Clinical Course Of Inflammatory Bowel Disease Research Articles

P0470 Albumin as a prognostic marker in IBD : Insights from a Tertiary Care Hepato-Gastroenterology Center Experience

Abstract Background Chronic inflammatory bowel diseases (IBD) are persistent conditions characterized by alternating phases of flare-ups and remissions, ranging from mild exacerbations to severe cases, such as those in ulcerative colitis (UC), which may require colectomy and significantly affect patients’ functional and vital outcomes. Over time, several predictive markers, particularly in Crohn’s disease (CD), have been identified at diagnosis. This raises an essential question: could hypoalbuminemia be considered a prognostic factor in the clinical course of IBD? Methods This retrospective descriptive and analytical study spanned 5 years and 2 months (January 2018 to March 2023) and included all IBD patients monitored in our department. Data analysis was conducted using SPSS, with chi-square tests and multivariate logistic regression employed to evaluate relationships Results 302 IBD patients were analyzed, with a mean age of 40.7 years and a female predominance ( sex ratio = 0.7).165 had Crohn’s disease (CD), and 143 had ulcerative colitis (UC), categorized as pancolitis (61 cases), UC E2 (46 cases), and UC E1 (30 cases). In the CD cohort, 30% (50 patients) underwent ileocecal resection. Smoking and alcoholism were reported in 14.9% and 6.6% of cases, respectively, while NSAID and PPI use were noted in 11.5% and 3.3%. Additionally, 8.6% reported phytotherapy use. Hypoalbuminemia was defined as serum albumin ≤35 mg/L, with 32% (97 patients) meeting this criterion. Patients with hypoalbuminemia were treatment-naïve and had serum albumin levels assessed at diagnosis, with follow-up for at least one year. Key findings included • Steroid Use: 78.35% of hypoalbuminemic patients required at least two courses of corticosteroids, compared to 12.68% with normal albumin levels (P=0.003). • Thiopurines and Anti-TNF: Thiopurines were used in 81% of hypoalbuminemic patients vs. 45.8% (P=0.001), and anti-TNF therapy in 42.2% vs. 16.58% (P=0.006). • Colectomy: Rates were higher in hypoalbuminemic patients (17.52%) compared to those with normal albumin (0.4%, P=0.009). • Anemia: Observed in 92.78% of hypoalbuminemic cases vs. 18.53% with normal albumin levels (P=0.001). Notably, only 7.2% of hypoalbuminemic patients were treated with combined oral and rectal 5-ASA, achieving sustained clinical and endoscopic remission over three years. Conclusion In conclusion, our study highlights hypoalbuminemia as a critical prognostic marker in the progression of IBD. Assessing albumin levels at diagnosis, particularly in UC, provides valuable insight for identifying patients at higher risk of severe disease, guiding the need for intensified treatment and closer follow-up. This reinforces the importance of early, comprehensive evaluation in optimizing IBD management strategies

The Role of Vitamin D and Vitamin D Receptor Gene Polymorphisms in the Course of Inflammatory Bowel Disease in Children.

Background: The etiopathogenesis of inflammatory bowel disease (IBD) is still unclear. Prior studies suggest genetic components that may influence the incidence and severity of the disease. Additionally, it was shown that low levels of serum vitamin D may have an impact on the clinical course of the disease due to its effect on the immunological system. Methods: We aimed to investigate the correlation between the incidence of vitamin D receptor (VDR) gene polymorphisms (rs11568820, rs10735810, rs1544410, rs7975232, and rs731236, commonly described as Cdx2, FokI, Bsm, ApaI, and TaqI, respectively) and vitamin D concentration with the clinical course of IBD (disease activity, extent of the intestinal lesions). Data were obtained from 62 patients with IBD (34 with Crohn's disease, 28 with ulcerative colitis), aged 3-18 years, and compared with controls (N = 47), aged 8-18 years. Results: Although there was no difference in the incidence of individual genotypes between the study groups (IBD, C) in all the polymorphisms examined, we described a significant increase in the chance of developing IBD for heterozygotes of Cdx2 (OR: 2.3, 95% CI 0.88-6.18, p = 0.04) and BsmI (OR: 2.07, 95% CI 0.89-4.82, p = 0.048) polymorphisms. The mean serum 25OHD level in patients with IBD was significantly higher compared with the controls (19.87 ng/mL vs. 16.07 ng/mL; p = 0.03); however, it was still below optimal (>30 ng/mL). Furthermore, a significant correlation was found between vitamin D level and TaqI in patients with IBD (p = 0.025) and patients with CD (p = 0.03), as well as with the BsmI polymorphism in patients with IBD (p = 0.04) and patients with CD (p = 0.04). A significant correlation was described between the degree of disease activity and genotypes for the FokI polymorphism in patients with UC (p = 0.027) and between the category of endoscopic lesions and genotypes for the Cdx2 polymorphism also in patients with UC (p = 0.046). Conclusions: The results suggest a potential correlation of VDR gene polymorphism with the chance of developing IBD, and the clinical course of the disease requires further studies in larger group of patients. Vitamin D supplementation should be recommended in both children with inflammatory bowel disease and in healthy peers.

