Introduction

As known, bIliary sludge has mostly asipmtomatic course, thus lack of data for biliary sludge diagnostics and treatment in Russia is observed.

Aims & Methods

Evaluation of the effectiveness and safety of therapy with UDCA in patients with the biliary sludge and early stage of cholelithiasis in routine practice.
Multicenter observational study (10 sites in total) has been conducted. Patients with the biliary sludge and/or early stage of cholelithiasis were enrolled. The main inclusion criteria were ultrasound (US) criteria (biliary sludge or low density stones less than 1 cm), history of uncomplicated cholelithiasis. Patients were given UDCA (10 mg/kg/day). Other medication were also given to address their abdominal symptoms (include pain that does not meet the criteria for biliary colic) in accordance with approved standards.The duration of the observation was 180 days.
Primary outcome was to evaluate the effect of complex therapy with UDCA on the patients’: quality of life, pain syndrome (include appearance biliary colic), changes in severity of other symptoms. The secondary outcomes were dynamics of US characteristics of the biliary system and the safety of UDCA.

Results

1056 patients were included in the study: with biliary sludge – 948 (89.8%), stones – 270 (25.6%), of which sludge plus stones – 162 (15.3%). At baseline, 40.2% patients had mild or medium abdominal pain, 44% - abdominal discomfort, 35.5% - sensitivity to abdominal palpation. The most common complaint was bitter taste in mouth (529 patients, 50.1%). Statistically significant increase of the quality of life and decrease the frequency of abdominal pain оn 60 days and 180 days of treatment was shown. There was a statistically significant decrease in the frequency of several symptoms such as: nausea, bitter taste in mouth, heartburn, feeling of fullness after eating, bloating, flatulence at the end of treatment compared to the baseline (p<0,001).

Parameter	Base	60 days	p(0-60 d)	Visit 7	p(0-180 d)
SF-36, physical, scores	49.9	53.5	<0.001	54.9	<0.001
SF-36, mental, scores	46.9	50.7	<0.001	52.5	<0.001
No pain, %	59.8	95.2	<0.001	99.3	<0.001

Results of repeated US showed the positive effect complex therapy with UDCA. The frequency of biliary sludge had decreased from 89.8% to 12%, the frequency of gallbladder stones - from 25.6% to 9.8%, simultaneous of biliary sludge and gallbladder stones - from 15,3% to 0.3%. There were no patients with enlargement of the gallbladder (against 8.5% at baseline).
In the vast majority of patients these parameters returned to normal level (ALT in 94.9% of cases, AST in 95.5%, direct bilirubin in 94.8%, total bilirubin in 92.2%, alkaline phosphatase in 95.0%). Among patients with normal values during treatment were recorded increase ALT (5 cases), total bilirubin (6), GGT (4), alkaline phosphatase (2).
High safety of treatment with UDCA was recorded: 4 adverse events associated with taking UDCA, no serious adverse events. Compliance in the vast majority of patients (fluctuations 83.3-90.1% of patients during the study) was high.

Conclusion

The results of this practice study have shown the effectiveness of complex therapy with UDCA in patients with cholelithiasis and biliary sludge. Complex therapy with UDCA improved patients’ quality of life, reduced the frequency of mild and moderate abdominal pain, prevents biliary colic. Results demonstrated that UDCA was highly safe. Thus, the UDCA may be extensively used in patients with biliary sludge & early stage of cholelithiasis and may prevent excessive surgery intervention.

Disclosure

Current study was conducted with the financial support of Binnopharm Group

Introduction

Pancreatic neuroendocrine tumors (pNETs) are a heterogeneous group of tumors with different treatment options depending on pathological grading, clinical staging, and presence of symptoms related to hormonal secretion. Their classification is made on mitotic count and Ki-67 index.
The current standard for Grading assessment is analysing the material obtained from EUS-guided fine needle aspiration/biopsy (EUS-FNA/FNB). However this technique is not free from adverse events and could be challenging for NETs localization.
The evidence of high grade of fibrosis and microvascular density decrease (MVD) on tumor pathological specimens has led many authors to search for undirected malignant features of pNET extrapolated from non-invasive techniques. The introduction of ancillary techniques, such as second-generation contrast agents (CH-EUS), has improved study of pNET. Particularly, at CH-EUS examination contrast pattern well correlates with behaviour and grading of NETs. However, the use of contrast agents entails a prolongation of procedure time and additional costs. An innovative ultrasound Doppler technique, Detective Flow Imaging EUS (DFI-EUS), involves no additional time or cost as it doesn’t require the administration of contrast agent. There is still no standardisation of this technique and few studies have validated its use.

