Introduction

Eosinophilic esophagitis (EoE) is an emerging disease in Latin America; however, little is known about medical practices related to its diagnosis, treatment, and follow-up. In Chile, the lack of a consensus-based practice guideline may lead to heterogeneous management among physicians. In contrast, standardized approaches and clinical recommendations have been established internationally.

Aims & Methods

To characterize current practices in the diagnosis, management, and follow-up of EoE in Chile.
A 55-item survey was developed to assess various aspects of eosinophilic esophagitis diagnosis, treatment, and monitoring. Five gastroenterologists reviewed a pilot version to evaluate its clarity and relevance. The survey invitation was emailed to all physician members of the Chilean Society of Gastroenterology. Additional open invitations were extended during the 50th Chilean Congress of Gastroenterology and through peer-to-peer contacts. Participants provided informed consent digitally, after which they received a link to complete the survey. The local ethics committee approved the study.

Results

The response rate was 11.9%, with 69 responses analyzed. The mean age of the participants was 50.4 years (SD ±12.77). Most respondents (66.7%) practiced in Santiago, and 91.3% were adult gastroenterologists. A total of 47.8% had more than 20 years of clinical experience, and 49.3% reported treating fewer than five EoE patients per year.
Among respondents, 82.6% generally or always performed esophageal biopsies in cases of dysphagia, and 69.6% for refractory reflux symptoms. The EREFS endoscopic classification was generally or always used by 52.2%. In emergency endoscopies for food impaction, 66.7% reported obtaining biopsies. Furthermore, 81.8% of endoscopists collected six or more biopsies when EoE was suspected.
Proton pump inhibitors (PPIs) were used as first-line therapy by 75.4% of respondents in over 75% of their patients, with esomeprazole being the most commonly prescribed PPI. 24.6% used topical corticosteroid as first-line treatment in over 75% of their patients. The most commonly used was liquid budesonide.
Regarding dietary therapy, whether as monotherapy or in combination with pharmacological treatment, the most frequent strategy was a two-food elimination diet with a step-up approach if needed. A total of 88.4% aimed for histologic remission as a therapeutic goal. In patients in clinical and histological remission without treatment changes, 55% reported follow-up intervals between three and six months.

Conclusion

There is variability among Chilean physicians in the diagnostic and therapeutic approaches to EoE. Most adhere to international biopsy standards and perform appropriately biopsies in patients with dysphagia. Many also align treatment with recommended therapeutic goals. However, biopsy collection during the index emergency endoscopy for food impaction should be reinforced to ensure timely diagnosis and early initiation of treatment. Overall, improved physician education and the development of national guidelines are needed to optimize and standardize the management of EoE in Chile.

Introduction

Endoscopists with baseline adenoma detection rates (ADRs) ≤26% who improve their ADRs significantly reduce their patients’ risk of post-colonoscopy colorectal cancer (PCCRC)¹. The recommended withdrawal time (WT) of 8–9 minutes is associated with higher ADRs; however, it includes time spent on therapeutic interventions, which may overestimate actual inspection time and limit its accuracy as a performance metric².

Aims & Methods

We aimed to determine the corrected withdrawal time (cWT)—defined as WT minus intervention time—required for low-performing endoscopists to achieve ADR thresholds of ≥26 and ≥35.
We prospectively analyzed 1,165 the recorded videos of elective colonoscopies performed by 17 endoscopists at Montreal University Hospital Center (IRB; CER22.013/ CER25.12283). Eligible cases were consecutive adults (≥18 years) undergoing elective colonoscopy. Exclusions were complex resections, sigmoidoscopies, incomplete exams, failed recordings, and procedures by endoscopists with <10 prior cases. A research assistant was present during each procedure and documented all periprocedural metrics in real-time. Endoscopists were stratified as low (ADR ≤25%) or high performers (ADR >25%). The primary outcome was the mean cWT required for low performers to achieve an ADR ≥26%. Secondary outcomes included the cWT needed to reach ADR ≥35% and the incremental impact of each additional minute of cWT on detection metrics. Multivariable generalized estimating equation (GEE) models adjusted for patient demographics, bowel preparation, indication of colonoscopy, time of day/month, CADe use, and endoscopist effect.