Navigating the Intersection: Sarcopenia and Sarcopenic Obesity in Inflammatory Bowel Disease.

Inflammatory bowel diseases (IBDs) are intricate systemic conditions that can extend beyond the gastrointestinal tract through both direct and indirect mechanisms. Sarcopenia, characterized by a reduction in muscle mass and strength, often emerges as a consequence of the clinical course of IBDs. Indeed, sarcopenia exhibits a high prevalence in Crohn's disease (52%) and ulcerative colitis (37%). While computed tomography and magnetic resonance imaging remain gold-standard methods for assessing muscle mass, ultrasound is gaining traction as a reliable, cost-effective, and widely available diagnostic method. Muscle strength serves as a key indicator of muscle function, with grip strength test emerging nowadays as the most reliable assessment method. In IBDs, sarcopenia may arise from factors such as inflammation, malnutrition, and gut dysbiosis, leading to the formulation of the 'gut-muscle axis' hypothesis. This condition determines an increased need for surgery with poorer post-surgical outcomes and a reduced response to biological treatments. Sarcopenia and its consequences lead to reduced quality of life (QoL), in addition to the already impaired QoL. Of emerging concern is sarcopenic obesity in IBDs, a challenging condition whose pathogenesis and management are still poorly understood. Resistance exercise and nutritional interventions, particularly those aimed at augmenting protein intake, have demonstrated efficacy in addressing sarcopenia in IBDs. Furthermore, anti-TNF biological therapies showed interesting outcomes in managing this condition. This review seeks to furnish a comprehensive overview of sarcopenia in IBDs, elucidating diagnostic methodologies, pathophysiological mechanisms, and clinical implications and management. Attention will also be paid to sarcopenic obesity, exploring the pathophysiology and possible treatment modalities of this condition.

The yin and yang of B cells in a constant state of battle: intestinal inflammation and inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract, defined by a clinical relapse-remitting course. Affecting people worldwide, the origin of IBD is still undefined, arising as a consequence of the interaction between genes, environment, and microbiota. Although the root cause is difficult to identify, data clearly indicate that dysbiosis and pathogenic microbial taxa are connected with the establishment and clinical course of IBD. The composition of the microbiota is shaped by plasma cell IgA secretion and binding, while cytokines such as IL10 or IFN-γ are important fine-tuners of the immune response in the gastrointestinal environment. B cells may also influence the course of inflammation by promoting either an anti-inflammatory or a pro-inflammatory milieu. Here, we discuss IgA-producing B regulatory cells as an anti-inflammatory factor in intestinal inflammation. Moreover, we specify the context of IgA and IgG as players that can potentially participate in mucosal inflammation. Finally, we discuss the role of B cells in mouse infection models where IL10, IgA, or IgG contribute to the outcome of the infection.

Severe acute respiratory syndrome coronavirus 2 infection does not worsen the course of inflammatory bowel disease in the long term.

