bloodstream infection. However, progression rates varied considerably across cohorts, likely reflecting differences in patient characteristics, antimicrobial exposure, and ICU practices rather than a consistent effect size. Biomarker studies showed reduced citrulline levels and elevated intestinal fatty acid-binding protein concentrations in patients with gastrointestinal dysfunction; however, these markers indicate enterocyte injury rather than directly measuring intestinal permeability or bacterial translocation. Microbiome analyses demonstrated reduced diversity and impaired colonization resistance, although the extent and timing of these changes were not uniform across studies. Taken together, the evidence supports a biologically plausible link between epithelial injury, dysbiosis, and infection risk, but does not establish a direct causal relationship, largely due to the observational design of available studies and the influence of confounding factors such as illness severity, antimicrobial exposure, and ICU environment. CONCLUSION Gut barrier dysfunction appears to contribute to the pathogenesis of MDR infection in critically ill adults; however, current evidence supports association rather than causation. Early recognition of intestinal colonization and strategies aimed at preserving mucosal integrity may offer potential clinical benefit, although their effectiveness requires confirmation in well-designed prospective and interventional studies.
Ulcerative colitis (UC) is a chronic inflammatory disorder of the colon. Its pathogenesis has been linked to chronic intestinal inflammation stemming from genetic predisposition, immune dysregulation, changes in gut microbiome, and various environmental factors. There is emerging evidence for autophagy dysfunction in the UC setting, suggesting a compromise of the intestinal epithelial barrier and microbial clearance in patients, resulting in chronic activation of the immune system. There is growing evidence that the appendix functions as a critical priming site for UC. Dysregulation of various lymphocyte subsets, dysbiosis, propagation of inflammation into the colon, as well as autophagy dysfunction, have been listed as contributing to this early appendiceal priming phase. While initially thought of as a vestigial organ, current evidence points towards the appendix as an active immunological and microbial hub. Epidemiological data demonstrate an inverse association between early appendectomy and UC risk, suggesting its potential as a therapeutic strategy. According to recent ACCURE (2025) and COSTA (2026) clinical trials, improved remission outcomes were observed post-appendectomy in selected patients, particularly in patients unresponsive to biologic therapy. Together, the evidence positions appendectomy as a legitimate adjunctive treatment option for UC, warranting further mechanistic and clinical investigation. In this narrative review, current evidence on the pathogenesis and risk factors of UC are summarized, including the emerging role of the appendix and the therapeutic potential of appendectomy in UC.
BACKGROUND Early hepatocellular carcinoma (HCC) detection in cirrhosis remains suboptimal despite semi-annual ultrasound and alpha-fetoprotein surveillance. Advanced fibrosis is a central driver of hepatocarcinogenesis, and liver stiffness measurement (LSM) is a non-invasive measure of liver stiffness that may be associated with HCC risk. AIM To evaluate whether LSM by transient elastography (TE) is associated with the presence of HCC among patients with established cirrhosis. METHODS A retrospective, matched case-control study at a tertiary liver center including adults with cirrhosis and a valid TE (≥ 10 valid acquisitions, interquartile range < 30% , success rate > 60%) was conducted. Cirrhotic patients with diagnosed HCC per standard guidelines were frequency matched for age, sex, etiology, and Child-Pugh class with controls (cirrhotic patients without HCC). Multivariable logistic regression tested the association between LSM and HCC. Discrimination and cut-off points were assessed using receiver operating characteristic (ROC) analysis and Youden’s index. RESULTS A total of 262 patients (133 with HCC; 129 controls) were enrolled. Median LSM was higher in the HCC cohort than in controls (31.7 kPa vs 22.6 kPa; P < 0.001). Multivariate regression analysis revealed that only LSM was significantly associated with HCC (adjusted odds ratio 1.09; 95%CI: 1.05-1.13; P = 0.0001). A cut-off of ≥ 47 kPa had excellent discriminatory power (area under the ROC curve: 0.88; 95%CI: 0.84-0.93). CONCLUSION A liver stiffness threshold of approximately 47 kPa may serve as a marker associated with risk of HCC, justifying intensified screening in high-risk cirrhosis; prospective validation, integration with multivariable risk models, and cost-effectiveness analyses remain essential.