Results

Low performers required a mean cWT of 10′58″ to achieve an ADR ≥26%, and 13′51″ to reach ≥35% compared to 4′01″ for high performers. Each additional minute of cWT increased ADR odds by 15.3% for low performers and 5.0% for high performers (P < .001). Similar improvements were observed across all detection metrics (Table 1). For every additional cWT minute, the odds of detecting advanced adenomas increased by 10.1%, sessile serrated lesions (SSLs) by 10.1%, and polyps by 16.5% (all P <  .001). Adenoma and polyp counts increased by 7.5% and 7.9%, respectively. Absolute gains per minute were greater in low performers, with ADR increases exceeding 3% beyond 12 minutes of cWT. After adjusting for covariates, each additional cWT minute was associated with a significant increase in the odds of detection: an increase of 6.5% (P = .002) for adenomas, 9.2% (P < .001) for advanced adenomas, 11.5% (P < .001) for SSLs, and 14.9% (P < 0.01) for polyps. With each additional cWT minute, the adenoma count increased by 7.3% and the polyp count increased by 7.8% (P < .001) (results not shown).

Table 1. Mean Detection Metrics and Their Incremental Increase Per Additional Minute of Corrected Withdrawal Time, Overall and Stratified by High vs Low Performers.

Conclusion

Longer cWT enhanced detection across all metrics, particularly for low performes. These findings support personalized cWT targets based on individual performance rather than uniform WT recommendations.

References

1. Pilonis ND, Spychalski P, Kalager M, et al. Adenoma detection rates by physicians and subsequent colorectal cancer risk. JAMA 2025;333:400–407.
2. Rex DK, Anderson JC, Butterly LF, et al. Quality indicators for colonoscopy. Gastrointest Endosc 2024;100:352–381.

Disclosure

Daniel von Renteln has received research funding from ERBE Elektromedizin GmbH, Ventage, Pendopharm, Fujifilm, and Pentax, and has received consultant or speaker fees from Boston Scientific Inc., ERBE Elektromedizin GmbH, and Pendopharm. Roupen Djinbachian has received speaker fees from Fujifilm. The remaining authors declare that they have no conflict of interest.

Introduction

It is not clear whether the inverse relationship between colonoscopists’ adenoma detection rate (ADR) and post-colonoscopy colorectal cancer (PCCRC) is seamless or subject to “plateau” effect.

Aims & Methods

Aim of the study was to model the pattern of association between ADR and PCCRC. The present study is a systematic review and meta-analysis of studies published up to December 2024 providing the crude incidence rate of PCCRC according to various colonoscopists’ ADR categories. The primary outcome was calculated as the cumulative incidence of PCCRC at the lowest bound of each ADR category, starting from highest to lowest colonoscopists’ ADR. A restricted cubic spline multilevel metaregression analysis was applied to model the inverse association between ADR and cumulative PCCRC.

Results

After applying selection criteria, 7 studies published in 2020-2024, including 2,178,822 patients were included. All studies were conducted in organized CRC screening programs: 5 studies were set in primary colonoscopy screening, whereas 2 studies assessed FIT+ patients undergoing colonoscopy with two different cut-offs (20 µg Hgb/g and 47 µg Hgb/g feces). Four studies were European, and three studies were conducted in the US. Median patient age ranged from 57 to 65 years (see Table 1).
In primary colonoscopy setting (5 studies with 2,025,296 patients), adjusting for standardized follow-up and standardized CRC risk, cumulative incidence of CRC after colonoscopy showed a marked decrease for each 1-unit increase in ADR up to 27%, with a more gradual decline between 27% and 34%. In absolute numbers, assuming a 10-year follow-up period, CRC after colonoscopy ranged from 258/100,000 at 1% ADR, to 228/100,000 at 27% ADR, and 220/100,000 at 34% ADR, yielding a total decrease of 38 CRC after colonoscopy cases per 100,000 patients in 10 years. Beyond this threshold, according to model-based projections, CRC after colonoscopy would be 212/100,000 at 50% ADR, 207/100,000 at 60% ADR, and 197/100,000 at 80% ADR, yielding only an additional decrease of 8 (ADR 50%), 13 (ADR 60%), and 23 (ADR 80%) CRC after colonoscopy cases per 100,000 patients in 10 years, as compared to ADR 34%. Data remained consistent after excluding the study by Pilonis et al. [1], confirming that CRC after colonoscopy plateaus after 34% ADR. Heterogeneity was low (I²=0%) and the visual inspection of the funnel plot revealed some publication bias possibly leading to overestimate the inverse association between ADR and CRC after colonoscopy.
In the FIT-based setting (2 studies, 153,526 patients), quantitative synthesis was not performed owing to the low number of studies and different FIT thresholds (i.e., ≥20 and ≥47 µg Hb/g feces). Nonetheless, when examining the individual studies, there appears to be a more linear decline in post-colonoscopy CRC risk with increasing ADR.