Aims & Methods

The aim of this study is to evaluate the DFI role in defining NET vascularization and its correlation with CH-EUS. The second aim of the study is to assess DFI role in predicting histological grading.
Single center retrospective analysis on consecutive patients with solid pancreatic lesions who underwent EUS at Therapeutic Digestive Endoscopy Unit of the Fondazione Policlinico Universitario Campus Bio-Medico in Rome.
After activation of DFI, each lesion was observed for at least 30 seconds. Lesions was classified into three grades, according to the degree of vascularisation at DFI: (grade 0 absence of microvascularization of the tumor; grade 1 minimal/isovascularization of the tumor; grade 2 markedly increased microvascularization).
All lesion with final hystological diagnosis of NET were enrolled.
Grading and Ki-67 index of tumors were reported.
Data about lesion’s features and procedure were collected.

Results

From April 2024 to February 2025, 17 patients were enrolled (58.8% male; mean age 57±12 years old). The majority of lesion (53%) were localized in the body of the pancreas and the mean lesion’ s size was 28±20 mm. The final histological diagnosis classified 50% lesions as G1, 38.8% G2 and 5.5% G3.
At the CEH-EUS the 70.6% of lesion showed hyper-enhancement. About the DFI evaluation the 17.6% of lesion was hypo-vascular, 17.6% Iso-vascular and 64.7% was hyper-vascular. There was excellent correlation between DFI characterization of the lesion and the CH-EUS (ICC 0.9)
Among the NET G1, 66.7% were Hypervascular at DFI and 33.3% Isovascular. Among the G2, 71.4% were Hypervascular at DFI and 28.6% Hypovascular. The only G3 lesion was Hypovascular.
There was inverse correlation between the NET grade and the DFI grade (Pearson coefficient -0.56; p 0.02).

Conclusion

DFI-EUS can provide a fast evaluation of the micro-vascularization of pNET with excellent correlation with CH-EUS. Hyper-vascular pattern at DFI correlates with low Ki-67 index.

Introduction

Computer Aided Detection (CADe) systems may improve detection of (pre-)malignant lesions by endoscopists. Most CADe systems are developed using homogeneous datasets collected by experts, which do not represent the heterogeneous imaging conditions of daily clinical practice. Such heterogeneity is caused by endoscopist-dependent variation (e.g. skill and experience) as well as endoscopist-independent variation (e.g. endoscopy equipment). Recently, we presented a CADe system for Barrett’s neoplasia¹. However, all training and test data originated from expert centers.

Aims & Methods

We aimed to develop an updated CADe system (CADe 2.0) demonstrating more robustness to the varied imaging conditions found in routine patient care.
Our previously published CADe system (CADe 1.0) was trained and internally validated on a high-quality dataset originating from 15 expert centers. The dataset included 6.337 neoplastic (1.362 patients) and 7.695 non-dysplastic images (1.139 patients).
The updated CADe system (CADe 2.0) underwent four improvements. First, we included more heterogeneous training data from our training set patient population. We extracted video frames from videos comprising various quality artefacts (e.g. blurred lenses or insufficient mucosal cleaning). Second, we applied advanced data augmentation methods to address the diversity of post-processing enhancement settings used by modern endoscopy systems. Third, we updated the CADe system with a Vision Transformer architecture², which has shown to improve performance on lower quality endoscopic images³. Finally, we transitioned our pretraining approach from semi-supervised to a self-supervised learning framework⁴.
Both CADe systems were evaluated using three prospectively collected, independent test sets. The first test set represented the true diversity and complexity encountered in daily clinical practice. This dataset comprised all videos captured from all included patients in five referral centers between April 2022 and January 2024 (431 ten-second BE videos from 115 patients). The second test set focused on endoscopist-dependent variation. It included three paired subsets with high, moderate and low-quality images from 122 patients. Quality was determined by factors such as esophageal expansion and mucosal cleaning. The third test set addressed endoscopist-independent variation. It contained 16 paired subsets of 396 images (122 patients). Every subset was based on a different post-processing enhancement setting of the endoscopy system.