BACKGROUND Occult constipation (OC) is defined by the absence of classical symptoms of constipation on initial clinical history, despite objective evidence of fecal retention, such as the presence of hard stool on digital rectal examination or fecal impaction identified on plain abdominal radiography. It is frequently undiagnosed in children and presents with a diverse array of symptoms, such as abdominal pain and frequent defecation with mucoid feces. These symptoms are strikingly similar to irritable bowel syndrome (IBS) with diarrhea (IBS-D). AIM To verify the hypothesis that OC may present with the features of IBS-D. METHODS This is a prospective observational study that involves consecutive children who were referred to our center as primarily diagnosed with IBS-D (consistent with Rome IV criteria) by another physician and did not improve after at least three months of treatment. Patients presenting with red-flag symptoms suggestive of organic disease were excluded from the study. Patients who exhibited fecal impaction on a plain abdominal radiograph were diagnosed as OC and were administered magnesium hydroxide (milk of magnesia; 400 mg/5 mL) for a period of two months, with a progressive taper over the course of one month. Outcomes were assessed based on changes in pain intensity, frequency, and stool characteristics after the commencement of treatment. RESULTS This study included 54 patients who were diagnosed with IBS-D by other consultants and were unresponsive to treatment. Of these patients, 49 (91%) had OC mimicking IBS-D. After commencing treatment for OC, 46 (94%) of the 49 patients demonstrated a positive clinical response (44 good, 2 satisfactory). CONCLUSION Children presenting with IBS-D related symptoms who are unresponsive to standard therapy may benefit from evaluation for OC before considering escalation to more invasive investigations.
Cronkhite-Canada syndrome (CCS) is a rare, non-hereditary gastrointestinal (GI) disorder characterized by diffuse polyposis in the GI tract, ectodermal abnormalities, and nutritional deficiencies. It is a multisystem disorder with a multifactorial origin, particularly autoimmune, with only about 500 cases reported from around the world. This narrative review aims to consolidate current knowledge on CCS, focusing on its epidemiology, clinical features, pathogenesis, diagnostic techniques, and treatment strategies. Clinically, patients with CCS present with chronic diarrhea, abdominal pain, protein-losing enteropathy, alopecia, onychodystrophy, and hyperpigmentation. These symptoms often overlap with other prevalent GI conditions like ulcerative colitis, leading to misdiagnosis of CCS in earlier stages of the disease. Diagnosis of CCS requires a combination of laboratory analyses facilitated with endoscopic visualization of characteristic polyps, histopathological evaluation, and exclusion of other polyposis syndromes. Treatment remains non-standardized, with corticosteroids being the mainstay of management. Other therapeutic regimens include immunosuppressants, biologic agents, non-steroidal anti-inflammatory drugs, and proton pump inhibitors, which are often used as adjunctive therapy with steroids and paired with nutritional supplementation. On the other hand, malignant polyps need to be surgically resected. The prognosis of CCS is improving owing to improved treatment strategies and better patient outcomes. Further research is crucial to enhance our understanding of the pathologic mechanisms of CCS, ultimately aiming to improve early detection and reduce long-term morbidity and mortality.
