Introduction

Improving the adenoma detection rate (ADR) can contribute to reducing the incidence and mortality of post-colonoscopy colorectal cancer (PCCRC). Texture and color enhancement imaging (TXI) enhances subtle tissue textures, selectively brightens dark areas, and emphasizes the differences between red and white colors^1,2. Several studies have investigated the visibility and color differences of TXI in vitro and reported its superiority over WLI^3-7. However, A few studies have evaluated the ADR of colonoscopy with TXI, which is a novel image-enhancing technology. This study aims to compare the detection of colorectal polyps using TXI to that using white light imaging (WLI).

Aims & Methods

This study was conducted retrospectively in a single center using propensity-matched scoring based on the patients’ baseline characteristics, such as age, sex, indication, bowel preparation, endoscopist, colonoscope type, and withdrawal time. This study compared the effectiveness of WLI and TXI in patients who underwent chromocolonoscopy with indigo carmine spraying. The study determined the differences in the adenoma, including high-risk adenoma, and sessile serrated lesion (SSL) detection rates and the mean number of detected adenomas and SSLs per colonoscopy between the TXI and WLI groups. High-risk adenomas were defined as three or more adenomas, an adenoma ≥10 mm, an adenoma with a villous component, and an adenoma with high-grade dysplasia. The Wald test with logistic regression was used to analyze the P values.

Results

After propensity score matching, 1970 patients were enrolled into each imaging modality group. The mean patient age was 57.2 ± 12.5 years, and 44.5% of the cohort were men. The ADR was higher in the TXI group than in the WLI group (55.0% vs. 49.4%, odds ratio: 1.25). High-risk ADR were more common in the TXI group than in the WLI group (17.6% vs. 12.8%; OR: 1.45). The mean number of adenomas per colonoscopy (APC) was higher in the TXI group than in the WLI group (1.187 vs. 0.943, OR: 1.12). APC with a 0-II morphology according to the Paris classification (1.093 vs. 0.848, OR: 1.14) and APC of <6 mm (0.992 vs. 0.757, OR: 1.16) were higher in the TXI group than in the WLI group. The adenoma plus SSL detection rate (ASDR) was higher in the TXI group than in the WLI group (58.8% vs. 53.2%, OR: 1.25). The mean number of adenomas plus SSLs per colonoscopy (ASPC) was greater in the TXI group than in the WLI group (1.287 vs. 1.025, OR: 1.13, Table).

Conclusion

A randomized controlled trial⁸ and a cross-over study⁹ previously showed that the ADR of TXI was higher than that of WLI. In this study, we found that the ADR, high-risk ADR, APC, ASDR, and ASPC of TXI were higher than those of WLI after propensity-score matching of patients who underwent chromoendoscopy. TXI may help prevent PCCRC.

References

1 Sato T. TXI: Texture and Color Enhancement Imaging for Endoscopic Image Enhancement. J Healthc Eng 2021; 2021.
2 Tani Y, et al. Gastrointestinal: Texture and color enhancement imaging is useful for detection of small gastric adenocarcinoma of fundic-gland type. J Gastroenterol Hepatol 2024.
3 Nishizawa T, et al. TXI (Texture and Color Enhancement Imaging) for Serrated Colorectal Lesions. J Clin Med 2021.
4 Toyoshima O, et al. Texture and color enhancement imaging in magnifying endoscopic evaluation of colorectal adenomas. World J Gastrointest Endosc 2022.
5 Tamai N, et al. Visibility evaluation of colorectal lesion using texture and color enhancement imaging with video. DEN Open 2022.
6 Yoshida N, et al. Analysis of Texture and Color Enhancement Imaging for Improving the Visibility of Non-polypoid Colorectal Lesions. Dig Dis Sci 2022.
7 Hiramatsu T, et al. Improved visibility of colorectal tumor by texture and color enhancement imaging with indigo carmine. World J Gastrointest Endosc 2023.
8. Antonelli G, et al. Texture and color enhancement imaging versus high definition white-light endoscopy for detection of colorectal neoplasia: a randomized trial. Endoscopy 2023.
9. Sakamoto T, et al. Detection of colorectal adenomas with texture and color enhancement imaging: Multicenter observational study. Dig Endosc 2023.

Disclosure

​Nothing

Introduction

Cyclical monoclonal antibody (mAB) therapy, defined as intermittent pausing of biological agents to reduce drug cost and risk of adverse events, has been proposed as a treatment strategy. There are few prospective discontinuation studies; most are uncontrolled, have small sample sizes, are retrospective, are short term, and do not directly compare multiple mABs. It is therefore unknown if treatment persistence is impaired following a drug holiday versus their initial trajectory. Whether persistence loss differs between mABs, is mitigated by immunomodulators or shorter drug holidays, is also unknown.