The long-term outcome of inflammatory bowel disease (IBD) patients after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is under investigation. To assess, in a prospective study, whether a recent SARS-CoV-2 infection increases the risk of IBD relapse within 12 months. From March to April 2021, all IBD patients with recent (<2 months) SARS-CoV-2 infection (Cases) were enrolled. For each enrolled Case, four IBD Controls with no history of infection were considered. Clinical course of IBD was recorded for 12 months. Inclusion criteria: well defined diagnosis of IBD; age ≥18 and ≤85 years; 12-month follow-up; consent. Exclusion criteria: incomplete data; SARS-CoV-2 infection after enrollment. Additional inclusion criteria: recent SARS-CoV-2 infection for Cases; no history of SARS-CoV-2 infection for Controls. Data expressed as median [range]. Statistical analysis: Student-t-Test, Mann-Whitney U-test, χ2 test, multivariate logistic regression model [odds ratio (95% confidence interval)], Kaplan-Meier curves. One hundred forty-three IBD patients were enrolled. The analysis included 118 patients (22 met the exclusion criteria, three lost at follow-up): 29 (24.6%) Cases and 89 (75.4%) Controls. Demographic and clinical characteristics were comparable between groups. During the 12-month study, the frequency of IBD relapse was comparable between Cases and Controls [8 (27%) vs 19 (21%); P = 0.65]. At univariate analysis, SARS-CoV-2 infection was not a risk factor for IBD relapse within 12 months [1.5 (0.6-3.9); P = 0.34]. At multivariate analysis, IBD activity at baseline was the only risk factor for relapse [3.2 (1.1-9.1); P = 0.03]. Kaplan-Meier curves showed that survival from IBD relapse was comparable between Cases and Controls (P = 0.33). In a prospective 12-month study, a recent SARS-CoV-2 infection did not increase the risk of clinical relapse of IBD in the long term.

Atopic dermatitis is associated with the clinical course of inflammatory bowel disease

Objectives There are a few studies about the relationship between inflammatory bowel disease (IBD) and atopic dermatitis (AD). It is implied that both diseases have common pathophysiologic mechanisms and can affect each other. However, little information is available on the effect of AD on the clinical course of patients with IBD. Methods This is a multi-center, retrospective, observational study. We define AD as a chronic eczematoid dermatosis diagnosed by dermatologists. Patients with concurrent IBD and AD were defined as a case group. Age, gender, and IBD subtype-matched patients without AD were included as a reference group. Results The numbers of patients in the case and reference groups were 61 and 122 respectively. There was a significantly shorter biologics-free survival in the case group than that in the reference group according to the multivariable-adjusted Cox regression analysis with the onset age, disease duration, smoking status, use of steroid, use of immunomodulator, initial C-reactive protein, initial erythrocyte sedimentation rate, presence of other allergic diseases and initial disease severity [hazard ratio (HR) 1.828, 95% confidence interval (CI) 1.022–3.271, p = .042]. The trend was consistent in the subgroup analysis with ulcerative colitis (HR 3.498, 95% CI 1.066–11.481, p = .039), but not with Crohn’s disease (HR 1.542, 95% CI 0.720–3.301, p = .265). Conclusions AD showed a significant effect on the biologics-free survival of patients with IBD and especially the UC subtype. Further mechanistic research is required to elucidate the pathogenesis of AD on the clinical course of IBD.

Positive correlation between latent Epstein-Barr virus infection and severity of illness in inflammatory bowel disease patients.

Emerging studies indicate the critical involvement of microorganisms, such as Epstein-Barr virus (EBV), in the pathogenesis of inflammatory bowel disease (IBD). Immunosuppressive therapies for IBD can reactivate latent EBV, complicating the clinical course of IBD. Moreover, the clinical significance of EBV expression in B lymphocytes derived from IBD patients' intestinal tissues has not been explored in detail. To explore the clinical significance of latent EBV infection in IBD patients. Latent EBV infection was determined by double staining for EBV encoded RNA and CD20 in colon specimens of 43 IBD patients who underwent bowel resection. Based on the staining results, the patients were divided into two groups, according to their latent EBV infection states - negative (n = 33) and positive (n = 10). Illness severity of IBD were assigned according to Crohn's disease activity index (ulcerative colitis) and Mayo staging system (Crohn's disease). The clinic-pathological data were analyzed between the two different latent EBV groups and also between the mild-to-moderate and severe disease groups. Systolic pressure (P = 0.005), variety of disease (P = 0.005), the severity of illness (P = 0.002), and pre-op corticosteroids (P = 0.025) were significantly different between the EBV-negative and EBV-positive groups. Systolic pressure (P = 0.001), variety of disease (P = 0.000), pre-op corticosteroids (P = 0.011) and EBV infection (P = 0.003) were significantly different between the mild-to-moderate and severe disease groups. IBD patients with latent EBV infection may manifest more severe illnesses. It is suggested that the role of EBV in IBD development should be further investigated, latent EBV infection in patients with serious IBD should be closely monitored, and therapeutic course should be optimized.

Rising Incidence of Inflammatory Bowel Disease in South Asian Children in New Zealand-A Retrospective Population-Based Study.