The gut microbiome, a complex ecosystem of trillions of microorganisms, plays a crucial role in immune system regulation and overall health. This review explores the intricate cross-talk between the gut microbiota and the host immune system, emphasizing how microbial communities shape immune cell differentiation, modulate inflammatory responses, and contribute to immune homeostasis. Key interactions between innate and adaptive immune cells - including macrophages, dendritic cells, natural killer cells, innate Lymphoid cells, T cells, and B cells - and gut microbiota-derived metabolites such as short-chain fatty acids are discussed. The role of commensal bacteria in neonatal immune system development, mucosal barrier integrity, and systemic immunity is highlighted, along with implications for autoimmune diseases, inflammatory conditions, and cancer immunotherapy. Recent advances in metagenomics, metabolomics, and single-cell sequencing have provided deeper insights into the microbiota-immune axis, opening new avenues for microbiome-based therapeutic strategies. Understanding these interactions paves the way for novel interventions targeting immune-mediated diseases and optimizing health through microbiome modulation.
BACKGROUND:Functional abdominal pain disorders (FAPDs) are common gut-brain interaction disorders with unclear pathophysiology. While impaired gastrointestinal motility is thought to play a key role, small intestinal dysmotility remains largely unexplored. Orocecal transit time (OCTT), an indirect indicator of small intestinal transit, offers an insight into its potential contribution to FAPD's pathophysiology. AIM:To assess OCTT in children with FAPDs compared with healthy children using the lactulose breath hydrogen test. METHODS:Thirty-four children (44.1% males, age 5-12 years, mean 7.2 ± 2.4 years) with FAPDs attending North Colombo Teaching Hospital, Ragama, Sri Lanka, were included in the analysis. FAPDs were diagnosed using the Rome IV criteria. None had clinical or laboratory evidence of organic diseases. They were compared with 19 healthy controls (47.1% males, age 5-12 years, mean 7.8 ± 2.7 years) from the same geographical area. OCTT was calculated after an 8-hour fast using a previously validated technique. Breath hydrogen levels were measured at baseline and 15-minute intervals for 180 minutes post-lactulose ingestion (10 g in 10% solution). At each time point, 3 breath samples were collected and analyzed. OCTT was quantified as the time taken to achieve a sustained breath hydrogen increase > 10 parts per million above baseline. Symptoms were recorded using the Rome IV questionnaire, and symptom severity was graded on a 0-4 Likert scale. RESULTS:Patients with FAPDs had increased OCTT (median, 90 minutes; interquartile range, 75-120 minutes) compared to controls (median, 75 minutes; interquartile range, 60-75 minutes) (P = 0.0045, Mann-Whitney U-test). Children with functional dyspepsia had the longest mean OCTT (110.8 ± 26.7 minutes). There was no significant correlation between abdominal pain severity and OCTT (r = 0.18, P = 0.35, Spearman correlation coefficient). OCTT did not differ between those exposed to stressful events and those not exposed to such events (P > 0.05). CONCLUSION:Children with FAPDs have longer OCTT than healthy controls. However, the lack of a significant correlation between OCTT and symptom severity suggests that delayed small intestinal transit alone is not a substantial contributor to FAPD pathophysiology.
BACKGROUND:The gut microbiome is integral to human health, with emerging research underscoring its potential impact on ocular health through the gut-eye axis. Various ocular disorders, such as dry eye syndrome, retinal vascular diseases, macular degeneration, and glaucoma, may be influenced by gut dysbiosis, which could significantly contribute to their development and progression. AIM:To evaluate the influence of the gut microbiome on the pathogenesis and progression of various ocular diseases. METHODS:An extensive search of the scientific literature was undertaken by adhering to Preferred Reporting Items for Systematic Reviews & Meta-Analyses standards, using PubMed (MEDLINE), Scopus, EMBASE, and the Cochrane Library as sources to locate studies addressing the relationship between the gut microbiome and human health. To capture all relevant publications, search terms were systematically applied across these major databases, without limiting the search by language or publication date. Inclusion criteria covered randomized controlled trials, non-randomized controlled trial, prospective studies, cross-sectional studies, and case-control studies. Out of the 3077 articles, 36 full texts were included in the review. RESULTS:Ocular health appears to be shaped by the gut microbial community through mechanisms such as immune regulation, preservation of the blood-retinal barrier, and the generation of protective metabolites. Disturbances in this microbial balance can provoke measurable alterations in host immunity, providing a plausible immunopathogenic pathway that connects intestinal dysbiosis with eye disease. Both laboratory models and early human data suggest that targeted interventions, including prebiotics, probiotics, synbiotics, and faecal microbiota transfer, hold therapeutic potential. CONCLUSION:The gut-eye relationship reflects a multifaceted interaction in which the intestinal microbiome contributes to ocular health through complex biological pathways. Integrating microbiome assessments into diagnostic methods can revolutionize disease management through early detection and targeted interventions. Further, randomised controlled clinical trials are necessary for ocular diseases to prove causal relationships.
