For severe forms of ulcerative colitis (UC), a chronic inflammatory bowel disease (IBD), biological therapies, including tumor necrosis factor inhibitors (anti-TNF), are often used. However, these drugs have a high variability in treatment response. Multiple factors, such as genetic variants, can affect this variability. The goal of the study was to verify if selected candidate variants could affect response to anti-TNF in UC treatment. This association study included 76 participants suffering from UC and past or current users of anti-TNF. Clinical data for phenotyping was collected through a single visit with the participant and a medical chart review. Blood or saliva samples were collected to extract DNA and to genotype eight selected candidate variants in genes TNF, TNFAIP3, TNFRSF1 A and TNFRSF1B. For anti-TNF users, 30% of individuals were non-responders, 70% suffered from AE and none of the studied variants was associated with the response's phenotype. However, for infliximab users only (n = 44), the TNFRSF1B-rs1061622 variant was associated with nonresponse to infliximab for the first time in a cohort of UC patients (p-value = 0.028). Next steps are to replicate this association in independent cohorts and to perform functional studies to gain more evidence on the variant.

Background: Pediatric-onset familial inflammatory bowel disease (IBD) may differ from sporadic pediatric-onset IBD in its genetic and environmental background and may have distinct clinical and therapeutic implications. Objective: To evaluate the influence of a positive family history of IBD on the use of medical therapies and surgical interventions in adult patients with pediatric-onset IBD. Methods: Retrospective case-control study using the Spanish ENEIDA registry, including adults diagnosed with pediatric-onset IBD since 2006. Familial forms (FFs) (defined by a first-degree relative with IBD) and sporadic forms (SF) (with no relatives of any grade with IBD) were matched 1:4 by type of IBD, sex, age at IBD diagnosis, disease location, disease pattern, development of perianal disease and smoking status at diagnosis. The study outcomes were the use of immunomodulators, biological therapies, intestinal surgery, and perianal surgery during follow-up. Results: Six-hundred and fifty-five Crohn's disease (CD) (131 FF) and 440 ulcerative colitis (UC) (88 FF) patients were included. Immunomodulators, biological therapy, and intestinal surgery were used evenly among FF and SF patients for both UC and CD. However, a higher requirement for perianal surgery among FF-CD patients (18.3% vs. 10.5%, p = 0.014), together with a shorter time to perianal surgery (11 vs. 20 months, log-rank p = 0.004), was observed. Conclusions: Patients with FF of pediatric-onset IBD do not exhibit an increased use of immunomodulators, biological agents, or intestinal surgery, but do exhibit a higher need for perianal surgery, as compared to patients with SF pediatric-onset IBD.

Background: Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract, defined by intestinal epithelial cell death. While ferroptosis and disulfidptosis have been linked to IBD pathogenesis, the functional significance of disulfidptosis-related ferroptosis genes (DRFGs) in this disease remains poorly characterized. This investigation sought to pinpoint DRFGs as diagnostic indicators and clarify their mechanistic contributions to IBD progression. Methods: Four IBD datasets (GSE65114, GSE87473, GSE102133, and GSE186582) from the GEO database were integrated to identify differentially expressed genes (DEGs) (|log2FC| > 0.585, adj. p < 0.05). A Pearson correlation analysis was used to link disulfidptosis and ferroptosis genes, followed by machine learning (LASSO and RF) to screen core DRFGs. The immune subtypes and single-cell sequencing (GSE217695) results were analyzed. A DSS-induced colitis Mus musculus (C57BL/6) model was used for validation. Results: Transcriptomic profiling identified 521 DEGs, with 16 defined as DRFGs. Nine hub genes showed diagnostic potential (AUC: 0.71-0.91). Functional annotation demonstrated that IBD-associated genes regulate diverse pathways, with a network analysis revealing their functional synergy. The PPI networks prioritized DUOX2, NCF2, ACSL4, GPX2, CBS, and LPCAT3 as central hubs. Two immune subtypes exhibited divergent DRFG expression. Single-cell mapping revealed epithelial/immune compartment specificity. The DSS-induced murine colitis model confirmed differential expression patterns of DRFGs, with concordant results between qRT-PCR and RNA-seq, emphasizing their pivotal regulatory roles in disease progression and potential for translational application. Conclusions: DRFGs mediate IBD progression via multi-signal pathway regulation across intestinal cell types, demonstrating diagnostic and prognostic potential.

In this review the nexus between genomic instability and human health is investigated, emphasizing the rising consumption of ultra-processed foods (UPFs). Introducing the NOVA food classification system, we explore the significant surge in UPF consumption over the past 3 decades and its correlation with heightened mortality rates. This exploration extends to the development of health issues such as obesity, cancer, type 2 diabetes, inflammatory bowel diseases, cardiovascular diseases, and depression. Existing evidence, including studies involving healthy adolescents and older adults, underscores a clear link between increased consumption of UPFs and heightened DNA damage. The primary objective of this review is to offer a comprehensive examination of the repercussions of elevated UPF consumption on human health. With a specific focus on unraveling the intricate relationship between these dietary choices and genomic instability, the review seeks to enhance our understanding. Through a targeted exploration of molecular pathways, the aim is to illuminate how dependence on UPFs may impact physical and mental well-being.

Inflammation is central in inflammatory bowel disease (IBD) pathogenesis. Because of diet's pro- and anti-inflammatory properties, multiple observational studies have explored the link between the dietary inflammatory potential and IBD-related outcomes. We aimed to systematically review the literature and provide a comprehensive overview of the dietary inflammatory potential and its association with the development and progression of IBD.

Literature was searched systematically on the 2nd of May 2024 in PubMed, Web of Science, Scopus, Cochrane Library, and Embase to identify the observational studies that explored the link between the dietary inflammatory potential and IBD-related outcomes. A higher dietary inflammatory potential was defined as the ability of a dietary pattern to promote inflammation in the body. Studies were included only if they quantified this using a dietary index, such as the dietary inflammatory index (DII) and the empirical dietary inflammatory pattern (EDIP). Two authors independently performed study selection and data extraction and assessed the risk of bias using the Newcastle-Ottawa scale.

