Introduction

There is a known discrepancy between symptoms reporting and histological disease activity in patients with eosinophilic esophagitis (EoE) such that patients with EoE in histological remission may still report symptoms while patients with histologically active EoE may report few or no symptoms. Esophageal symptom-specific anxiety, hypervigilance, and adaptive behaviours at mealtime may affect dysphagia reporting in EoE but this has not been investigated.

Aims & Methods

We investigated the role of esophageal symptom-specific anxiety, hypervigilance, and adaptive behaviours at mealtime on dysphagia reporting in patients with EoE.
Consecutive adults (>18 years) with histologically active or inactive EoE (i.e., ≥15 or <15 eosinophils/high-power field) at their last upper endoscopy (EGD) were prospectively enrolled. For each patient, esophageal hypervigilance, anxiety, and adaptive behaviours were assessed prior to the EGD by a physician who was blind to patients’ treatment status and histological disease activity. Esophageal anxiety and hypervigilance were assessed using the validated Esophageal Hypervigilance and Anxiety Scale (EHAS) with a 30-day recall, while the validated Dysphagia Symptom Questionnaire (DSQ) and Dysphagia Symptom Score (DSS) were used for quantification of dysphagia. A structured interview (Pisa adaptation questionnaire, PiEAQ) was used for the assessment of adaptive behaviours (including: drinking water to push the bolus, lubricating food, chewing for long, and blending food) over the 30 days prior to the EGD. Kruskal-Wallis Rank Sum Test and Pearson’s Chi-squared were used for comparisons as appropriate. ROC curve analysis was used to calculate the diagnostic accuracy (AUC). Significance threshold was p<0.05.

Results

Seventy-one patients were included. Sixty-two percent (n=44) had histologically active EoE and 38% (n=27) were in histological remission. High anxiety, hypervigilance, and use of adaptive behaviours were found in 49.3%, 46.5%, and 56.3% of patients, respectively. Higher levels of anxiety were associated with an increased severity of dysphagia according to DSQ and DSS scores (p=0.02 and p=0.003, respectively), whereas this was not true for hypervigilance (p=0.79 and p=0.24, respectively). Adaptive behaviours were significantly more commonly used by histologically active EoE compared to EoE in remission (72.3% vs 29.6%, p<0.001). The DSQ and DSS scores of patients using any or a combination of adaptive behaviours were comparable to those of patients not using any adaptive behaviour at mealtime (p>0.1 for all comparisons), suggesting a marginal impact of adaptive behaviours on dysphagia reporting. Based on ROC curve analysis, the AUC of the DSQ for the assessment of histological disease activity was 0.72 (DeLong 95% CI, 0.60-0.83), while the AUC of the DSS was 0.69 (DeLong 95% CI, 0.56-0.82). Dysphagia reporting adjustments based on anxiety or hypervigilance sub-scores of the EHAS or on the presence of adaptive behaviours at mealtime did not modify the performance of the DSQ and DSS.

Conclusion

Esophageal anxiety, hypervigilance, and adaptive behaviours can be found in half of EoE patients regardless of histological disease activity. Esophageal anxiety contributes to dysphagia severity in patients with EoE, while hypervigilance does not. The use of adaptive behaviours is associated with histologically active EoE and represents a clinical marker of disease activity but does not affect dysphagia reporting.

Introduction

With the recent rise in the occurrence of esophageal adenocarcinoma (EAC) in Western nations, there is an escalating worry regarding Barrett’s esophagus (BE). In contrast, Asian countries exhibit a lower prevalence of BE compared to their Western counterparts. Given the annual increase in chronic gastroesophageal reflux disease (GERD) cases, there is an expectation of a concurrent rise in the prevalence of BE. Consequently, we are embarking on a multicenter prospective study to assess the current prevalence of BE and pinpoint its risk factors in Taiwan.

Aims & Methods

Aim: to evaluate current prevalence and risk factors of Barrett's esophagus in Taiwan.
Methods: We carried out a prospective multicenter study involving consecutive outpatients who underwent upper gastrointestinal endoscopy for various upper gastrointestinal symptoms. Biopsies were taken from endoscopically suspected esophageal metaplasia (ESEM), clearly visible at least 1 cm above the gastroesophageal junction during endoscopy. The biopsy procedure involved obtaining standardized random samples, with four pieces taken every 2 cm from the four quarters of the esophagus exhibiting the ESEM lesion. BE was defined based on the histological confirmation of specialized intestinal metaplasia in the metaplastic esophageal epithelium.