Results

For test set 1, CADe 1.0 reached a sensitivity and specificity of 84% and 73%. CADe 2.0 scored 93% and 76%. For test set 2, CADe 2.0 reached higher sensitivity and specificity scores on high-quality images compared to CADe 1.0. In addition, CADe 2.0 performance loss on moderate and low-quality images was smaller. On test set 3 CADe 1.0 scores substantially varied depending on the test sets enhancement setting (82-94% sensitivity, 52-83% specificity). Variation of CADe 2.0 was limited to 91-95% and 81-88%.

Table 1. Results of CADe 1.0 and CADe 2.0

Test Set	Metric	CADe 1.0	CADe 2.0
Test set 1: Video Performance	Sensitivity Specificity	84% 73%	93% 76%
Test set 2: High Quality Images Test set 2: Moderate Quality Images Test set 2: Low Quality Images	Sensitivity Specificity Sensitivity (loss) Specificity (loss) Sensitivity (loss) Specificity (loss)	93% 68% 76% (-17%) 69% (+1%) 61% (-32%) 76% (+8%)	96% 85% 85% (-11%) 87% (+2%) 72% (-24%) 90% (+5%)
Test set 3: Enhancement Setting	Sensitivity range (min-max) Specificity range (min-max)	12% (82-94) 31% (52-83)	4% (91-95) 8% (81-88)

Conclusion

The updated CADe system displayed improved performance for detection of Barrett’s neoplasia in videos. More importantly, this CADe system also displayed less performance loss when exposed to lower image quality and less performance variability when confronted with differing post-processing enhancement settings.

References

1. Fockens N, Jong MR, Jukema JB, Pouw RE, Duits LC, Van Munster SN, et al. A deep learning system for detection of early Barrett's neoplasia: a model development and validation study. The Lancet Digit Health. 2023;5:905-21.
2. Yu W, Si C, Zhou P, Luo M, Zhou Y, Feng J, et al. MetaFormer Baselines for Vision2022 October 01, 2022:[arXiv:2210.13452 p.]. Available from: https://ui.adsabs.harvard.edu/abs/2022arXiv221013452Y.
3. Kusters CHJ, Boers TGW, Jaspers TJM, Jukema JB, Jong MR, Fockens KN, et al., editors. CNNs vs. Transformers: Performance and Robustness in Endoscopic Image Analysis. Applications of Medical Artificial Intelligence; 2024 2024//; Cham: Springer Nature Switzerland.
4. Caron M, Touvron H, Misra I, Jégou H, Mairal J, Bojanowski P, et al. Emerging Properties in Self-Supervised Vision Transformers2021 April 01, 2021:[arXiv:2104.14294 p.]. Available from: https://ui.adsabs.harvard.edu/abs/2021arXiv210414294C.

Introduction

Aspiration Pneumonia is a well described complication of upper digestive endoscopy. However, limited data are available on incidence, risk factors and clinical consequences of post- Endoscopic retrograde cholangiopancreatography (ERCP) aspiration pneumonia (pEP).

Aims & Methods

All consecutive ERCPs performed under anesthesiologist-administered sedation at the Endoscopy Unit of the University of Verona between April 1st 2022 and August 31st 2024 were retrospectively evaluated. Demographical, clinical and endoscopic data were collected.

Results

One-thousand-one-hundred-forty consecutive ERCPs were included. Main indication was malignant biliary stricture and patient’s mean age was 68±13.9 years. Overall incidence of pEP was 2.7%. American Society of Anesthesiologists (ASA) score, presence of active cholangitis before ERCP and performance of endoscopic ultrasound (EUS) and ERCP in the same sedation session were significantly associated to higher risk of pEP at both univariable and multivariable analysis. pEP was an independent risk factor for post-ERCP 30-days-mortality and for prolonged hospital stay.

