Micro- and nanoplastics (MNPs) are pervasive environmental contaminants with growing recognition as potential contributors to human disease. Widespread human exposure occurs primarily through ingestion of contaminated food and water, and MNPs have been detected in multiple human tissues, including the gastrointestinal tract. Experimental evidence provides a plausible biological basis for disease associations, including impairment of intestinal barrier integrity, activation of mucosal immune pathways, and alteration of gut microbial communities caused by MNP exposure. Although human data remain limited, early studies demonstrate MNP detection in stool and suggest potential correlations with inflammatory biomarkers such as fecal calprotectin. These findings, together with mechanistic data from in vitro and animal models, raise concern that MNP exposure represents a paradigm shift in the pathogenesis or modulation of inflammatory bowel disease (IBD); however, methodological variability, small sample sizes, and contamination challenges currently limit definitive conclusions. The aim of this review is to evaluate the current understanding of MNP exposure and its impact on intestinal health, particularly in relation to IBD. We synthesize mechanistic and early clinical evidence linking MNPs to IBD and highlight critical research gaps. Future standardized exposure assessment, mechanistic validation in human systems, and longitudinal studies are essential to clarify causal relationships. Given the modifiable nature of environmental plastic exposure, advancing this field may offer new opportunities for IBD prevention and intervention.

Identifying patients at high risk for poor bowel preparation preceding a colonoscopy is critical to successful colorectal cancer screening. High-risk patients, such as those who are obese, diabetic, opioid users, or former smokers, often have comorbidity, medication, and sociodemographic factors that lead to suboptimal bowel preparation even when following protocol. Suboptimal preparation results in missed lesions, longer procedure times, and increased healthcare costs. Optimal visualization of the colon mucosa is achieved through effective bowel preparation. Polyethylene glycol (PEG) solutions are preferred for their safety, especially in patients with kidney or cardiac disease. Split-dose PEG regimens with a low-residue diet are recommended by the American Gastroenterological Association to promote cleansing and patient tolerance. Tailored regimens can be employed in high-risk patients, including those with chronic constipation, opioid dependence, or diabetes. Educational interventions, such as written and verbal instructions, patient navigators, and mobile device reminders, improve compliance. Medical strategies include split-dose PEG-electrolyte lavage solution with bisacodyl, additional purgatives for select patients, and avoidance of sodium phosphate in elderly or renally impaired individuals. Open-access colonoscopy services have expanded following the COVID-19 pandemic to manage backlogs and improve access. Improving education, simplifying regimens, and targeting interventions can reduce repeat procedures and enhance colorectal cancer detection. This narrative review summarizes patient-, medication-, and system-level risk factors for inadequate bowel preparation in high-risk populations and synthesizes practical, evidence-based strategies to optimize colonoscopy quality, including in open-access settings.

Cholelithiasis and gallstone-related complications remain one of the most prevalent gastrointestinal diseases globally. Age, gender, body mass index, physical activity, dietary factors, and genetics play a role in the development of gallstones. More than 20% of patients with gallstones will develop symptomatic disease during their lifetime, which can often lead to complications and significant morbidity. Laparoscopic cholecystectomy is considered the standard of care for symptomatic gallstone disease. Still, in select patient populations and in those who are non-surgical candidates, medical management, with bile acid therapy such as ursodeoxycholic acid (UDCA) or mechanical therapy such as extracorporeal shock wave lithotripsy, is preferred. UDCA is a hydrophilic bile acid that lowers biliary cholesterol saturation and aids in dissolving small, cholesterol-rich gallstones. UDCA appears to be well tolerated in the populations studied. While serious adverse events were uncommon in the available literature, UDCA’s efficacy is limited by a high recurrence rate. The aim of this review is to summarize the current evidence and developments regarding the role of UDCA therapy in the management of cholelithiasis and choledocholithiasis.