Results

A total of 8925 subjects were enrolled in this study. The prevalence of BE was 2.6%. A total of 228 subjects with BE were detected among 751 ESEM subjects. Short segment BE (78.1 % , n = 178) was more prevalent than long segment BE (22.9 % , n = 50). The prevalence of GERD symptoms, erosive esophagitis (EE), and hiatal hernia (HH) was 52.5%, 27.3% and 7.85%, respectively. Multivariate analysis disclosed that old age [odds ratio (OR) = 1.59; 95% CI, 1.20-2.11; P <0.01], male gender (OR = 2.27; 95%CI, 1.65-3.11; P < 0.01),alcohol consumption (OR = 1.70, 95%CI, 1.19-2.44; P< 0.01), GERD symptoms (OR = 1.45, 95%CI, 1.10-1.92; P< 0.01), EE (OR = 1.94, 95%CI, 1.47-2.56; P< 0.01) and presence of hiatal hernia (OR = 2.49; 95%CI, 1.78-3.47; P < 0.001) were significant risk factors predicting BE.
Risk factors for Barrett esophagus: multivariable analysis.

Conclusion

The prevalence of BE was identified as 2.6%. Notably, advanced age (>50), male gender, alcohol consumption, symptoms of gastroesophageal reflux disease (GERD), erosive esophagitis, and the presence of hiatal hernia emerged as independently significant risk factors for Barrett's esophagus.

References

1. Sharma P. Barrett Esophagus: A Review. Jama. 2022;328(7):663-71.
2. Marques de Sá I, et al. The global prevalence of Barrett's esophagus: A systematic review of the published literature. United European Gastroenterol J. 2020;8(9):1086-105.
3. Chang CY, et al. Current status of Barrett's esophagus research in Asia. J Gastroenterol Hepatol. 2011;26(2):240-6.
4. Shiota S, et al. Prevalence of Barrett's Esophagus in Asian Countries: A Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol. 2015;13(11):1907-18.
5. Chang CY, et al. The application of Prague C and M criteria in the diagnosis of Barrett's esophagus in an ethnic Chinese population. Am J Gastroenterol. 2009;104(1):13-20.
6. Fock KM, et al. Asia-Pacific consensus on the management of gastro-oesophageal reflux disease: an update focusing on refractory reflux disease and Barrett's oesophagus. Gut. 2016;65(9):1402-15.
7. Eusebi LH, et al. Global prevalence of Barrett's oesophagus and oesophageal cancer in individuals with gastro-oesophageal reflux: a systematic review and meta-analysis. Gut. 2021;70(3):456-63.
8. Akiyama T, et al. Alcohol consumption is associated with an increased risk of erosive esophagitis and Barrett's epithelium in Japanese men. BMC Gastroenterol. 2008;8:58.
9. Andrici J,et al. Hiatal hernia and the risk of Barrett's esophagus. J Gastroenterol Hepatol. 2013;28(3):415-31.

Introduction

Lifestyle factors are significant contributors to fatigue, which affects approximately 45% of patients with Inflammatory Bowel Disease (IBD) in remission.

Aims & Methods

In this study, we evaluated the effect of a digital multimodal lifestyle intervention on fatigue in patients with IBD. Patients with IBD in biochemical remission (fecal calprotectin <150 mg/kg) were enrolled in a multicenter, non-randomized, controlled interventional study. The intervention group participated in a 12-month lifestyle program—provided by the non-profit organization Voeding Leeft—that included digital group meetings with a nutritionist and a lifestyle coach focusing on gradual and sustainable behavior change regarding nutrition, physical activity, sleep, and stress management. In addition, the program encouraged patients to exercise more self-control over their personal health. Following the initial six months, attendance at online sessions was not mandatory; however, patients could attend online sessions every six to 12 weeks to stay motivated and foster the lifestyle habits they acquired throughout the course. Patients in the control group received standard care that included an informational leaflet about the potential causes of fatigue in IBD, the leaflet also included basic lifestyle information and advice to exercise more, eat a healthier diet, stop smoking, reduce alcohol intake, improve sleeping habits, and manage stress. The allocation to a study group was determined by the availability within the group and participant’s ability to attend the scheduled intervention. Clinical data and patient-reported outcomes were collected. Fatigue was measured with the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F); any increase in FACIT-F after six months was considered a positive response to the intervention. The Minimal Clinically Important Difference (MCID) for fatigue was at least a four-point increase in the FACIT-F score¹. Inverse probability treatment weighting was used to correct confounding by indication.