Conclusion

pEP is a relatively frequent adverse event after ERCP. In patent with high ASA score, active cholangitis and scheduled EUS and ERCP in the same sedation session, preventive medical and/or anesthesiological strategies might be considered. Additional prospective studies are needed to confirm these data.

References

Incidence rates of post-ERCP complications: a systematic survey of prospective studies. Complications of ERCP: a prospective study.
ERCP-related adverse events: European Society of Gastrointestinal Endoscopy (ESGE) Guideline.
Unrecognised aspiration pneumonitis during enteroscopy: two case report.
Efficecay and safety of therapeutic endoscopic retrograde cholangiopancreatography in patients with native papillae with a performance status score of 3 or 4: a single-center retrospective study.
A prospective assessment of sedation-related adverse events and patient and endoscopist satisfaction in ERCP with anesthesiologist-administred sedation.
Increased ERCP-related adverse event from premature urgent ERCP following symptom onset in acute biliary pancreatitis with cholangitis.
Acute sedation-associated complications in GI endoscopy (ProSed 2 Study): results from the prospective multicentre electronic registry of sedation-associated complications.
Deep sedation without intubation for ERCP is appropriate in healthier, non-obese patients.
Comparative efficacy and safety of anesthetic and sedative regimens for endoscopic retrograde cholangiopancreatography: a network meta-analysis.
International consensus recommendations for difficult biliary access.
Intraprocedural quality in endosocpic retrograde cholangiopancreatography: e meta-analysis.
Criteria for difficult biliary cannulation: start to count.
Safety and efficacy of therapeutic endoscopic retrograde cholangiopancreatography for patients over 90 years of age.
Risk factors for post-endoscopic retrograde cholangiopancreatography complications in very elderly patients aged 90 years or older-no additional risk.

Disclosure

I have no conflict of interest

Introduction

Acute pancreatitis (AP) can progress to recurrent acute pancreatitis (RAP) or chronic pancreatitis (CP).

Aims & Methods

This systematic review and meta-analysis aimed to identify risk factors associated with this progression. The protocol was registered on PROSPERO (CRD42022368931). A comprehensive search was conducted in three (Medline, Embase, Cochrane) databases on October 25th, 2022. Articles reporting and risk factors associated with AP progression into RAP or CP were included. Pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated using the random effects model. Heterogeneity was evaluated using the I² statistic. The risk of bias assessment was performed using the Quality in Prognostic Studies (QUIPS) tool.

Results

A total of 71 articles were included in the meta–analysis, and several risk factors were identified for the progression of AP into RAP and CP. We found the following risk factors of AP recurrence: younger age, male gender, smoking, alcoholic etiology, hypertriglyceridemia, diabetes mellitus, pseudocyst, etc. The pooled OR for the male gender was 1.45 (95% CI: 1.29-1.64, I²=24%), for smoking was 1.45 (95% CI: 1.16-1.81, I²=62%), for alcoholic etiology was 1.76 (95% CI: 1.38-2.25, I²=81%), for hypertriglyceridemia was 2.45 (95% CI: 2.07-2.90, I²=9%), for diabetes mellitus was 1.49 (95% CI: 1.24-1.80, I²=0%), for pseudocyst was 2.19 (95% CI: 1.52-3.15, I²=0%). We also found risk factors of RAP progression into CP. The risk of bias was moderate in the majority of the included studies.

Conclusion

Our study identified multiple modifiable risk factors which can be treated to prevent the progression of pancreatitis.

Introduction

Disordered eating is reported to be common in disorders of gut-brain interaction. In this study, we aimed to identify symptoms compatible with disordered eating, including ARFID and other eating disorders (i.e., anorexia and bulimia nervosa) in a large population-based cohort with bowel symptoms.