High rates of inflammatory bowel disease (IBD) are reported in children of South Asian (SA) descent in some western countries. This population-based study describes the incidence and clinical course of IBD in SA children compared to non-South Asian (NSA) children in New Zealand (NZ). Children (≤15 years) with new-onset IBD presenting to a centralized tertiary referral center in Auckland, NZ from 2010 to 2020 were identified. Disease phenotype, clinical characteristics, response to exclusive enteral nutrition, clinical remission rates at 3 and 12 months, biologic use, corticosteroid exposure, and disease complications were compared by ethnicity; IBD incidence was calculated. There were 127 (26 SA; 101 NSA) children with Crohn disease, 41 (10 SA; 31 NSA) with ulcerative colitis, and 10 (3 SA; 7 NSA) with IBD-unclassified. IBD incidence in SA and NSA children was 14.1 per 100,000 and 4.3 per 100,000 respectively ( P < 0.001). IBD incidence increased by 5.6% per year ( P = 0.022), due to a greater rise in incidence in SA (SA 16.8% per year, P = 0.015; NSA 4.5% per year, P = 0.317). At presentation, SA children had worse biochemical parameters, severe colitis, and vitamin D deficiency. SA children had lower rates of remission following exclusive enteral nutrition (28.5% vs 65.0%, P < 0.001) or biologic induction (35.7% vs 70.8%, P = 0.020), at 3-month (35.3% vs 69.8%, P < 0.001) and 12-month follow-up (29.4% vs 55.0%, P = 0.005). No significant differences were found in disease location or corticosteroid burden. Increasing incidence of IBD was disproportionately represented by SA children with more severe disease and lower remission rates following exclusive enteral nutrition or biologic therapy.

P135 Atopic dermatitis is associated with the clinical course of inflammatory bowel disease

Abstract Background There are a few studies about the relationship between inflammatory bowel disease (IBD) and atopic dermatitis (AD). It implies that both diseases have common pathophysiologic mechanisms and can affect each other. However, little information is available on the effect of AD on the clinical course of patients with IBD. Methods This is a multicenter, retrospective, observational study. Patients with concurrent IBD and AD were defined as case group. AD was defined as chronic eczematoid dermatosis diagnosed by dermatologists. Age-, gender-, and IBD subtype-matched patients without AD were included as reference group. The ratio of the case and reference group is 1:2. Results The numbers of patients in the case and reference group were 61 and 122, respectively. There was a significantly shorter biologics-free survival in the case group than that in the reference one after the multivariable adjusted Cox regression analysis with the onset age, disease duration, smoking status, use of steroid, use of immunomodulator, presence of other allergic diseases and initial disease severity [hazard ratio (HR) 1.743, 95% confidence interval (CI) 1.048-2.901, p = 0.032]. The trend was shown consistently in the subgroup analysis with ulcerative colitis (HR 4.769, 95% CI 1.625-13.995, p = 0.004), but not with Crohn’s disease (HR 1.393, 95% CI 0.736-2.636, p = 0.308). Conclusion AD showed a significant effect on the biologics-free survival of patients with IBD, especially UC. Further mechanistic research is required to elucidate the pathogenesis of AD on the clinical course of IBD.

New insights into bacterial mechanisms and potential intestinal epithelial cell therapeutic targets of inflammatory bowel disease.

The global incidence of inflammatory bowel disease (IBD) has increased rapidly in recent years, but its exact etiology remains unclear. In the past decade, IBD has been reported to be associated with dysbiosis of gut microbiota. Although not yet proven to be a cause or consequence of IBD, the common hypothesis is that at least some alterations in the microbiome are protective or pathogenic. Furthermore, intestinal epithelial cells (IECs) serve as a protective physical barrier for gut microbiota, essential for maintaining intestinal homeostasis and actively contributes to the mucosal immune system. Thus, dysregulation within the intestinal epithelium increases intestinal permeability, promotes the entry of bacteria, toxins, and macromolecules, and disrupts intestinal immune homeostasis, all of which are associated with the clinical course of IBD. This article presents a selective overview of recent studies on bacterial mechanisms that may be protective or promotive of IBD in biological models. Moreover, we summarize and discuss the recent discovery of key modulators and signaling pathways in the IECs that could serve as potential IBD therapeutic targets. Understanding the role of the IECs in the pathogenesis of IBD may help improve the understanding of the inflammatory process and the identification of potential therapeutic targets to help ameliorate this increasingly common disease.