BACKGROUND:Gastric motility is an essential gastrointestinal function. It can be influenced by age, gender, body composition, and metabolic status. However, published data on these associations remains limited. AIM:To assess the relationship between gastric motility and adiposity, and metabolic indicators in a cohort of Sri Lankan office workers. METHODS:A cross-sectional study was conducted among 130 office workers (58.5% females) aged 20-50 years (mean 36.81, SD 8.85 years) of the University of Kelaniya, Sri Lanka. Gastric motility was assessed by real-time ultrasonography, using a previously validated method. Fasting antral area (FAA), postprandial antral areas at 1 minutes and 15 minutes (AA1, AA15), and antral contraction frequency (FAC) were measured, and gastric emptying rate (GER) and antral motility index were calculated. Anthropometric parameters were obtained using sensitive scales. Glycated hemoglobin, lipid profile, and liver enzyme levels were measured at an accredited laboratory. RESULTS:The mean body mass index (BMI) was 24.36 (SD 4.09) kg/m2, and 39.2% were overweight or obese. Increased abdominal adiposity was detected in 29.2% and 40.8% had high waist-to-hip ratios. Prediabetes/diabetes were observed in 20.0%, hypercholesterolemia in 47.7%, hypertriglyceridemia in 14.7%, high low-density lipoproteins in 39.2%, and elevated aspartate transaminase and alanine transaminase in 5.4% and 21.5% respectively. FAA had a weak negative correlation with high-density lipoprotein level (r = -0.227, P = 0.009), and a positive correlation with waist circumference (r = 0.235, P = 0.007), and waist-to-hip ratio (r = 0.244, P = 0.005). GER and AA1 correlated weakly with triglyceride (GER: r = 0.174, P = 0.048; AA1: r = 0.194, P = 0.027) and VLDL levels (GER: r = 0.183, P = 0.038; AA1: r = 0.195, P = 0.026). In females, AA1 positively correlated with triglycerides (r = 0.333, P = 0.003), and VLDL levels (r = 0.337, P = 0.003), and AA15 with BMI (r = 0.284, P = 0.013) and hip circumference (r = 0.229, P = 0.047). FAC negatively correlated with BMI (r = -0.234, P = 0.042) and hip circumference (r = -0.247, P = 0.032). CONCLUSION:Gastric motility parameters showed weak associations with metabolic indicators, particularly lipid profiles, and to a lesser extent, with adiposity indicators. The greater number of correlations observed in females suggests the possibility of sex-specific differences in these associations. These findings highlight potential relationships that require confirmation through longitudinal studies.