Results

Thirty-six patients in the intervention group and 32 in the control group were compared. After six months, more patients in the intervention group (82.1% of patients) than in the control group (54.2% of patients) experienced improvement in fatigue, P = 0.029. Likewise, significantly more patients in the intervention group (71.4% of patients) than the control group (33.3% of patients) achieved a MCID regarding fatigue; P = 0.006. The improvements in fatigue were sustained throughout the study period in the intervention group. Acceptance of the health status was a significant factor for improvement in fatigue (β 7.813, SE 1.908, P < 0.001). Compared to the control group, quality of life improved in the intervention group; these patients gained 0.05 more quality-adjusted life years throughout the study. Last but not least, significant improvements in dietary quality were observed as early as three months after the baseline in the intervention but not the control group; these improvements in the intervention group were sustained throughout the study period.

Conclusion

Multimodal lifestyle intervention improves fatigue, quality of life, and dietary quality in patients with IBD who are in remission. Acceptance of the health status appears essential for fatigue improvement; instruments evaluating acceptance could help to personalize treatment and maximize its effectiveness.

References

1. Cella D, Yount S, Sorensen M, et al. Validation of the Functional Assessment of Chronic Illness Therapy Fatigue Scale relative to other instrumentation in patients with rheumatoid arthritis. J Rheumatol 2005;32:811-9.

Disclosure

AEvdMdJ received unrestricted research grants from Galapagos, Norgine, Vedanta, Nestle, including speaker’s fees from Galapagos, Tramedico, Takeda, Ferring, and Janssen Pharmaceuticals. PWV has received speaker fee from Galapagos and Takeda and served on the advisory board of Lilly, Galapagos, Janssen, BMS, Takeda, and Abbvie. RL has received travel expenses from Galapagos and Cablon Medical and served on the advisory board at Cablon Medical. NW and MJHB are employed by the non-profit organization Voeding Leeft and were a part of the team that guided participants in the intervention group. All other authors have no conflicts of interest to declare.

Introduction

Cendakimab is a recombinant, humanized, high-affinity, neutralizing monoclonal antibody that binds to interleukin 13 (IL-13) and blocks interaction with both its receptors, IL-13Rα1 and IL-13Rα2. IL-13 is a cytokine implicated in the pathogenesis of atopic dermatitis (AD) and is thought to be a key driver of the complex pathophysiology of eosinophilic esophagitis (EoE). IL-13 signals through both IL-13Rα1 and IL-13Rα2 to regulate cellular and molecular pathways across a variety of cell types. The binding of IL-13 to IL-13Rα1 promotes a Type 2 immune response and eosinophil recruitment, whereas the binding of IL-13 to IL-13Rα2 is believed to play a role in fibrosis and epithelial tissue remodeling. Several biomarkers associated with Type 2 inflammatory diseases are known to be regulated by IL-13. Eotaxin-3, a key biomarker, plays a central role in attracting eosinophils to the site of inflammation. Periostin, an extracellular matrix protein linked to activated fibroblasts, is implicated in tissue remodeling and fibrosis. Another enzyme governed by IL-13 is matrix metalloproteinase-12 (MMP-12)—this enzyme contributes to tissue remodeling and breakdown of extracellular matrix components. Here, we evaluate the pharmacodynamic effects of IL-13 inhibition with cendakimab on the key serum biomarkers eotaxin-3, periostin, and MMP-12 in patients with AD, with a focus on exploring potential implications for EoE.