Fourteen of the 165 identified records met the inclusion criteria. Seven investigated the risk of developing IBD, but with mixed results. Nine investigated the progression of IBD, which indicated that a higher dietary inflammatory potential contributed to higher disease activity and associated symptoms.

The evidence suggested that a higher dietary inflammatory potential worsens the condition of IBD patients, while the link with the risk of developing the disease was less clear. To elucidate this, high-quality intervention studies are needed.

Many of the patients with inflammatory bowel disease (IBD) are children and adolescents, and the incidence of pediatric IBD is increasing. However, understanding epidemiological trends is crucial for effective prevention and treatment and reducing the local and global burden of IBD. Little data exist regarding the incidence of IBD in the child population in the Kujawsko-Pomorskie Voivodeship. The aims of this study were to evaluate the incidence of IBD in the period 2011 - 2022 and to compare the data regarding three types of IBD, namely ulcerative colitis (UC), Crohn's disease (CD), and unclassified inflammatory bowel disease (IBD-U), from the first half, i.e. 2011 - 2016, to the second half, i.e. 2017 - 2022.

This retrospective study analyzed the medical records of 118 IBD patients hospitalized at the Department of Pediatrics, Allergology and Gastroenterology from the central-northern part of Poland.

Of the 118 patients diagnosed with IBD, 48 (40.68%) had CD, 57 (48.31%) had UC, and 13 (11.01%) had IBD-U. Between 2011 and 2016, 48 new IBD patients were diagnosed, with a further 70 new cases added between 2017 and 2022, representing a significant increase over the period (P = 0.033). Also, a significant increase was seen for UC, i.e. rising from 19 new cases between 2011 and 2016, to 38 between 2017 and 2022 (P = 0.015). The increase in CD was not significant.

The incidence of pediatric IBD in the central-northern district of Poland is lower than other countries, it nonetheless appears to be increasing, particularly in children with UC. The number of IBD diagnoses in children has increased by nearly 50% over the last 6 years.

The differences in the clinical course of Crohn's disease (CD) and ulcerative colitis (UC) among Asian countries remain unknown. Thus, we compared the clinical characteristics, treatment, and one-year outcomes of newly diagnosed inflammatory bowel disease (IBD) patients between Vietnam and Korea.

A retrospective cohort study was conducted at seven tertiary hospitals in these countries between January 2020 and January 2021. Data on demographics, diseases, treatment, and outcomes during 1 year after diagnosis were collected.

Among 225 patients (60 from Vietnam and 165 from Korea), 140 and 85 were diagnosed with UC and CD, respectively. Severe activity (p < 0.01) and extensive colitis (p < 0.01) in UC, along with complicated behavior in CD (p < 0.01), were more frequently observed in Vietnamese patients compared to Korean patients. The proportion of UC patients using corticosteroids (p < 0.01), immunomodulators (p < 0.01), and biologics (p = 0.026) was significantly higher in Vietnam. In contrast, the proportion of UC patients using topical mesalamine (p < 0.01) was significantly higher in Korea. The intervals from CD diagnosis to biologic therapy initiation (p = 0.04), as well as from UC diagnosis to corticosteroid (p < 0.01), immunomodulator (p < 0.01), and biologic therapy (p < 0.01) commencement, were significantly shorter in Vietnamese patients compared to Korean patients. However, the proportions of endoscopic healing and complications at 1-year follow-up did not significantly differ between the countries (p > 0.05).

Although Vietnamese IBD patients had higher baseline clinical and phenotypic severity than their Korean counterparts, no significant differences in short-term outcomes were observed, potentially reflecting the impact of the higher rate and early biologic usage in Vietnamese patients.

Inflammatory bowel disease (IBD) is a non-specific inflammatory disease of digestive tract, primarily manifesting as ulcerative colitis (UC) and Crohn's disease (CD). The precise etiology of IBD remains elusive. The interplay of genetic factors, environmental influences, and intestinal microbiota contributes to the establishment of an uncontrolled immune environment within the intestine, which can progressively lead to atypical hyperplasia and ultimately to malignancy over a long period. This colorectal malignant tumor that arises from chronic IBD is referred to as colitis-associated colorectal cancer (CAC). Dysregulation in the quantity and functionality of neutrophils plays a significant role in the onset, progression, and recurrence of IBD, as well as in the transition from IBD to CAC. Neutrophils affect the pathophysiology of IBD through various mechanisms, including the production of reactive oxygen species (ROS), degranulation, the release of inflammatory mediators and chemokines, and the formation of neutrophil extracellular traps (NETs). These processes can induce DNA mutations, thereby facilitating the development of colon cancer. Given the incomplete understanding of the disease mechanisms underlying IBD and CAC, effective treatment and prevention strategies remain challenging. Consequently, a comprehensive review of the functional roles of neutrophils in IBD and CAC is essential for advancing our understanding of IBD pathogenesis and identifying potential therapeutic targets.

Chronic gastrointestinal disorders such as inflammatory bowel diseases (IBDs) and irritable bowel syndrome (IBS) impose significant health burdens globally. IBDs, encompassing Crohn's disease and ulcerative colitis, are multifactorial disorders characterized by chronic inflammation of the gastrointestinal tract. On the other hand, IBS is one of the principal gastrointestinal tract functional disorders and is characterized by abdominal pain and altered bowel habits. Although the precise etiopathogenesis of these disorders remains unclear, mounting evidence suggests that non-coding RNA molecules play crucial roles in regulating gene expression associated with inflammation, apoptosis, oxidative stress, and tissue permeability, thus influencing disease progression. miRNAs have emerged as possible reliable biomarkers, as they can be analyzed in the biological fluids of patients at a low cost. This review explores the roles of miRNAs in IBDs and IBS, focusing on their involvement in the control of disease hallmarks. By an extensive literature review and employing bioinformatics tools, we identified the miRNAs frequently studied concerning these diseases. Ultimately, specific miRNAs could be proposed as diagnostic biomarkers for IBDs and IBS. Their ability to be secreted into biofluids makes them promising candidates for non-invasive diagnostic tools. Therefore, understanding molecular mechanisms through the ways in which they regulate gastrointestinal inflammation and immune responses could provide new insights into the pathogenesis of IBDs and IBS and open avenues for miRNA-based therapeutic interventions.