BACKGROUND:Various therapeutic options are available for the treatment of Crohn's disease (CD). About 30%-40% patients experience primary non-response, and 20%-30% secondary loss of response to biological therapy. Predicting therapeutic response is challenging and an area of active research. Gut microbiota has emerged as an important player in the pathogenesis of CD and also appears to be a promising biomarker for predicting therapeutic response. AIM:To systematically review the literature on the current status of gut microbiota as a tool to predict response to treatment in adults with CD. METHODS:We searched the literature database (PubMed, Scopus, and Cochrane database) from inception to August 2025. We screened for studies reporting on adult patients with CD receiving biologic or immunomodulator therapies, with baseline microbiome analyses performed prior to treatment. Papers reporting on baseline gut microbiota as a predictor of therapeutic response were finally included. The utility of bacterial diversity, microbial community structure, and the role of specific operational taxonomic units as biomarkers of therapeutic response was reviewed. The results were grouped based on the bacterial parameters studied and presented in separate tables. The quality of the included studies was assessed using the MINORS criteria. The review was registered prospectively in PROSPERO. RESULTS:After applying the selection criteria, sixteen studies were included in this systematic review. The majority of the papers were from Europe and the United States. All except two papers assessed gut bacterial population using 16S rRNA gene sequencing. Ten of the sixteen studies were of high quality. Among the sixteen studies included, most identified an association between microbial taxa and treatment response, while the relation with alpha-diversity was inconsistent. The functional characteristics were reported in only four studies and were found to be useful. The best prediction was achieved when microbial characteristics were combined with clinical and other parameters, with area under the curve values up to 0.96. CONCLUSION:The overall results suggest good performance of microbial parameters as a novel biomarker of therapeutic response. However, there are variations across individual studies, probably related to the methodology of assessing microbial communities and the therapeutic agent used. Future multicenter studies integrating microbial, clinical, and metabolomic data are warranted to develop predictive models for personalized therapy in CD.
Acute appendicitis remains one of the most common causes of emergency abdominal surgery globally. Imaging plays a pivotal role in confirming or excluding the diagnosis and identifying complications that influence management pathways. This narrative review synthesizes contemporary evidence and consensus-based imaging protocols for appendicitis, with a focus on computed tomography, magnetic resonance imaging, and ultrasound. The article explores advanced diagnostic criteria, interpretation challenges, imaging algorithms derived from professional society guidelines, and special considerations including pregnancy and pediatric populations. Clinical practice recommendations by the World Society of Emergency Surgery, European Association of Endoscopic Surgery, American College of Radiology, and Infectious Diseases Society of America are incorporated to frame best practices.
BACKGROUND:Colorectal cancer remains as one of the most common cancers that are diagnosed and remains as a significant contributor to morbidity and mortality. Despite advances in techniques, improving access to diagnostic modalities and increasing awareness, it often presents at a later stage and can recur despite treatment. Recurrence can be variable and can occur years after treatment. Liver is the most common location for metastasis to occur followed by lungs. However, atypical sites of metastasis can occur although unusual and colorectal cancer can spread to the spleen, hilum of the liver, adrenals, bone, skeletal muscles, skin, prostate, brain, parotid gland, thyroid gland and even the cardiac muscle. It is crucial to recognize the metachronous nature of the metastasis and to only present at a single site as within this lies the rarity of the case. The mass itself mimicked a cholangiocarcinoma or a Klatskin's tumor initially and only through pathology was the diagnosis established. We present an unusual case of recurrent colorectal cancer that occurred several years post treatment and presented as an isolated metastasis to the hilum of the liver leading to biliary obstruction without any other identifiable lesions including in the colon itself. CASE SUMMARY:A 68-year-old male with history of colon cancer presented with obstructive jaundice to the hospital. After evaluation with imaging studies was diagnosed with mass at the hilum of the liver that was leading to obstruction. With percutaneous biopsies obtained by interventional radiology, the diagnosis of metastatic adenocarcinoma originating from the colon was established. He was deemed not to be a surgical candidate and is currently pursuing chemotherapy. CONCLUSION:A metastatic adenocarcinoma of the colon that presents as a hilar mass and mimics cholangiocarcinoma is very rare. The metachronous nature along with the isolated metastasis involving the hilum of the liver makes this case unique. Diagnosis can be challenging and needs a tissue specimen along with immunostaining to achieve an accurate diagnosis and provide appropriate treatment. Biliary decompression is performed either endoscopically or percutaneously and is part of the multidisciplinary approach involving medical and surgical oncology teams.