Aims & Methods

In this phase 2, multicenter, global, randomized, double-blinded, placebo-controlled, parallel-group study (NCT04800315), 220 adults with moderate-to-severe AD received cendakimab 360 mg Q2W, 720 mg QW, 720 mg Q2W, or placebo for 16 weeks. Blood samples were collected, and a panel of biomarkers were assessed. The current analysis focuses on the assessment of serum levels of eotaxin-3, periostin, and MMP-12 using Proximity Extension Assay pre- and post-treatment on day 1 (baseline), at week 1 and week 2, and then biweekly until week 16. The least square mean percent change from baseline at week 16 for each treatment group was evaluated.

Results

For all 3 doses of cendakimab, there was a significant decrease from baseline in the levels of eotaxin-3, periostin, and MMP-12 as early as week 1 post-treatment and continued through week 16 of cendakimab treatment (Table). Compared with placebo, cendakimab resulted in significantly greater reductions in these biomarker levels through week 16.

Conclusion

Cendakimab decreased levels of key inflammatory and remodeling biomarkers over 16 weeks of treatment in patients with AD. These findings suggest that cendakimab modulates pathways of inflammation, fibrosis, and tissue remodeling in AD and add to the existing clinical evidence of its modulation in other Type 2 inflammatory diseases such as EoE.
​
Table. Least square mean percent change from baseline in key serum biomarker levels at week 16 in patients with AD

Disclosure

ESD served as a consultant for Abbott, Abbvie, Adare/Ellodi, Aimmune, Akesobio, Alfasigma, ALK, Allakos, Amgen, Aqilion, Arena/Pfizer, Aslan, AstraZeneca, Avir, Biorasi, Calypso, Celgene/Receptos/ Bristol Myers Squibb, Celldex, Eli Lilly, EsoCap, Eupraxia, Dr. Falk Pharma, Ferring, GlaxoSmithKline, Gossamer Bio, Holoclara, Invea, Knightpoint, Landos, LucidDx, Morphic, Nexstone Immunology/Uniquity, Nutricia, Parexel/Calyx, Phathom, Regeneron, Revolo, Robarts/Alimentiv, Salix, Sanofi, Shire/Takeda, Target RWE, Upstream Bio, received research funding from Adare/Ellodi, Allakos, Arena/Pfizer, AstraZeneca, Eupraxia, Ferring, GSK, Meritage, Miraca, Nutricia, Celgene/Receptos/ Bristol Myers Squibb, Regeneron, Revolo, Shire/Takeda, and received educational grant from Allakos, Aqilion, Holoclara, and Invea. JL, SH, LG, CDO, and CC are employees and stockholders of Bristol Myers Squibb. JS served as consultant for Abbvie, Alamar, Aldena, Amgen, AObiome, Apollo, Arcutis, Arena, Asana, Aslan, Attovia, BioMX, Biosion, Bodewell, Boehringer-Ingelheim, Bristol Myers Squibb, Cara, Castle Biosciences, Celgene, Connect Biopharma, Corevitas, Dermavant, Eli Lilly, FIDE, Galderma, GlaxoSmithKline, Incyte, Invea, Kiniksa, Leo Pharma, Merck, My-Or Diagnostics, Nektar, Novartis, Optum, Pfizer, RAPT, Recludix, Regeneron, Sandoz, Sanofi-Genzyme, Shaperon, TARGET-RWE, Teva, Union, UpToDate, participated on a data safety monitoring board or advisory board for Biosion and Sanofi, received grants or contracts from Galderma, Incyte, Pfizer, received honoraria from Abbvie, Eli Lilly, Leo Pharma, Pfizer, Regeneron, Sanofi-Genzyme.

Introduction

Fatigue is a prevalent and debilitating symptom among patients with Crohn’s disease (CD) or ulcerative colitis (UC). However, due to its subjective nature and the lack of effective management strategies in CD/UC, fatigue often goes under-recognized and under-treated.¹ The Communicating Needs and Features of IBD Experiences (CONFIDE) study explored patient and healthcare professional (HCP) perspectives on the experiences and impact of CD/UC-related symptoms in Europe (France, Germany, Italy, Spain, and UK), the United States (US) and Japan.