Acute and chronic bowel pathologies can often be mistaken for manifestations of inflammatory bowel disease (IBD), and there are many entities with imaging and clinical features that overlap with IBD, making diagnosis difficult. We describe multiple inflammatory, infectious, neoplastic, and vascular entities with imaging and clinical features that may mimic IBD, and highlight differentiating features to assist in diagnosis.

Inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis, is a nonspecific chronic inflammation of the gastrointestinal tract. Despite recent advances in therapeutics and newer management strategies, IBD largely remains untreatable. Helminth therapy is a promising alternative therapeutic for IBD that has gained some attention in the last two decades. Helminths have immunomodulatory effects and can alter the gut microbiota. The immunomodulatory effects include a strong Th2 immune response, T-regulatory cell response, and the production of regulatory cytokines. Although concrete evidence regarding the efficacy of helminth therapy in IBD is lacking, clinical studies and studies done in animal models have shown some promise. Most clinical studies have shown that helminth therapy is safe and easily tolerable. Extensive work has been done on the whipworm Trichuris, but other helminths, including Schistosoma, Trichinella, Heligmosomoides, and Ancylostoma, have also been explored for pre-clinical and animal studies. This review article summarizes the potential of helminth therapy as an alternative therapeutic or an adjuvant to the existing therapeutic procedures for IBD treatment.

Inflammatory bowel disease (IBD), encompassing Crohn's disease (CD) and ulcerative colitis (UC), has a significant genetic component and is increasingly prevalent due to environmental factors. Current polygenic risk scores (PRS) have limited predictive power and cannot inform time of symptom onset. Circulating proteomics profiling offers a novel, non-invasive approach for understanding the inflammatory state of complex diseases, enabling the creation of proteomic risk scores (ProRS). This study utilizes data from 51,772 individuals in the UK Biobank to evaluate the unique and combined contributions of PRS and ProRS to IBD risk prediction. We developed ProRS models for CD and UC, assessed their predictive performance over time, and examined the benefits of integrating PRS and ProRS for enhanced risk stratification. Our findings are the first to demonstrate that combining genetic and proteomic data improves IBD incidence prediction, with ProRS providing time-sensitive predictions and PRS offering additional long-term predictive value. We also show that the ProRS achieves better predictive performance among individuals with high PRS. This integrated approach highlights the potential for multi-omic data in precision medicine for IBD.

Previous studies suggest that appendectomy has a protective effect against ulcerative colitis (UC); however, relatively few studies focusing on this topic have been reported in China.

To explore the correlation between appendectomy and the onset of UC.

A total of 313 patients with newly diagnosed UC and 313 healthy individuals were selected for this study. According to whether their appendix was removed before the diagnosis of UC, patients were divided into appendectomized and non-appendectomized groups. Their general clinical data, appendectomy history, disease severity, extent of involvement, and blood routine test results were collected to evaluate the relationship between appendectomy and the onset of UC.

The study revealed that the average time interval for the diagnosis of UC after appendectomy was 14.72 ± 13.87 years. 55.81% patients were diagnosed with UC five years after appendectomy. Among them, eight patients underwent appendectomy before the age of 20 years and were diagnosed with UC five years later. In the appendectomized group, the onset age of UC was higher, and the degree of disease activity was significantly lower. This group had a higher proportion of patients in clinical remission or with mild disease and a lower proportion of patients with severe disease. The extent of lesions in the appendectomized group was limited, with a higher proportion of E1 and E2, whereas a lower proportion of E3 lesions.

Appendectomy may delay the onset of UC, reduce disease severity, and lessen the scope of involvement.

The intestinal microbiota plays a key role in the pathogenesis of inflammatory bowel disease (IBD), with its composition varying based on geographic location and dietary factors. This study was performed to examine and compare the bacterial composition of the gut microbiota in Mexican and Spanish individuals with IBD and healthy controls, while also considering the nutritional aspects. This study involved 79 individuals with IBD and healthy controls from Mexico and Spain. The fecal microbiota composition was analyzed using 16S rRNA gene sequencing, and the dietary intake and anthropometric measurements were collected. Alpha diversity analysis revealed a lower Chao1 index of the bacterial genera in the IBD groups. Beta diversity analysis showed significant differences in the bacterial composition, suggesting inter-individual variability within the healthy and IBD groups. Additionally, the relative abundance of the bacterial genera varied across the four groups. Faecalibacterium was more abundant in the IBD groups; Prevotella was found exclusively in the Mexican groups, and Akkermansia was found only in the Spanish groups. Akkermansia was positively correlated with meat and protein intake, Prevotella with lean mass, and Bacteroides with calorie intake. These findings highlight the importance of considering geographic and nutritional factors in future research on the gut microbiome's role in IBD pathogenesis.

Biotherapeutics are among the therapeutics that have revolutionized standard inflammatory bowel disease (IBD) treatment, which was previously limited to mesalamine, 5-aminosalicylic acid, corticosteroids, and classical immunosuppressants. Self-administrable biotherapeutics for IBD would enable home-based treatment and reduce the burden on medical infrastructure. Self-administration is made possible through subcutaneous injectable, oral, and rectal dosage forms. Nevertheless, the full benefits of self-administration cannot be realized without first addressing the issue of medication adherence, which remains woefully inadequate for IBD biotherapies. Some of the major barriers to medication adherence in IBD are the route of administration, frequency of administration, and undesired side effects. In this review, we identify the main physiological and engineering constraints that underlie these three barriers to adherence. We then highlight key technological and behavioral innovations-spanning multiple scientific disciplines-that can be leveraged to design novel therapies and interventions that improve adherence to self-administered IBD biotherapies.