Aims & Methods

We aimed to evaluate the persistence of Crohn’s disease (CD) mABs with- and without drug holiday using a real world data registry. We interrogated the prospective population-based Persistence Australian National IBD Cohort (PANIC)5 registry of CD subjects up until Dec 2021. The PANIC registry includes the entire Australian population on advanced therapies. Drug holiday was defined as mAB discontinuation with recommencement of the same mAB after a >6-month dispensing gap. Non-persistence was defined as subsequent cessation of treatment for >6-months. Kaplan Meier survival curves were generated for persistence and compared using the log-rank test. Propensity score matched Cox proportional hazards regression models calculated hazard ratios (HR) and 95% confidence intervals (CI). P<0.05 was deemed statistically significant (SPSS, IBM, USA).

Results

In total 19,078 consecutive CD subjects (44.5% male, median age 39.0 years, 79,677 patient-years of prospective follow-up) were identified with 3,383 episodes of drug holiday (mean duration of 414 days) versus 28,584 episodes of continuous treatment as controls. Patients who resumed mAB therapy following a drug holiday had a statistically significant lower median persistence of 23 months versus 41 months for controls (-18 months; HR: 0.63, 95% CI: 0.60-0.66, P<0.001). TNF inhibitors (TNFi) and ustekinumab (UST) demonstrated significant loss of persistence following a drug holiday (both P<0.001) but not vedolizumab (P=0.63; Figure 1). Shorter versus longer median drug holiday duration did not impact persistence (P>0.05). Use of immunomodulator abrogated the loss of persistence of UST (P=0.15) but not TNFi (P<0.001). Propensity score matched independent predictors of non-persistence were drug holiday (HR: 0.72 [95%CI: 0:67-0.76]), TNFi, monotherapy, females, and bio-exposed status.

Conclusion

This study that recruited all CD subjects on advanced therapy in Australia showed pausing mAB therapy to be associated with a 37% decline in medication persistence for TNFi and UST, but not VED. Immunomodulator combination therapy mitigated the loss of persistence with UST but not TNFi. mAB drug holiday should be discouraged and closely monitored for disease relapse. These data do not support the cyclical use of mABs.

Disclosure

RL: advisory board: AbbVie, Aspen, BMS, Celgene, Celltrion, Chiesi, Ferring, Glutagen, Hospira, Janssen, Lilly, MSD, Novartis, Pfizer, Prometheus Biosciences, Takeda; research grants: Joanna Tiddy USYD, McCusker Charitable Foundation, Celltrion, Shire, Janssen, Takeda, Gastroenterological Society of Australia, NHMRC, Gutsy Group, Pfizer, MRFF

Introduction

Nonalcoholic fatty liver disease (NAFLD) is a widespread metabolic disorder associated with intestinal dysbiosis, low-grade systemic inflammation, and small intestinal bacterial overgrowth (SIBO). Targeting the gut-liver axis through microbiome-modulating therapies may represent a promising approach to disease management.

Aims & Methods

The aim was to investigate gut microbiota alterations in NAFLD patients and assess the efficacy of microbiota-based therapy on metabolic, inflammatory, and structural liver parameters. The study included 152 NAFLD patients and 47 controls. Gut microbiota composition was evaluated using qRT-PCR, and SIBO was diagnosed via hydrogen breath testing. The therapeutic protocol included rifaximin (200 mg TID for 14 days), Saccharomyces boulardii CNCM I-745 (1 capsule BID for 30 days), and essential phospholipids (600 mg TID for 30 days). Liver function tests, inflammatory markers, and steatometry were assessed before and after treatment.

Results

Alterations in gut microbiota composition indicative of dysbiosis—including increased Firmicutes/Bacteroides ratio and Actinobacteria abundance—were identified in NAFLD. Strong correlations emerged between the F/B index and triglycerides (r = 0.78), TNF-α (r = 0.77), and between Actinobacteria and hsCRP (r = 0.66). SIBO rates declined significantly post-treatment (51% → 17%). Liver enzymes, inflammatory markers, and steatometric parameters improved substantially (p<0.05).