Depression is associated with increased disease activity in patients with ulcerative colitis: A propensity score-matched analysis using a nationwide database in Japan.

The incidence and prevalence of psychiatric disorders are elevated in patients with inflammatory bowel disease (IBD). Whether psychiatric disorders could affect the clinical course of IBD is uncertain and controversial. We aimed to evaluate the impact of psychiatric disorders, particularly depression, on the clinical course of IBD using a nationwide database in Japan. We collected data on admissions with IBD using the Diagnosis Procedure Combination database system introduced in Japan. We divided eligible admissions into IBD with and without depression groups using propensity score matching and compared the rates of surgery, use of molecular targeted drugs and biologics, systemic steroid administrations, and in-hospital death. We also conducted a logistic regression analysis to identify clinical factors affecting surgery, the use of molecular targeted drugs and biologics, and systemic steroid administrations. The rates of surgery, use of two or more molecular targeted drugs, systemic steroid administrations, and in-hospital deaths in the ulcerative colitis (UC) with depression group were higher than in the UC without depression group. Multivariate analysis of UC showed that depression increased the odds of systemic steroid administrations, use of two or more molecular targeted drugs, and surgery. However, analysis of Crohn's disease showed that only steroid administrations were associated with depression. Our study demonstrated an association between a worse clinical course of UC and depression. Although this result indicates that depression might be associated with increased disease activity in patients with UC, the causal relationship is still unclear. Further prospective studies are warranted.

Histopathological assessment of the microscopic activity in inflammatory bowel diseases: What are we looking for?

Advances in diagnostics of inflammatory bowel diseases (IBD) and improved treatment strategies allowed the establishment of new therapeutic endpoints. Currently, it is desirable not only to cease clinical symptoms, but mainly to achieve endoscopic remission, a macroscopic normalization of the bowel mucosa. However, up to one-third of IBD patients in remission exhibit persisting microscopic activity of the disease. The evidence suggests a better predictive value of histology for the development of clinical complications such as clinical relapse, surgical intervention, need for therapy escalation, or development of colorectal cancer. The proper assessment of microscopic inflammatory activity thus became an important part of the overall histopathological evaluation of colonic biopsies and many histopathological scoring indices have been established. Nonetheless, a majority of them have not been validated and no scoring index became a part of the routine bioptic practice. This review summarizes a predictive value of microscopic disease activity assessment for the subsequent clinical course of IBD, describes the most commonly used scoring indices for Crohn's disease and ulcerative colitis, and comments on current limitations and unresolved issues.

Protective SARS-CoV-2 Antibody Response in Children With Inflammatory Bowel Disease.

BackgroundTo date, there's no evidence of an increased risk of SARS-CoV-2 infection or more severe COVID-19 in patients with inflammatory bowel disease (IBD). However, whether COVID-19 alters the clinical course of IBD or whether IBD treatment affects the immunological response to SARS-CoV-2 is still under investigation, especially in children.AimTo assess the serological response to SARS-CoV-2 in children with IBD, and to evaluate the impact of COVID-19 on the clinical course of IBD.Material and MethodsThis prospective study enrolled children (0–18 years) followed-up at the University Hospital of Padova for IBD, who acquired a confirmed SARS-CoV-2 infection between 02.2020 and 02.2021. The anti-SARS-CoV-2 S-RBD IgG titer was evaluated at 3 months after infection and compared to that of a control group of healthy children matched for age, sex, and COVID-19 severity.ResultsTwelve children with IBD (M = 5; median age 14 years) contracted COVID-19 during the study period. 11/12 patients were under immunomodulatory treatment (4/12 steroids; 6/12 azathioprine; 3/12 anti-TNFs; 2 vedolizumab; 1 ustekinumab). SARS-CoV-2 infection remained asymptomatic in 4/12 children and caused mild COVID-19 in the remaining 8. Mean anti-SARS-CoV-2 IgG S-RBD titer was similar between IBD patients and controls (27.3 ± 43.8 vs. 36.8 ± 35.3 kAU/L, p = ns). No children experienced IBD flares nor required gastroenterological support during the infection period.DiscussionChildren with IBD can mount a protective humoral response against SARS-CoV-2, which is comparable to that of their healthy peers regardless of ongoing immunomodulatory treatment. This study also supports the favorable course of PIBD during COVID-19 and vice-versa.