Management of ulcerative colitis and Crohn's disease, the main subtypes of inflammatory bowel disease (IBD), focuses on the induction and maintenance of remission. Tacrolimus, a member of a group of drugs termed calcineurin inhibitors, may have a role in the medical management of IBD when given either systemically or topically. This review aimed to evaluate the available data focusing on the use of topical tacrolimus in the management of IBD. Reports of the use of topical tacrolimus in IBD were extracted from databases up to 31 May 2024. Topical tacrolimus therapy appears to have reasonable efficacy in the induction and maintenance of remission in patients with refractory IBD, with an acceptable safety profile. Overall, the available data are supportive of the use of topical tacrolimus in selected patients. Further comparative clinical studies are required to more fully delineate the role of this drug.

Endoplasmic reticulum stress (ERS) becomes a significant factor in inflammatory bowel disease (IBD), like Crohn's disease (CD) and ulcerative colitis (UC). Our research was aimed at identifying molecular markers to enhance our understanding of ERS and inflammation in IBD, recognizing risk factors and high-risk groups at the molecular level, and developing a predictive model on the grounds of based on ERS-associated genes. This research adopted the least absolute shrinkage and selection operator (LASSO) regression and logistic regression to build a predictive model, and categorized IBD patients into high- and low-risk groups, and then identified four gene clusters. Our key findings included a significant increase in drug target gene expression in high-risk groups, notable discrepancies in immune levels, and functions between high-risk and low-risk groups. Notably, the TAP1 gene emerged as a strong predictor with the highest diagnostic value (area under the curve [AUC] = 0.941). TAP1 encodes proteins required for antigenic peptide transfer across the endoplasmic reticulum (ER) membrane, and its potential as a diagnostic marker and therapeutic target is reflected by its overexpression in IBD tissues. Our study established a new ERS-associated gene model which could forecast the risk, immunological status, and treatment efficacy of patients with IBD. These findings suggest potential targets for personalized therapy and highlight the significance of ERS in the etiology and therapy of IBD. Future studies should explore the therapeutic potential of targeting TAP1 and other ERS-related genes for IBD management.

The intestines are the largest barrier organ in the human body. The intestinal barrier plays a crucial role in maintaining the balance of the intestinal environment and protecting the intestines from harmful bacterial invasion. Single‑cell RNA sequencing technology allows the detection of the different cell types in the intestine in two dimensions and the exploration of cell types that have not been fully characterized. The intestinal mucosa is highly complex in structure, and its proper functioning is linked to multiple structures in the proximal‑distal intestinal and luminal‑mucosal axes. Spatial localization is at the core of the efforts to explore the interactions between the complex structures. Spatial transcriptomics (ST) is a method that allows for comprehensive tissue analysis and the acquisition of spatially separated genetic information from individual cells, while preserving their spatial location and interactions. This approach also prevents the loss of fragile cells during tissue disaggregation. The emergence of ST technology allows us to spatially dissect enzymatic processes and interactions between multiple cells, genes, proteins and signals in the intestine. This includes the exchange of oxygen and nutrients in the intestine, different gradients of microbial populations and the role of extracellular matrix proteins. This regionally precise approach to tissue studies is gaining more acceptance and is increasingly applied in the investigation of disease mechanisms related to the gastrointestinal tract. Therefore, this review summarized the application of ST in gastrointestinal diseases.

Infectious causes of diarrhea contribute significantly to morbidity in Asia. We conducted a systematic review and meta-analysis of the prevalence of infectious etiologies of persistent and chronic diarrhea in Asian adults. Searches were performed on PubMed and Scopus for studies from January 1, 1970, to May 30, 2023. Sixteen studies were identified and included. The meta-analysis was conducted with the random-effects method, estimating the pooled prevalence of groups of infectious pathogens as causes of persistent and chronic diarrhea among Asian adults. The findings were highly heterogeneous and indicative of publication bias. The majority of studies were conducted on persons living with human immunodeficiency virus infection (PLHIV). The studies were predominantly from low-income and middle-income Asian countries. The most common cause was parasitic, with a pooled prevalence of 0.52 (95% confidence interval 0.28-0.65, I2 = 99%, Cochran's Q = 1027.44, P < 0.01), followed by bacterial, fungal, and viral causes, which were substantially rarer. Negative microbiological testing was also common, with a pooled prevalence for a negative test being 0.37 (95% confidence interval 0.17-0.52, I2 = 99%, Cochran's Q = 1027.44, P < 0.01). Subgroup analyses of studies conducted among PLHIV, from year 2000 and among those conducted in Southeast Asia showed a similar prevalence of parasitic causes of diarrhea. In conclusion, in Asian adults with persistent and chronic diarrhea, parasitic causes were most prevalent. However, the estimate of true prevalence is limited by significant heterogeneity among the available studies. More study in this field is required, especially examining PLHIV in the post-antiretroviral therapy era and from high-income countries.

Recent research indicates that the microbiome has a significant impact on the progression of inflammatory bowel disease (IBD) and that creating therapies that change its composition could positively impact the outcomes of IBD treatment. This review summarizes the results of extensive studies that examined IBD patients undergoing several therapies, including anti-TNF medication, vedolizumab, ustekinumab, probiotics, and fecal microbiota transplantation (FMT), and the alterations in their gut microbiota's composition and function. The objective was to investigate the variety and effectiveness of microbial species in order to discover new biomarkers or therapeutic targets that could improve the outcome of treatment for these patients. This research aimed to offer useful insights into personalized medicine techniques for managing IBD. Beneficial bacteria such as Faecalibacterium prausnitzii and Roseburia have been consistently linked to favorable clinical outcomes, whereas pathogenic bacteria such as Escherichia coli and Clostridioides difficile are associated with worsening disease conditions. Although many studies have examined the role of gut microbiota in IBD, there is still a need for more targeted research on the connection between specific microbial communities and treatment outcomes. This study sought to address this gap by exploring the intricate relationship between the gut microbiota composition and the effectiveness of IBD medications.