Aims & Methods

Online, quantitative, cross-sectional surveys were conducted separately among patients with moderate-to-severe CD/UC and HCPs who make prescribing decisions for patients. Moderate-to-severe CD/UC were defined using criteria based on previous treatment, steroid use, and/or hospitalization. Descriptive statistics were used here to summarize the European and US data related to fatigue.

Results

A total of 547 European (55.4% male, mean age: 38.0 years) and 215 US (54.9% male, 40.9 years) patients with CD and 556 European (57.4% male, 38.9 years) and 200 US (61.5% male, 40.4 years) patients with UC completed the surveys. The proportions of patients who received advanced therapies at the time of survey completion were 63.4% and 58.1% among European and US patients with CD. Among patients with UC, the percentages were 54.1% and 76.5% of European and US patients.

Overall, 34.2% European and 35.8% US patients with CD, and 20.9% European and 27.5% US patients with UC reported currently experiencing fatigue (in the past month). Similar results were observed among patients receiving advanced therapies: CD (Europe: 34.3%; US: 36.0%); UC (Europe: 19.9%; US: 25.5%). Fatigue was ranked among the top five symptoms with greatest impact on patients by 44.5% European and 52.9% US patients with CD, and 55.2% European and 37.5% US patients with UC. Among patients who reported currently experiencing fatigue, 29.9% European and 36.4% US patients with CD, and 22.4% European and 40.0% US patients with UC discussed it with their HCPs at every appointment. Among patients who did not discuss fatigue with their HCPs at every appointment, at least two-thirds indicated that they would like to discuss it more frequently: CD (Europe: 75.6%; US: 67.3%); UC (Europe: 74.4%; US: 66.7%).

Surveys were completed by 503 European (70.8% male) and 200 US (78.0% male) HCPs, of which 92.5% were gastroenterologists/internal medicine practitioners. A minority of HCPs reported fatigue among the top five symptoms with the greatest impact on patients: CD (Europe: 33.9%; US: 22.0%); UC (Europe: 22.7%; US: 11.5%). More than half of HCPs reported proactively discussing fatigue at a routine appointment with patients: CD (Europe: 69.4%, US: 59.5%); UC (Europe: 64.6%, US: 59.0%). Among HCPs not proactively discussing fatigue, the most common reason was that they expected patients to bring it up if it is an issue: CD (Europe: 39.0%, US: 30.9%); UC (Europe: 37.1%, US: 32.9%).

Conclusion

For both patients with CD/UC, fatigue was a common and impactful symptom, despite the use of advanced therapies. A substantial proportion of patients experiencing fatigue who did not discuss it at every HCP appointment, reported a desire to discuss fatigue more frequently. Although more than half of HCPs reported proactive discussion of fatigue with their patients, some HCPs expected patients to bring it up. This indicates a communication gap between patients and HCPs and highlights the underappreciation of the impact of fatigue in CD/UC.