Gluten has multiple harmful effects that compromise human health, not only in gluten-dependent diseases but also in non-gluten-affected chronic inflammatory conditions. After consumption, the indigestible gluten peptides are modified by luminal microbial transglutaminase or transported through the gut epithelium to interact with the highly populated mucosal immune cells. As a disruptor of gut permeability, gluten peptides compromise tight junction integrity, allowing foreign immunogenic molecules to reach internal compartments. Gliadin peptides are distributed systemically to remote organs, where they encounter endogenous tissue transglutaminase. Following post-translational deamidation or transamidation, the peptides become immunogenic and pro-inflammatory, inducing organ dysfunction and pathology. Cross-reactivity and sequence homology between gluten/gliadin peptides and human epitopes may contribute to molecular mimicry in autoimmunity induction. A gluten-free diet can prevent these phenomena through various mechanisms. As proof of concept, gluten withdrawal alleviates disease activity in chronic inflammatory, metabolic, and autoimmune conditions, and even in neurodegeneration. We recommend combining the gluten-free and Mediterranean diets to leverage the advantages of both. Before recommending gluten withdrawal for non-gluten-dependent conditions, patients should be asked about gut symptomatology and screened for celiac-associated antibodies. The current list of gluten-induced diseases includes celiac disease, dermatitis herpetiformis, gluten ataxia, gluten allergy, and non-celiac gluten sensitivity. In view of gluten being a universal pro-inflammatory molecule, other non-celiac autoinflammatory and neurodegenerative conditions should be investigated for potential gluten avoidance.

Alcohol consumption is responsible for approximately 6% of all deaths and 5.1% of the global disease burden. The most common alcohol-related causes of death include liver cirrhosis (50% of cases), pancreatitis (25%), and esophageal cancer (22%). In this review, we provide an overview of ethanol metabolism and highlight the major diseases caused by alcohol consumption in the liver and gastrointestinal tract. Due to its central metabolic role, the liver is particularly susceptible to ethanol, which is known to cause a wide spectrum of conditions, including steatosis, steatohepatitis, alcohol-associated hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma). The gastrointestinal tract is often one of the first areas to show signs of damage from excessive alcohol consumption. Chronic alcohol abuse is a well-established risk factor for both acute and chronic pancreatitis, as well as pancreatic cancer. Approximately 70% of acute pancreatitis cases and 30% of chronic pancreatitis cases are attributable to alcohol abuse. Epidemiological studies have consistently demonstrated a negative correlation between alcohol intake and the prevalence of gallstones. Moreover, alcohol is an important risk factor for gastroenteropancreatic cancer, as ethanol metabolism produces acetaldehyde, a potent carcinogen for humans. In conclusion, chronic ethanol intake, through one of its main metabolic products, acetaldehyde, causes pathological changes in the gastrointestinal tract, liver, pancreas, and gallbladder. Even moderate amounts of alcohol may increase the risk of cancers, such as colorectal cancer. Therefore, if there is clinical suspicion of excessive alcohol intake in a patient with persistent digestive symptoms (e.g., abdominal pain, nausea, vomiting, diarrhea, and bloody stools), immediate medical evaluation is essential. Referral to specialized centers with expertise in alcohol use disorder is a key management option for patients with established alcohol use disorder.

The incidence and prevalence of inflammatory bowel diseases (IBD), including ulcerative colitis and Crohn’s disease, are rapidly increasing. Currently, colonoscopy is the gold standard for diagnosing and monitoring the course of IBD. However, the recently implemented “treat-to-target” strategy, which involves meticulously pursuing multiple therapeutic objectives, has opened avenues for non-invasive diagnostic and monitoring tools. These tools aim to assess disease activity and predict the likelihood of recurrence. Research studies into serum and fecal biomarkers in IBD have been ongoing for several years. Among the most relevant biomarkers, fecal calprotectin and C-reactive protein have shown the best accuracy, with good-to-optimal correlation with endoscopic, histologic, or transmural activity. Numerous studies have explored the potential advantages of using multi-target tools that combine serum and fecal biomarkers with clinical activity indexes to enhance diagnostic and monitoring effectiveness. Encouraging findings have emerged for fecal lactoferrin, autoantibodies, micro-RNA, gene expression, and many other serological and fecal markers. However, limited evidence has hindered their widespread adoption in routine clinical practice. This review aimed to summarize the available data on the utilization of biomarkers in IBD.