The etiology of Inflammatory Bowel Disease (IBD) is not fully understood but is believed to involve a dysregulated immune response to intestinal microbiota in genetically susceptible individuals. Individuals with IBD are at increased risk of infections due to immunosuppressive treatments, comorbidities, and advanced age. Current evidence indicates that IBD patients are not at higher risk of SARS-CoV-2 infection compared to the general population, though the risk of severe outcomes remains debated. A retrospective observational study was conducted using Apulian regional health data from 2020 to 2022. This study included 1029 IBD patients and 3075 controls, matched by age and sex. COVID-19 incidence, hospitalization, and case fatality rates were analyzed alongside vaccination coverage. No significant differences in COVID-19 incidence (IRR = 0.97), hospitalization (p = 0.218), or lethality (p = 0.271) were evidenced between IBD patients and the general population. Vaccination rates were high in both groups, with slightly higher uptake in IBD patients. Multivariate analysis identified age and male sex as risk factors for severe COVID-19 outcomes, while vaccination significantly reduced hospitalization and lethality risks. IBD patients in Apulia do not have an increased risk of COVID-19 infection or severe outcomes compared to the general population. Vaccination is crucial in protecting IBD patients, and ongoing efforts to promote vaccination within this population are essential. Future research should focus on the impact of specific IBD treatments on COVID-19 outcomes and the long-term effectiveness of vaccines.

The term "inflammatory bowel disease" (IBD) describes a class of relapse-remitting conditions that affect the gastrointestinal (GI) tract. Among these, Crohn's disease (CD) and ulcerative colitis (UC) are two of the most globally prevalent and debilitating conditions. Several articles have brought attention to the significant role that inflammation and oxidative stress cooperatively play in the development of IBD, offering a different viewpoint both on its etiopathogenesis and on strategies for the effective treatment of these conditions. Marine ecosystems may be a significant source of physiologically active substances, supporting the search for new potential clinical therapeutics. Based on this evidence, this review aims to comprehensively evaluate the activity of marine algae and deriving biomolecules in decreasing pathological features of CD and UC. To match this purpose, a deep search of the literature on PubMed (MEDLINE) and Google Scholar was performed to highlight primary biological mechanisms, the modulation of inflammatory and oxidative stress biochemical parameters, and potential clinical benefits deriving from marine species. From our findings, both macroalgae and microalgae have shown potential as therapeutic solutions for IBD due to their bioactive compounds and their anti-inflammatory and antioxidant activities which are capable of modulating markers such as cytokines, the NF-κB pathway, reactive oxidative and nitrosative species (ROS and RNS), trefoil factor 3 (TFF3), lactoferrin, SIRT1, etc. However, while we found promising preclinical evidence, more extensive and long-term clinical studies are necessary to establish the efficacy and safety of marine algae for IBD treatment.

The impact of type 1 diabetes (T1D) on inflammatory bowel disease (IBD) remains unclear.

To analyze the causal relationship between T1D and IBD using Mendelian ran-domization (MR).

Single nucleotide polymorphisms were sourced from FinnGen for T1D, IBD, ulcerative colitis (UC) and Crohn's disease (CD). Inverse variance-weighted, MR-Egger, and weighted median tests were used to assess exposure-outcome causality. The MR-Egger intercept was used to assess horizontal pleiotropy. Co-chran's Q and leave-one-out method were used to analyze heterogeneity and sensitivity, respectively.

Our MR analysis indicated that T1D was associated with a reduced risk of IBD [odds ratio (OR): 0.959; 95% confidence interval (CI): 0.938-0.980; P < 0.001] and UC (OR: 0.960; 95%CI: 0.929-0.992; P = 0.015), with no significant association observed in terms of CD risk (OR: 0.966; 95%CI: 0.913-1.022; P = 0.227). The MR-Egger intercept showed no horizontal pleiotropy (P > 0.05). Cochran's Q and leave-one-out sensitivity analyses showed that the results were not heterogeneous (P > 0.05) and were robust.

This MR analysis suggests that T1D serves as a potential protective factor against IBD and UC but is independent of CD.

To examine possible geographical and temporal differences in the incidence of childhood-onset inflammatory bowel disease (IBD) in Norway, motivated by previous research indicating relevant environmental factors explaining changing epidemiology.

We analysed data from children born in Norway from 2004 to 2012 (n = 541 036) in a registry-based nationwide study. After validating registry diagnoses against medical records, we defined IBD as ≥2 entries of International Classification of Diseases, 10th revision (ICD-10) codes K50, K51 and K52.3 in the Norwegian Patient registry. We estimated hazard ratios (HR) for IBD across four geographical regions with a south-to-north gradient and the incidence by period of birth.

By the end of follow-up on 31 December 2020, 799 IBD diagnoses were identified (Crohn's disease: n = 465; ulcerative colitis, n = 293, IBD: unclassified, n = 41). Compared to children in the southernmost region, there was almost a two-fold HR for IBD in children in the most Northern region (HR = 1.94, 95% Cl = 1.47-2.57; Mid region: HR = 1.68, 95% CI = 1.29-2.19, ptrend <0.001). These estimates remained largely unchanged after adjustment for potential confounding factors. The cohorts born in 2004-2006 and 2010-2012 had comparable cumulative incidences, with a slightly higher incidence for those born in 2007-2009.

We observed an increase in the risk of IBD by increasing latitude which may suggest that environmental factors influence the development of IBD, although non-causal explanations cannot be ruled out.