P310 Atopic dermatitis is associated with the clinical course of Inflammatory Bowel Disease

Abstract Background There are a few studies about the relationship between inflammatory bowel disease (IBD) and atopic dermatitis (AD). It implicates that both diseases have common pathophysiologic mechanism and are able to affect each other. However, little information is available for the effect of AD on the clinical course of patients with IBD. Methods This is a retrospective, observational case-control study. Patients with concurrent IBD and AD were defined as case group and those with IBD only as control group. Diagnosis of AD was defined as chronic eczematoid dermatosis diagnosed by dermatologists. Age-, gender-, and IBD subtype-matched patients with a confirmed diagnosis of IBD were included as control group. The ratio of the case and control group was set as, 1:2. Trend in the duration from diagnosis of IBD to first use of biologics, first IBD-related operation and first IBD-related bowel resection were estimated with Cox regression analysis. Results The numbers of patients in the case and control group were, 31 and, 62, respectively. Compared with the control group, the case group showed an earlier disease onset (unit: years, 22.13 ±, 10.66 vs., 17.68 ±, 8.07, p = 0.043) and longer disease duration of IBD (unit: months, 98.37 ±, 69.24 vs., 150.77 ±, 83.45, p = 0.002). In addition, the proportion of biologics use (35% vs., 61%, p = 0.018) and the total numbers of biologics usages (0.48 ±, 0.76 vs., 1.06 ±, 1.12, p = 0.013) were higher in patients in the case group than those in the control group. In the Cox-regression analysis, there was a significant decrease of the duration for the biologics free survival in the case group compared with the control one after the adjustment with age, IBD subtype, onset age and disease duration (p &amp;lt; 0.001). Conclusion Patients having concurrent IBD and AD exhibited different characteristics compared with those having IBD only, particularly in terms of disease onset and severity. Furthermore, AD showed an significant effect on the time for the initiation of biologics. Further research is required to elucidate the common pathogenesis and the role of AD on the clinical course of IBD.

P626 Anti-TNF monotherapy is associated with an adverse clinical outcome in female Inflammatory Bowel Disease patients who stop Anti-TNF treatment during the third trimester of pregnancy

Abstract Background Anti-TNF drugs are safe during pregnancy in inflammatory bowel disease (IBD), but they cross the placenta most actively in the third trimester, and some guidelines still recommend stopping them during this period. There few data that examines the impact of anti-TNF discontinuation on the clinical course of IBD, so we aimed to explore the clinical outcomes of IBD pregnant patients who stopped anti-TNF at the third trimester. Methods We performed a retrospective, longitudinal study on female IBD patients receiving anti-TNF agents at our IBD clinic. We included IBD pregnant patients who discontinued the anti-TNF in the third trimester of pregnancy, and we matched these cases in a 1:1 ratio with non-pregnant female IBD patients by age, type of IBD, type of anti-TNF, duration of treatment, location, and behavior of IBD. Demographic and clinical variables were collected from 18 months before anti-TNF discontinuation and 12 months after discontinuation, and when available endoscopic indices (SES CD and UC). We determined whether subjects presented any adverse clinical outcome during the follow-up defined as development of disease flare, corticosteroid use, hospital admission, need for surgery, biologic dose escalation, or switch. Results We included 34 pregnant patients and 34 controls. Patients who stopped anti-TNF more frequently presented an adverse clinical outcome during the follow-up year when compared to the control group (47.1% vs. 23.5% p = 0.04) and flare activity (35, 3 vs. 11.8%, p = 0.02). We found no differences in escalation or biologic switch, hospital admission, or surgery between the subjects. We also found an association between the development of an adverse clinical outcome and anti-TNF monotherapy (p=0.009) and a higher SESCD in the previous year (p=0.017). In the multivariate analysis, anti-TNF monotherapy was the only independent factor for developing an adverse clinical outcome up to 1 year after anti-TNF discontinuation (OR: 3.47, CI 95%: 1.16–10.4, p=0.026). Conclusion In our cohort of female IBD patients on anti-TNF, monotherapy was independently associated with an adverse clinical outcome in the following year after anti-TNF discontinuation.