Conclusion

Microbiota-targeted therapy combining rifaximin, S. boulardii, and phospholipids effectively corrected dysbiosis, reduced inflammation, improved metabolic parameters, and promoted liver structural recovery in NAFLD patients. These findings support incorporating microbiome-focused interventions into routine clinical practice for NAFLD. ​

Introduction

Ulcerative proctitis (UP) is associated with disabling symptoms such as diarrhea, hematochezia and bowel urgency¹. Adequate therapy is crucial for symptom control and may reduce the risk of proximal disease extension. Although prior studies have explored risk factors for disease progression, they are limited by small sample sizes and have conflicting results^2,3.

Aims & Methods

We aimed to (1) assess the incidence and (2) identify risk factors for disease progression in newly diagnosed UP patients. We included all patients diagnosed with UP (inflammation ≤15 cm beyond the anal verge) between January 2000 and January 2024 in a large, non-academic hospital in the Netherlands. Data were collected from diagnosis until the end of follow-up. Disease progression was defined as endoscopic extension of UP (Montreal E1) to either left-sided (E2) or pancolitis (E3). To avoid overestimating the risk of disease progression, we used a Fine & Gray (F&G) regression model to account for patients in long-term remission who had no in-hospital follow-up. Patients who were referred back to primary care and/or had no in-hospital follow-up for ≥2 years were considered in long-term remission, which was used as a competing event in the F&G model. The cumulative incidence of disease progression was calculated at 1-, 5- and 10-years follow-up and compared to the progression rates of traditional Kaplan-Meier survival estimates.

Results

In total, 486 UP patients were included; 283 (58%) were female and median age at diagnosis was 39 years (IQR 29-53). 371 (76%) patients were in clinical remission at last follow-up. Of those, 291 (78%) were treated with topical and/or oral 5-aminosalicylates (5-ASA) and/or topical steroids; 202 (54%) required only topical and/or oral 5-ASA. 50 (10%) patients had refractory UP and required treatment with immunosuppressants or advanced therapies. During a median follow-up of 6.2 years (IQR 2.1-12.2), disease progression occurred in 112 patients (23%), of whom 80 (16%) progressed to E2 and 32 (6.6%) to E3. Median time to progression was 57 months (IQR 22-103). The cumulative incidence of disease progression was 2.8% (95% CI 1.4-4.4%) at 1 year, 13.2% (95% CI 9.9-16.4%) at 5 years and 23.9% (95% CI 19.4-28.4%) at 10 years after diagnosis and would have been overestimated with traditional Kaplan-Meier analysis (5.1% [95% CI 1.9-8.1%] at 1 year, 24.6% [95% CI 14.9-33.3%] at 5 years and 46.3% [95% CI 30.3-58.6%] at 10 years). F&G analyses demonstrated that age <18 years at diagnosis (HR 2.61, p=0.009) and the absence of steroid-free remission at 3 months (HR 1.97, p=0.005) were significant predictors for disease progression (Table 1).

Conclusion

In this large cohort of newly diagnosed UP patients, the 10-year cumulative incidence of disease progression was 23.9%. Most patients responded well to conventional treatment, as 60% reached clinical remission with only topical and/or oral 5-ASA and/or topical steroids. Absence of steroid-free remission at 3 months and age <18 at diagnosis were significant predictors for disease progression. Better prediction of disease progression could help identify high-risk patients who may benefit from tailored monitoring strategies, as well as low-risk patients that may be suitable for referral back to primary care.

References

1. Meucci G, Vecchi M, Astegiano M, et al. The natural history of ulcerative proctitis: a multicenter, retrospective study. Gruppo di Studio per le Malattie Infiammatorie Intestinali (GSMII). Am J Gastroenterol. 2000;95(2):469-473
2. Huguet JM, Ferrer-Barceló L, Suárez P, et al. Endoscopic progression of ulcerative proctitis to proximal disease. Can we identify predictors of progression?. Scand J Gastroenterol. 2018;53(10-11):1286-1290.
3. Walsh E, Chah YW, Chin SM, et al. Clinical Predictors and Natural History of Disease Extension in Patients with Ulcerative Proctitis. Inflamm Bowel Dis. 2017;23(11):2035-2041.
4. Andersen PK, Geskus RB, de Witte T, Putter H. Competing risks in epidemiology: possibilities and pitfalls. Int J Epidemiol. 2012;41(3):861-870.

Disclosure

RJBP, JH, RAJP, REAvD and AGLB have nothing to disclose. LAAPD has served on advisory boards for Abbvie, Janssen, Galapagos, and Pfizer, and has received independent research funding from Pfizer. ACdV has has served on advisory boards for Takeda, Janssen, Bristol Myers Squibb, Abbvie, Pfizer, and Galapagos and has received unrestricted research grants from Takeda, Janssen, and Pfizer.