The timely introduction and adjustment of the appropriate drug in accordance with previously well-defined treatment goals is the foundation of the approach in the treatment of inflammatory bowel disease (IBD). The therapeutic approach is still evolving in terms of the mechanism of action but also in terms of the possibility of maintaining remission. In patients with achieved long-term remission, the question of de-escalation or discontinuation of therapy arises, considering the possible side effects and economic burden of long-term therapy. For each of the drugs used in IBD (5-aminosalycaltes, immunomodulators, biological drugs, small molecules) there is a risk of relapse. Furthermore, studies show that more than 50% of patients who discontinue therapy will relapse. Based on the findings of large studies and meta-analysis, relapse of disease can be expected in about half of the patients after therapy withdrawal, in case of monotherapy with aminosalicylates, immunomodulators or biological therapy. However, longer relapse-free periods are recorded with withdrawal of medication in patients who had previously been on combination therapies immunomodulators and anti-tumor necrosis factor. It needs to be stressed that randomised clinical trials regarding withdrawal from medications are still lacking. Before making a decision on discontinuation of therapy, it is important to distinguish potential candidates and predictive factors for the possibility of disease relapse. Fecal calprotectin level has currently been identified as the strongest predictive factor for relapse. Several other predictive factors have also been identified, such as: High Crohn's disease activity index or Harvey Bradshaw index, younger age (< 40 years), longer disease duration (> 40 years), smoking, young age of disease onset, steroid use 6-12 months before cessation. An important factor in the decision to withdraw medication is the success of re-treatment with the same or other drugs. The decision to discontinue therapy must be based on individual approach, taking into account the severity, extension, and duration of the disease, the possibility of side adverse effects, the risk of relapse, and patient's preferences.

Studies exploring the association between inflammatory bowel disease (IBD) and pancreatic cancer have reported inconsistent results.

To provide a comprehensive overview of the risk of pancreatic cancer development in patients with IBD.

We searched Embase, PubMed, Scopus and ProQuest from inception to 31 October 2023. We included population-based cohort studies examining the risk of incident pancreatic cancer in adult patients with IBD compared to the non-IBD population. We also retrieved Mendelian randomisation (MR) studies investigating the relationship of IBD with pancreatic cancer risk. We conducted random-effects meta-analyses and provided pooled relative risks (RRs) with 95% confidence intervals (CIs).

We included 13 studies. Among 11 cohort studies, the risk of developing pancreatic cancer increased by 79% in patients with IBD (RR = 1.79 [95% CI: 1.16-2.75]; I2 = 95.7%). Patients either with Crohn's disease (RR = 1.42 [95% CI: 1.24-1.63]) or ulcerative colitis (RR = 1.50 [95% CI: 1.17-1.92]) had increased risk (p for interaction = 0.72). The annual incidence of pancreatic cancer potentially attributable to IBD increased by 55 cases (95% CI: 17-103) per million. Two MR studies demonstrated that genetic liability to IBD was associated with an increased risk of pancreatic cancer.

Our results suggest a moderate increase in the risk of pancreatic cancer in patients with IBD, which may be further heightened by genetic predisposition to IBD. The increased risk of pancreatic cancer is probably similar in Crohn's disease and ulcerative colitis.

Inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), is a heterogeneous state of chronic intestinal inflammation. Intestinal innate immunity, including innate immune cells, defends against pathogens and excessive entry of gut microbiota, while preserving immune tolerance to resident intestinal microbiota, and may be characterized by its capacity to produce a rapid and nonspecific reaction. The association between microbiota dysbiosis and the pathogenesis of IBD is complex and dynamic. When the intestinal ecosystem is in dysbiosis, the reduced abundance and diversity of intestinal gut microbiota make the host more vulnerable to the attack of exogenous and endogenous pathogenic gut microbiota. The aim of our study was to comprehensively assess the relationship between microbial populations within UC, the signaling pathways of pathogenic gut microbe therein and the inflammatory response, as well as to understand the effects of using PE&AFWE (poppy extract [Papaver nudicaule L.] and Artemisia frigida Willd. extract) on UC modulation.

A UC mouse model was established by inducing SPF-grade C57BL/6 mice using dextrose sodium sulfate (DSS). Based on metagenomic sequencing to characterize the gut microbiome, the relationship between gut microbiota dysbiosis and gut microbiota was further studied using random forest and Bayesian network analysis methods, as well as histopathological analysis.

(1) We found that the 5 gut microbiota with the highest relative abundance of inflammatory bowel disease UC model gut microbiota were consistent with the top 5 ranked natural bacteria. There were three types of abundance changes in the model groups: increases (Chlamydiae/Proteobacteria and Deferribacteres), decreases (Firmicutes), and no significant changes (Bacteroidetes). The UC model group was significantly different from the control group, with 1308 differentially expressed species with abundance changes greater than or equal to 2-fold. (2) The proportion of the fecal flora in the UC group decreased by 37.5% in the Firmicutes and increased by 14.29% in the proportion of Proteobacteria compared to the control group before treatment. (3) The significantly enriched and increased signaling pathways screened were the 'arachidonic acid metabolic pathway' and the 'phagosomal pathway', which both showed a decreasing trend after drug administration. (4) Based on the causal relationship between different OTUs and the UC model/PE&AFWE administration, screening for directly relevant OTU networks, the UC group was found to directly affect OTU69, followed by a cascade of effects on OTU12, OTU121, OTU93, and OTU7, which may be the pathway of action that initiated the pathological changes in normal mice. (5) We identified a causal relationship between common differentially expressed OTUs and PE&AFWE and UC in the pre- and post-PE&AFWE-treated groups. Thereby, we learned that PE&AFWE can directly affect OTU90, after which it inhibits UC, inhibiting the activity of arachidonic acid metabolic pathway by affecting OTU118, which in turn inhibits the colonization of gut microbiota by OTU93 and OTU7. (6) Histopathological observation and scoring (HS) of the colon showed that there was a significant difference between the model group and the control group (p < 0.001), and that there was a significant recovery in both the sulfasalazine (SASP)and the PE&AFWE groups after the administration of the drug (p < 0.0001).

We demonstrated causal effects and inflammatory metabolic pathways in gut microbiota dysbiosis and IBD, with five opportunistic pathogens directly contributing to IBD. PE&AFWE reduced the abundance of proteobacteria in the gut microbiota, and histopathology showed significant improvement.