P311 Depression and anxiety are associated with poor clinical outcomes in Inflammatory Bowel Disease: A Nationwide Population-Based Study in South Korea

Abstract Background The increase in prevalence of depression and anxiety disorder in Inflammatory Bowel Disease (IBD) is demonstrated from previous studies, but it is uncertain whether the patients with depression and anxiety are at higher risk of poor outcomes of IBD. Therefore we aimed to determine the impact of depression and anxiety on clinical outcomes in patients with IBD. Methods We conducted a nationwide, population-based retrospective cohort study using the Korean national health insurance claims data between, 2010 and, 2017. Patients with Crohn’s Disease and Ulcerative Colitis were targeted through the registration program for rare/intractable diseases, and patients with depression and anxiety were also identified by the International Classification of Disease, tenth revision (ICD-10) code. The primary outcome of this study is the poor IBD-related outcomes and we defined the poor IBD-related outcomes as IBD-related emergency room visits, hospitalization, and surgery in this study. Results A total of, 36,379 IBD patients (10,754 Crohn’s disease (CD) and, 25,625 ulcerative colitis (UC)) were enrolled in this study between, 2010 and, 2017 and among them, 4,335 (11.9%) had depression/anxiety. Multivariate analysis showed that CD patients with depression/anxiety were at an increased risk of ER visits (HR, 1.858, 95% CI, 1.5–2.301) and hospitalization (HR, 1.727, 95% CI, 1.315–2.269). UC patients with depression/anxiety were also at increased risk for ER visits (HR, 1.339, 95% CI, 1.084–1.654) and hospitalization (HR, 1.367, 95% CI, 1.059–1.764). While the risk of surgery in patients with depression/anxiety was not different from those without depression/anxiety in both CD and UC. Conclusion Depression and anxiety disorder was associated with a higher risk for poor clinical outcomes in patients with IBD. The results of this study suggest that psychologic co-morbidities such as depression and anxiety might improve the clinical course of IBD

High Sugar-Sweetened Beverage Consumption Is Associated with Increased Health Care Utilization in Patients with Inflammatory Bowel Disease: A Multiyear, Prospective Analysis

BackgroundDietary factors like sugar-sweetened beverage (SSB) consumption are known to influence disease course in a variety of illnesses; however, long-term outcomes are not well documented for inflammatory bowel disease. ObjectiveDoes high consumption of SSBs lead to high healthcare utilization (ie, hospitalizations and emergency department visits), inflammation, and disease severity in patients with inflammatory bowel disease? DesignA prospective cohort study was conducted from 2015 to 2019. Patients enrolled in the discovery study cohort were followed for 3 years, whereas patients in the validation cohort were followed for 2 years. They underwent nutrition assessment and received routine care. Dietary intakes of SSBs and fiber were quantified by a validated, self-reported questionnaire. Participants/settingFor the discovery study cohort, 1133 adult patients were recruited from the University of Pittsburgh Medical Center Digestive Disease Clinic in Pittsburgh, PA. Eligible patients had a preexisting diagnosis of Crohn’s disease or ulcerative colitis and had at least annual follow-up at this tertiary referral center. High SSB consumption was defined as 7 or more SSBs per week. Moderate was defined as > 2 but < 7 SSBs per week. Low SSB consumption was defined as 2 or fewer SSBs per week. Main outcome measuresPrimary outcome was time to hospitalization and emergency department visits. Secondary outcomes assessed laboratory markers of disease severity and inflammation. Tertiary outcomes assessed time to hospitalization and emergency department visits in a subsequent independent cohort of patients. Statistical analysis performedMultivariable logistic regression, Kaplan-Meier, and Cox proportional hazards modeling ResultsThe discovery cohort included of 1,133 adult patients with inflammatory bowel disease (58% women, 70% with Chron’s disease, 30% with ulcerative colitis, median age 46 years). Low SSB consumption, moderate SSB consumption, and high SSB consumption occurred in 57%, 17%, and 26% in the discovery cohort, respectively. Among patients without active disease at enrollment, high SSB consumption was associated with decreased time to hospitalization and emergency department visits when compared with low SSB consumption (hazard ratio 1.55, 95% CI 1.06 to 2.27; and hazard ratio 1.53, 95% CI 1.10 to 2.13). In terms of disease severity and inflammatory biomarkers, high SSB consumption was associated with increase odds of elevated erythrocyte sedimentation rate (odds ratio 2.04, 95% CI 1.31 to 3.18), elevated C-reactive protein level (odds ratio 1.60, 95% CI, 1.07-2.37), eosinophilia (odds ratio 1.88, 95% CI 1.06 to 3.335), and monocytosis (odds ratio 1.81, 95% CI 1.18 to 2.79) when compared with low SSB consumption after adjusting for baseline differences. Lastly, the validation cohort produced similar results to our primary outcome (ie, high SSB consumption was associated with decreased time to hospitalization and emergency department visits when compared with low SSB consumption). ConclusionsHigh SSB consumption was associated with decreased time to hospitalization and emergency department visits. Furthermore, high SSB consumption is associated with disease severity biomarkers and inflammation. Prospective studies assessing the therapeutic influence of nutrition counseling and decreased SSB consumption on long-term inflammatory bowel disease clinical course are warranted.