Conclusion

In primary colonoscopy screening, achieving an ADR of at least 27% is essential. While increasing ADR beyond 27% continues to reduce risk, the benefit plateaus beyond ADR 34%, suggesting limited additional clinical advantage. Of note, the absolute risk reduction in CRC after colonoscopy is overall modest. Additional quality measures could provide a more comprehensive assessment of colonoscopy effectiveness.

References

Pilonis ND, Spychalski P, Kalager M, et al. Adenoma Detection Rates by Physicians and Subsequent Colorectal Cancer Risk. JAMA. Published Online First: 16 December 2024.
Wisse PHA, Erler NS, de Boer SY, et al. Adenoma Detection Rate and Risk for Interval Postcolonoscopy Colorectal Cancer in Fecal Immunochemical Test-Based Screening : A Population-Based Cohort Study. Ann Intern Med. 2022;175:1366–73.
Zorzi M, Antonelli G, Barbiellini Amidei C, et al. Adenoma Detection Rate and Colorectal Cancer Risk in Fecal Immunochemical Test Screening Programs : An Observational Cohort Study. Ann Intern Med. 2023;176:303–10.
Schottinger JE, Jensen CD, Ghai NR, et al. Association of Physician Adenoma Detection Rates With Postcolonoscopy Colorectal Cancer. JAMA. 2022;327:2114–22.
Waldmann E, Penz D, Šinkovec H, et al. Interval cancer after colonoscopy in the Austrian National Screening Programme: influence of physician and patient factors. Gut. 2021;70:1309–17.
Lam AY, Li Y, Gregory DL, et al. Association between improved adenoma detection rates and interval colorectal cancer rates after a quality improvement program. Gastrointest Endosc. 2020;92:355-364.e5.
Polychronidis G, He M-M, Vithayathil M, et al. Risk of colorectal neoplasia after removal of conventional adenomas and serrated polyps: a comprehensive evaluation of risk factors and surveillance use. Gut. 2024;73:1675–83.

Clinical Case Summary

A 27-year-old male with diarrhea and rectal bleeding was diagnosed with moderate ulcerative colitis (UC) (Montreal: E3, Mayo endoscopic subscore: 2). He was started on mesalazine 4 g/day and oral prednisolone 40 mg/day, with clinical remission after 2 weeks. Prednisolone was successfully tapered off over the course of 8 weeks. He was not taking other medications. After starting therapy, the patient reported intermittent red urine discoloration, without other symptoms or association with respiratory tract infections.
Extensive investigation of hematuria was negative, including ANA, ANCA, anti-dsDNA and anti-GBM antibodies and imaging studies. Urine samples were macroscopically normal, with no red blood cells, casts or crystals. Urethrocystoscopy and urine cytology were unremarkable. Renal biopsy was considered.
The patient remained on mesalazine, with clinical, analytical and endoscopic response. During one episode, he noticed that the urine only became reddish after contact with toilet water disinfected with bleach. After stopping bleach toilet disinfection, there was no recurrence. He was diagnosed with mesalazine induced pseudohematuria and did not undergo further investigation.
Mesalazine is the first-line treatment for mild-to-moderate UC. Although uncommon, nephrotoxicity has been described and may result in urine discoloration or hematuria. Mesalazine is excreted in the urine and, when in contact with sodium hypochlorite (the active component of household bleach), oxidises, resulting in red-brown urine discoloration. Rare cases of patients reporting similar situations have been described in the literature. The role of gastroenterologists in recognizing this phenomenon is crucial, since mesalazine is a widespread efficient drug with an otherwise favorable safety profile. As our case illustrates, knowledge of this harmless reaction is desirable to avoid additional tests and potentially harmful unnecessary interventions, such as renal biopsy.

References

Figure 1 - Reaction between the urine of a patient taking mesalazine and the sodium hypochlorite present in household bleach (1A - before addition of bleach; 1B - after addition of bleach).