Crohn's disease, a chronic inflammatory process of the gastrointestinal tract defined by flares and periods of remission, is increasing in incidence. Despite advances in multimodal medical therapy, disease progression often necessitates multiple operations with high morbidity. The inability to treat Crohn's disease successfully is likely in part because the etiopathogenesis is not completely understood; however, recent research suggests the gut microbiome plays a critical role. How traditional perioperative management, including bowel preparation and preoperative antibiotics, further changes the microbiome and affects outcomes is not well described, especially in Crohn's patients, who are unique given their immunosuppression and baseline dysbiosis. This paper aims to outline current knowledge regarding perioperative management of Crohn's disease, the evolving role of gut dysbiosis, and how the microbiome can guide perioperative considerations with special attention to perioperative antibiotics as well as treatment of Mycobacterium avium subspecies paratuberculosis. In conclusion, dysbiosis is common in Crohn's patients and may be exacerbated by malnutrition, steroids, narcotic use, diarrhea, and perioperative antibiotics. Dysbiosis is also a major risk factor for anastomotic leak, and special consideration should be given to limiting factors that further perturb the gut microbiota in the perioperative period.

Genetic factors of chronic intestinal ulcers are increasingly garnering attention. We present a case of chronic intestinal ulcers and bleeding associated with mutations of the activin A receptor type II-like 1 (ACVRL1) and phospholipase A2 group IVA (PLA2G4A) genes and review the available relevant literature.

A 20-year-old man was admitted to our center with a 6-year history of recurrent abdominal pain, diarrhea, and dark stools. At the onset 6 years ago, the patient had received treatment at a local hospital for abdominal pain persisting for 7 d, under the diagnosis of diffuse peritonitis, acute gangrenous appendicitis with perforation, adhesive intestinal obstruction, and pelvic abscess. The surgical treatment included exploratory laparotomy, appendectomy, intestinal adhesiolysis, and pelvic abscess removal. The patient's condition improved and he was discharged. However, the recurrent episodes of abdominal pain and passage of black stools started again one year after discharge. On the basis of these features and results of subsequent colonoscopy, the clinical diagnosis was established as inflammatory bowel disease (IBD). Accordingly, aminosalicylic acid, immunotherapy, and related symptomatic treatment were administered, but the symptoms of the patient did not improve significantly. Further investigations revealed mutations in the ACVRL1 and PLA2G4A genes. ACVRL1 and PLA2G4A are involved in angiogenesis and coagulation, respectively. This suggests that the chronic intestinal ulcers and bleeding in this case may be linked to mutations in the ACVRL1 and PLA2G4A genes. Oral Kangfuxin liquid was administered to promote healing of the intestinal mucosa and effectively manage clinical symptoms.

Mutations in the ACVRL1 and PLA2G4A genes may be one of the causes of chronic intestinal ulcers and bleeding in IBD. Orally administered Kangfuxin liquid may have therapeutic potential.

Inflammatory bowel disease (IBD) is a collective term for a group of chronic inflammatory enteropathies which are characterized by intestinal inflammation and persistent or frequent gastrointestinal signs. This disease affects more than 3.5 million humans worldwide and presents some similarities between animal species, in particular, dogs and cats. Although the underlying mechanism that triggers the disease is not yet well understood, the evidence suggests a multifactorial etiology implicating genetic causes, environmental factors, microbiota imbalance, and mucosa immune defects, both in humans and in dogs and cats. Conventional immunomodulatory drug therapies, such as glucocorticoids or immunosuppressants, are related with numerous adverse effects that limit its long-term use, creating the need to develop new therapeutic strategies. Mesenchymal stromal cells (MSCs) emerge as a promising alternative that attenuates intestinal inflammation by modulating inflammatory cytokines in inflamed tissues, and also due to their pro-angiogenic, anti-apoptotic, anti-fibrotic, regenerative, anti-tumor, and anti-microbial potential. However, this therapeutic approach may have important limitations regarding the lack of studies, namely in veterinary medicine, lack of standardized protocols, and high economic cost. This review summarizes the main differences and similarities between human, canine, and feline IBD, as well as the potential treatment and future prospects of MSCs.

The aim of this study was to assess the prevalence of malnutrition risk in patients with IBD using different scales to evaluate their usefulness as first-step screening tools for the diagnosis of malnutrition using the GLIM criteria in patients with inflammatory bowel disease. This study included 82 patients with IBD. The Mini Nutritional Assessment, Malnutrition Universal Screening Tool, Saskatchewan IBD-Nutrition Risk and Malnutrition Screening Tool were used to assess malnutrition risk in the study group. In order to diagnose malnutrition, the GLIM criteria were used. According to the GLIM recommendations, malnutrition was diagnosed in 60 patients with IBD (73.17%). Depending on the applied screening tools, the prevalence of moderate and/or high-risk malnutrition in patients with IBD ranged from 20.25% to 43.59%. The highest level of accuracy (ACC) was noted for the MST and MUST questionnaires (92.50% and 90%, respectively), followed by the SASKIBD-NR test (89.97%) and the MNA questionnaire (83.33%). The results of our study indicate a high prevalence of malnutrition in patients with IBD. Thus, there is a need to conduct routine assessments of malnutrition risk using validated scales. The MUST scale seems promising in the assessment of malnutrition risk in patients with IBD as a first step in the assessment of malnutrition using the GLIM criteria.

Inflammatory bowel diseases are a conglomerate of disorders causing inflammation of the gastrointestinal tract, which have gained a significant increase in prevalence in the 21st century. As they present a challenge in the terms of diagnosis as well as treatment, IBDs can present an overwhelming impact on the individual and can take a toll on healthcare costs. Thus, a quick and precise diagnosis is required in order to prevent the high number of complications that can arise from a late diagnosis as well as a misdiagnosis. Although endoscopy remains the primary method of evaluation for IBD, recent trends have highlighted various non-invasive methods of diagnosis as well as reevaluating previous ones. This review focused on the current non-invasive methods in the diagnosis of IBD, exploring their possible implementation in the near future, with the goal of achieving earlier, feasible, and cheap methods of diagnosis as well as prognosis in IBD.