References

1. Farrell D, et al. (2020) Cochrane Database Syst Rev. 4(4), CD012005.

Disclosure

Remo Panaccione, Consultant for: Abbott, AbbVie, Abbivax, Alimentiv (formerly Robarts), Amgen, AnaptysBio, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Celltrion, Cosmos Pharmaceuticals, Eisai, Elan, Eli Lilly, Ferring, Galapagos, Fresenius Kabi, Genentech, Gilead Sciences, Glaxo-Smith Kline, JAMP Bio, Janssen, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pendopharm, Pfizer, Progenity, Prometheus Biosciences, Protagonist Therapeutics, Roche, Sandoz, Satisfai Health, Shire, Sublimity Therapeutics, Spyre Therapeutics, Takeda Pharmaceuticals, Theravance Biopharma, Trellus, Union Biopharma, Viatris, Ventyx, UCB; Speaker’s Fees for: AbbVie, Amgen, Arena Pharmaceuticals, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Gilead Sciences, Janssen, Merck, Organon, Pfizer, Roche, Sandoz, Shire, Takeda Pharmaceuticals; Advisory Boards for: AbbVie, Alimentiv (formerly Robarts), Amgen, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Genentech, Gilead Sciences, Glaxo-Smith Kline, JAMP Bio, Janssen, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pfizer, Progenity, Protagonist Therapeutics, Roche, SandozShire, Sublimity Therapeutics, Takeda Pharmaceuticals, Ventyx.
Stefan Schreiber, Consultancy fees: AbbVie, Arena, Biogen, Bristol-Myers Squibb, Celgene, Celltrion, Falk, Fresenius, Gilead Sciences, IMAB, Janssen, Eli Lilly and Company, Hikma, MSD, Mylan, Pfizer Inc, Protagonist, Provention Bio, Takeda, Ventyx, and Theravance.
Simon Travis, Grants: AbbVie, ECCO, Eli Lilly and Company, Helmsley Trust International, International Organization for the Study of Inflammatory Bowel Disease, Norman Collision Foundation, Pfizer, Takeda, UCB Pharma, UKIERI, Vifor Pharma; Honoraria: Ferring Pharmaceuticals, Takeda, Eli Lilly and Company, Bristol Myers Squibb, Janssen, Violicom; Travel grants: AbbVie, Eli Lilly and Company, Janssen, Pfizer, Takeda, Ferring Pharmaceuticals, Amgen, Biogen; Consultancy fees: AbbVie, Allergan, Amgen, Apexian, Bioclinica, Biogen, Bristol Myers Squibb, ChemoCentryx, Cosmo Pharmaceuticals, Endpoint Health, Eli Lilly and Company, Enterome, Equillium, Ferring Pharmaceuticals, Genentech/Roche, GlaxoSmithKline, Immunocore, Immunometabolism, Janssen, Merck, Merck Sharp & Dohme, Mestag Therapeutics, Novartis, Pfizer, Protagonist Therapeutics, Proximagen, Receptos, Roche, Sanofi, Satisfai Health, Sensyne Health, Sorriso Pharmaceuticals, Takeda, UCB Pharma, VHsquared, Vifor Pharma.
Marla C. Dubinsky, Consultancy fees: AbbVie, Abivax, Astra Zeneca, Boehringer Ingelheim International GmbH, Bristol Myers Squibb, Celgene Corporation, Eli Lilly and Company, F. Hoffman-La Roche Ltd, Genentech Inc., Gilead Sciences, Janssen, LLC, Merck, Pfizer, Prometheus Biosciences, Takeda Pharmaceuticals USA, Inc., and UCB; Stock options: TrellusHealth Inc.; Research support: AbbVie, Janssen, LLC, Pfizer, and Prometheus Labsa; and licensing fees: Takeda.
Toshifumi Hibi, Personal fees: Abbvie GK, EA Pharma, Janssen Pharmaceutical K.K, JIMRO, Mitsubishi-Tanabe, Mochida Pharmaceutical, Pfizer Japan, Sandoz K.K, Takeda Pharmaceutical, Zeria Pharmaceutical, Celltrion Healthcare Japan, Eli Lilly Japan, Gilead Sciences, Miyarisan Pharmaceutical, Alfresa Pharma Corporation, Kyorin Pharmaceutical; Grants: JIMRO, Mochida Pharmaceutical, Zeria Pharmaceutical, Miyarisan Pharmaceutical, Alfresa Pharma Corporation, and Kyorin Pharmaceutical.
Christian Atkinson, Employment: Adelphi Real World.
David Rubin, Grant support: Takeda; Consultant: Abbvie, Altrubio, Apex, Avalo Therapeutics, Bristol-Myers Squibb, Buhlmann Diagnostics Corp, Celgene, Connect BioPharma, Intouch Group, Iterative Health, Janssen Pharmaceuticals, Lilly, Pfizer, Samsung Neurologica, and Takeda. Board of Trustees: Crohn’s & Colitis Foundation; Board of Directors: Cornerstones Health.
Alison Potts Bleakman, Theresa Hunter Gibble, Tommaso Panni, Cem Kayhan, Eoin J. Flynn, and Angelo D. Favia are employees and stockholders of Eli Lilly and Company.

Introduction

Managing decompensated cirrhosis is a significant challenge due to high morbidity and mortality rates. The recently proposed Baveno VII criteria provide a standardized definition to assess recompensation. In this study, we validated the Baveno VII definition of recompensation and aimed to evaluate recompensation factors in patients with decompensated viral cirrhosis.