Disclosure

No conflict of interest to declare.

Introduction

Acute upper gastrointestinal bleeding and timing to endoscopy are a recognised as risk factors for mortality. European Guidelines * suggest that the hemodynamical resuscitation could be performed before the endoscopy, however, indications are lacking about the timing of blood transfusions.

Aims & Methods

The aim of the study is to evaluate the transfusion timing to reduce death risk in patients with upper gastrointestinal bleeding. This is a prospective multicentre cohort study, including all consecutive hospitalized patients with upper gastrointestinal bleeding (UGIB). Clinical, endoscopic source of bleeding, medical and endoscopic treatment, time to endoscopy, and timing to transfusion were collected. We adopted the ESGE* guidelines to define the need for transfusion, timing to endoscopy and mortality. We considered timing to transfusion before or after the endoscopic procedure. Statistics: multivariate backward logistic regression was used to estimate the adjusted odds ratio death risk for variables with main clinical relevance or highly statistical significance at univariate analyses. Variables identified by the logistic regression were used into the propensity-score matching to compare the death risk between the two groups.

Results

2,017 out of 3324 patients received a transfusion and were included in the analysis; the mean age was 69.7 [±15.1], male was 1,365 (67.7%); the source of bleeding was non-variceal in 1634 patients (81 %), 178 patients died (8.8%); 69 out of 700 (9.9 %) died in the group transfusion before endoscopy; 109 out 1317 (8.3 %) in the group transfusion after endoscopy with an OR 1.2 (C.I. 95% .86 to 1.68) p<= 0.23. Mortality between the two groups did not significantly differ when haemoglobin levels at admission were considered, nor after adjustment for potential confounding variables, including ASA score, in-hospital bleeding, haematemesis at presentation, shock at admission, altered mental status and timing to endoscopy. Propensity score matching analysis indicated that among patients who received a transfusion, the risk of death decreased when the transfusion was administered before the endoscopy and the haemoglobin level was below 7 g/dL (coefficient = -0.06, p = 0.06; see Table).

Conclusion

Red pack cell transfusions before or after endoscopy did not modify the death risk in patients with acute upper gastrointestinal bleeding; the death risk was less frequent in patients transfused before endoscopy and with a haemoglobin value lower than 7 gr/l. However, this risk increased in those patients transfused before endoscopy and with a haemoglobin value > 8 gr/l.

References

* Ian M. Gralnek et al. Endoscopy 2021; 53: 300–332

Introduction

Individuals with Lynch syndrome (LS) are predisposed to different tumors, including gastric (GC) and duodenal (DC) cancer, especially those with specific mutations or familial aggregation. However, the role of esophagogastroduodenoscopy (EGD) in these patients is still uncertain, with heterogeneous recommendations among different guidelines.

Aims & Methods

To estimate the overall incidence of GC and DC in individuals with LS, to determine the incidence of GC and DC in higher-risk subgroups within these patients, as well as to clarify the usefulness of screening or surveillance by EGD.

Systematic search of Pubmed and Embase for cohort studies and clinical trials from inception to April 2024. Incidences of GC and DC were calculated, as well as the relative risk (RR) and their respective 95% confidence intervals in those studies comparing patients under surveillance with EGD vs without. A meta-analysis was performed using a random-effects model. Heterogeneity was assessed with the I² statistic.

Results

A total of 584 studies were obtained, of which 30 were finally included, with a total of 31264 patients with LS. The overall incidence of GC was 2.04% (95%CI 1.63-2.45). The incidence of GC was 2.60% (95%CI 1.61-3.60) in MLH1 carriers and 2.91% (95%CI 1.63-2.45) in MSH2 carriers. In those with LS and family history, the incidence of GC was 25.94% (95%CI 15.01-36.87). The incidence of DC was 1.61% (95%CI 1.21-2.00).
Only 3 studies compared patients with LS in follow-up with EGD vs those without follow-up, evidencing a protective effect of EGD for GC [RR 0.31 (95%CI 0.14-0.69)], but not for DC [RR 0.65 (95%CI 0.22-1.32)].

Conclusion

The incidence of GC and DC in patients with LS is higher than that of the general population, especially in those patients with MLH1, MSH2 mutations or family aggregation. Surveillance with EGD could help to reduce this incidence through the diagnosis of premalignant lesions.