We investigated the role of ChiA and its associated polymorphisms in the interaction between Crohn's disease (CD)-associated adherent-invasive Escherichia coli (AIEC) and intestinal mucosa. We observed a higher abundance of chiA among the metagenome of CD patients compared to healthy subjects. In dextran sulfate sodium-induced colitis mice model, AIEC-LF82∆chiA colonization was reduced in ileal, colonic and fecal samples compared to wild-type LF82. The binding of ChiA to recombinant human CHI3L1 or mucus was higher with the pathogenic polymorphism. The strength of ChiA-mucin interaction was 300-fold stronger than ChiA-rhCHI3L1. ChiA was able to degrade mucin to promote its growth and enabled LF82 to get closer to epithelial cells. The pathogenic polymorphism of ChiA had a stronger impact on mucus degradation than on the binding capability of AIEC to adhere to the intestinal epithelium. We observed that ChiA could favor an efficient bacterial invasion of intestinal crypts, and that ChiA, especially its pathogenic polymorphism, gives LF82 an advantage to uptake within Peyer's patches, macrophages and mesenteric lymph nodes. All together, these data support the role of ChiA in the virulence of AIEC and show that it could be a promising target to reduce AIEC colonization in patients with CD.

This study aimed to investigate whether transdiagnostic treatment as well as acceptance and commitment therapy (ACT) could improve treatment adherence and alleviate gastrointestinal symptoms plus perceived stress in patients suffering from irritable bowel syndrome.

Research has shown that people with chronic diseases often have negative attitudes toward medications, especially when they also have psychiatric disorders. This, along with the complex dosing requirements and inadequate knowledge about medication adherence among irritable bowel syndrome patients, can affect the treatment efficacy.

A randomized clinical trial was conducted using a pre-test-post-test design. The statistical population included patients with irritable bowel syndrome referring to Taleghani Hospital in Tehran between winter 2021 and spring 2022. Convenience sampling was used to select 30 individuals, with 15 people assigned to each group. Two types of psychotherapy were provided online and individually to the participants. The desired treatments were given to the transdiagnostic treatment and ACT groups in eight weekly sessions of 45-60 minutes.

There was no significant difference between the transdiagnostic treatment pre-test and ACT regarding perceived stress, medication adherence, and gastrointestinal symptoms (P>0.05). There was no significant difference either between the transdiagnostic treatment and ACT post-test. However, there was a significant difference between the pre-test and post-test phases of ACT regarding adherence, gastrointestinal symptoms, plus perceived stress (P<0.05) and transdiagnostic treatment regarding gastrointestinal symptoms (P<0.05).

Specialists may use transdiagnostic treatment and ACT as effective psychological treatments to alleviate gastrointestinal symptoms and perceived stress, thereby increasing treatment adherence in patients with irritable bowel syndrome.

Inflammatory bowel disease (IBD) is a multifactorial disease, which is thought to be an interplay between genetic, environment, microbiota, and immune-mediated factors. Dysbiosis in the gut microbial composition, caused by antibiotics and diet, is closely related to the initiation and progression of IBD. Differences in gut microbiota composition between IBD patients and healthy individuals have been found, with reduced biodiversity of commensal microbes and colonization of opportunistic microbes in IBD patients. Gut microbiota can, therefore, potentially be used for diagnosing and prognosticating IBD, and predicting its treatment response. Currently, there are no curative therapies for IBD. Microbiota-based interventions, including probiotics, prebiotics, synbiotics, and fecal microbiota transplantation, have been recognized as promising therapeutic strategies. Clinical studies and studies done in animal models have provided sufficient evidence that microbiota-based interventions may improve inflammation, the remission rate, and microscopic aspects of IBD. Further studies are required to better understand the mechanisms of action of such interventions. This will help in enhancing their effectiveness and developing personalized therapies. The present review summarizes the relationship between gut microbiota and IBD immunopathogenesis. It also discusses the use of gut microbiota as a noninvasive biomarker and potential therapeutic option.

Crohn's Disease (CD) is an Inflammatory Bowel Disease and is characterized by an immune-mediated nature. Its etiology results from the interaction between genetic, enviromental and microbial factors. Regarding pathophysiology, it involves high levels of interleukin (IL)-12, IL-17, and Th1 profile, along with loss of tolerance mechanisms, an increase in pro-inflammatory interleukins, beyond the possibility to affect any part of the gastrointestinal tract. Its symptoms include abdominal pain, chronic diarrhea, weight loss, anorexia, and fatigue, as well as blood in the stool or rectum. Additionally, conditions comprising musculoskeletal, cutaneous, ocular, hepatic, and hematological alterations may be associated with this scenario and extra-intestinal presentation, such as erythema nodosum, anterior uveitis, osteoporosis, and arthritis can also occur. Today, clinical history, exams as fecal calprotectin, ileocolonocopy, and capsule endoscopy can be performed in the diagnosis investigation, along with treatments to induce and maintain remission. In this sense, anti-inflammatory drugs, such as corticosteroids, immunomodulators, and biological agents, as well as surgery and non-pharmacological interventions plays a role in its therapy. The aim of this review is to bring more current evidence to clinical management of CD, as well as to briefly discuss aspects of its pathophysiology, surveillance, and associated disorders.

Crohn's disease (CD) is a chronic inflammatory granulomatous disease that can affect the entire gastrointestinal tract. It is characterized by various extraintestinal manifestations (EIMs), of which oral manifestations (OMs) are often possible. One of the possible OMs is periodontal disease (PD), a chronic inflammatory condition of the supporting tissues of the teeth. This study aimed to show the existence of a mutual relationship between the clinical activity of PD and the clinical and endoscopic activity of CD.

One clinical and two endoscopic indexes were used for the assessment of CD activity and clinical attachment loss (CAL), bleeding on probing (BOP), pocket probing depth (PPD), and radiographic bone loss (RBL) in a dental panoramic tomogram to assess PD in CD patients.

A total of 38 patients underwent the entire study process, of which 20 patients had CD and 18 patients had CD and PD. Considering all CD activity scores, there were 26 patients with active disease; half of them had PD, and 85.7% of operated patients had active CD. The values of CAL, PPD, BOP, and RBL were higher in active CD patients than those in remission, except for BOP when comparing to the CDAI score, which was higher in those in remission of CD.

The results of this study indicate that there is a connection between the activity of CD and worse conditions of the supporting tissues of the gums in the oral cavity, so it is important to keep in mind the necessity of referring patients with CD to a dentist for timely and adequate therapeutic measures.