Aims & Methods

This is a retrospective descriptive study over a 10-year period between 2012 and 2022, enrolling 99 patients from the hepato-gastroenterology department of Mohamed Taher Maamouri Hospital in Nabeul who had been treated for decompensated viral cirrhosis B or C and achieved sustained virological response with a follow-up of at least 12 months.

Results

A total of 99 patients with decompensated viral cirrhosis (B or C), who had received treatment and achieved sustained virological response, were included in the study. The mean age was 62 ± 11 years, and 56 patients were female. The most common mode of decompensation was ascites, observed in 81.8% of the patients. The mean MELD score was 15 ± 4, and the majority (59.7%) were classified as Child-Pugh class B. Overall, 45.5% of the decompensated patients achieved recompensation during the study period. The recompensation rate was higher in patients with hepatitis B-related cirrhosis (51.1%) compared to those with hepatitis C-related cirrhosis (40.4%).
According to the results of logistic regression, four independent factors associated with recompensation were found: albumin ( OR = 2.033, IC95% [1,461-2,827], p<0.001 ), diabetes ( OR =0.003, IC95%[0.000-0.045], p<0.001 ), Child Pugh score ( OR=0.162, IC95% [0.057-0.459], p=0.001 ), INR ( OR =0.017, IC95%[0.000-0.939].

Conclusion

This study identified key factors associated with recompensation in patients with viral decompensated cirrhosis, including serum albumin levels, INR values, history of diabetes, and severity of liver disease. The knowledge of recompensated indicators may help support the development of different prevention strategies to reduce the incidence of acute decompensation.

Introduction

With the advent of EUS guided biliary interventions, there is a lot of hype created that ERCP will cease to be performed. The most important and limiting factor for ERCP is successful bile duct cannulation. We have studied a large series of our cases and tried to study the impact of properly performed precut on success of bile duct cannulation.

Aims & Methods

Aim: To analyze the efficacy of freehand precut for selective cannulation in difficult ERCP and its role in improving technical success rate, obviating need for EUS guided / other rendezvous techniques.
Methods: Retrospective analysis of 3000 patients undergoing ERCP from 2017 till date for varied etiologies. No. of patients required precut accessotomy were noted and technical success rate was measured.

Results

No. of patients analyzed- 3000. Selective biliary cannulation- 2452 (81.74%). Difficult cannulations requiring freehand precut accessotomy- 548 (18.26%). Technical success after precut achieving biliary access- 539 (98.36%). Failure of biliary cannulation even after precut- 09 (1.64%). Most common etiology in precut casesstone disease 360 (65.70%) followed by malignant lesions 118 (21.53%), benign strictures 28 (5.11%), post cholecystectomy biliary leak 28 (5.11%), post traumatic biliary leak 10 (1.82%), post hydatid surgery biliary leak 02 (0.36%), post central hepatectomy biliary leak 02 (0.36%). Most common cause for failure in precut cases was extensive edema and deformed anatomy. Of all failed cases 3 were large stones who were subjected to surgery and 6 were malignant lesions who were subjected to EUS guided biliary drainage.

Conclusion

Free hand precut technique, done correctly, is a savior in difficult cannulation cases and it increases the success rate of selective biliary cannulation significantly avoiding the need for other costlier techniques such as EUS guided / Rendezvous techniques.

References

Mariani A, Di Leo M, Giardullo N, Giussani A, Marini M, Buffoli F, Cipolletta L, Radaelli F, Ravelli P, Lombardi G, D'Onofrio V, Macchiarelli R,
Iiritano E, Le Grazie M, Pantaleo G, Testoni PA. Early precut sphincterotomy for difficult biliary access to reduce post-ERCP pancreatitis: a randomized trial. Endoscopy. 2016 Jun;48(6):530-5. doi: 10.1055/s-0042-102250. Epub 2016 Mar 18. PMID: 26990509.
Davee T, Garcia JA, Baron TH. Precut sphincterotomy for selective biliary duct cannulation during endoscopic retrograde cholangiopancreatography. Ann Gastroenterol. 2012;25(4):291-302. ​PMID: 24714256; PMCID: PMC3959408.