Emerging therapeutic options in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a chronic disease that requires chronic treatment throughout the evolution of the disease, with a complex physiopathology that entails great challenges for the development of new and specific treatments for ulcerative colitis and Crohn´s disease. The anti-tumor necrosis factor alpha therapy has impacted the clinical course of IBD in those patients who do not respond to conventional treatment, so there is a need to develop new therapies and markers of treatment response. Various pathways involved in the development of the disease are known and the new therapies have focused on blocking the inflammatory process at the gastrointestinal level by oral, intravenous, subcutaneous, and topical route. All these new therapies can lead to more personalized treatments with higher success rates and fewer relapses. These treatments have not only focused on clinical remission, but also on achieving macroscopic changes at the endoscopic level and microscopic changes by achieving mucosal healing. These treatments are mainly based on modifying signaling pathways, by blocking receptors or ligands, reducing cell migration and maintaining the integrity of the epithelial barrier. Therefore, this review presents the efficacy and safety of the new treatments that are currently under study and the advances that have been made in this area in recent years.

Natural history of inflammatory bowel disease: a comparison between the East and the West.

Over the past decades, there has been a rapid increase in the incidence and prevalence of inflammatory bowel disease (IBD) in Asia. The natural history of IBD in Asian patients could be different from that in Western patients due to variations in disease phenotypes and genotypes as well as the healthcare environment between the 2 populations. To adequately cope with this disease, it is important to fully understand the potential differences in its natural history among different populations. In this review, we evaluated the differences in the clinical course of IBD between Asian and Western patients with regards to phenotypic progression, hospitalization, major surgery, risk of colorectal cancer, and mortality, mainly based on the results of population-based studies. The findings of our narrative review suggest that the clinical course of Asian patients with IBD, especially ulcerative colitis, is better than that of Western patients, as indicated by the lower rates of major surgery and hospitalization. In addition, similar to Western patients, the clinical course of Asian patients with IBD has been improving as evidenced by the decreasing rates of disease behavior progression (in Crohn's disease), hospitalization, and major surgery.

Clinical Course of Hepatitis B Viral Infection in Patients Undergoing Anti-Tumor Necrosis Factor α Therapy for Inflammatory Bowel Disease.

Background/AimsLittle is known about the clinical course of hepatitis B virus (HBV)-infected patients undergoing anti-tumor necrosis factor α (TNF-α) therapy for inflammatory bowel disease (IBD). We aimed to investigate the clinical course of HBV infection and IBD and to analyze liver dysfunction risks in patients undergoing anti-TNF-α therapy.MethodsThis retrospective multinational study involved multiple centers in Korea, China, Taiwan, and Japan. We enrolled IBD patients with chronic or resolved HBV infection, who received anti-TNF-α therapy. The patients’ medical records were reviewed, and data were collected using a web-based case report form.ResultsOverall, 191 patients (77 ulcerative colitis and 114 Crohn’s disease) were included, 28.3% of whom received prophylactic antivirals. During a median follow-up duration of 32.4 months, 7.3% of patients experienced liver dysfunction due to HBV reactivation. Among patients with chronic HBV infection, the proportion experiencing liver dysfunction was significantly higher in the non-prophylaxis group (26% vs 8%, p=0.02). Liver dysfunction occurred in one patient with resolved HBV infection. Antiviral prophylaxis was independently associated with an 84% reduction in liver dysfunction risk in patients with chronic HBV infection (odds ratio, 0.16; 95% confidence interval, 0.04 to 0.66; p=0.01). The clinical course of IBD was not associated with liver dysfunction or the administration of antiviral prophylaxis.ConclusionsLiver dysfunction due to HBV reactivation can occur in HBV-infected IBD patients treated with anti-TNF-α agents. Careful monitoring is needed in these patients, and antivirals should be administered, especially to those with chronic HBV infection.