Aims & Methods

An internet-based survey was completed by individuals (18-70 years) who met symptom thresholds to diagnose a functional bowel disorder. The survey included self-report measures for quality of life (QoL), bowel and gastroduodenal disorders of gut-brain interaction, gastrointestinal (GI) symptom severity, body mass index, non-GI symptoms, GI-specific anxiety, general anxiety, depression, symptoms of ARFID (NIAS), and screening for anorexia and bulimia nervosa (SCOFF). Validated cutoffs for NIAS (≥10 Picky eating; ≥ 9 Appetite; ≥10 Fear) and SCOFF (total score ≥2) were used to detect ARFID and other eating disorders, respectively. Hence, we identified three groups: 1) ARFID (≥ cutoff for any NIAS subscale and SCOFF <2); 2) eating disorder (SCOFF ≥2); 3) no disordered eating.

Results

In total, 825 adults participated (age 34.0±15.0 years (mean ± SD); 66.2% females). Of these, 65.1% fulfilled the Rome IV criteria for a FBD, and 15.5% met the criteria for functional dyspepsia. A positive screening for anorexia and bulimia was more common among participants with FD and overlapping FBD and FD compared to participants with only FBD (44.7% and 50.6% respectively vs 30.3%, p<.001), which in turn was higher compared to participants that did not fulfill diagnostic criteria for FBD or FD (14.9%, p<.001). Symptoms of ARFID were more common among participants with overlapping FBD and FD compared to participants with only FD, only FBD or participants who did not fulfill diagnostic criteria for FBD or FD (27.2% vs 14.9%, 9.9% and 14.1% respectively, p<.001). Both groups with disordered eating consisted of more females and reported more severe non-GI somatic and GI symptoms, general anxiety, depression as well as lower QoL compared to the group with no disordered eating (Table). Body weight/shape related disordered eating had also more GI-specific anxiety whilst symptoms of ARFID was associated with a lower body weight.

Conclusion

Symptoms of ARFID and other eating disorders are very common in adults with bowel symptoms. Presence of disordered eating is associated with comorbid functional dyspepsia, more severe GI, non-GI, and psychological symptoms, as well as reduced quality of life. It is important to identify these individuals to optimize their medical, psychological, and dietary treatment.

Table. Demographics and symptoms in adults with bowel symptoms grouped by presence or absence of disordered eating.

	No disordered eating (n=481)	ARFID (n=108)	Eating disorder (n=236)	P
Female sex, %	60.1*	75.9§	74.2#		<0.001
Age (years)	40.2 ± 15.4	36.8 ± 14.4§	31.8 ± 12.5#		<0.001
BMI (kg/m2)	26.5 ± 6.0*	24.5 ± 6.7§	27.3 ± 6.2		<0.001
Non-GI somatic symptoms (PHQ-12)	7.5 ± 3.8*	9.4 ± 4.7	10.5 ± 4.5#		<0.001
GI-specific anxiety (VSI)	33.3 ± 17.0	36.4 ± 16.6	37.7 ± 13.1#		.001
Anxiety (PHQ-4)	1.5 ± 1.7*	2.4 ± 2.1	2.9 ± 1.9#		<0.001
Depressive symptoms (PHQ-4)	1.5 ± 1.6*	2.5 ± 2.0	3.0 ± 2.0#		<0.001
Overall GI symptom severity (IBS-SSS)	90.3 ± 99.8*	132.0 ± 116.1	156.5 ± 111.8#		<0.001
Quality of life (EQ-5D)	0.89 ± 0.11*	0.83 ± 0.16	0.82 ± 0.14#		<0.001

Data are mean ± SD or proportions (%) and groups were compared by Chi-square tests and ANOVA with pairwise comparisons (Bonferroni correction).
* P<0.05, No disordered eating vs. ARFID;
§ P<0.05, ARFID vs. eating disorder;
# P<0.05, No disordered eating vs. eating disorder.

Disclosure

No conflict of interest

Introduction

Etrasimod is an investigational, once-daily, oral, selective sphingosine 1‑phosphate (S1P)_1,4,5 receptor modulator in development for the treatment of moderately to severely active ulcerative colitis (UC). In the ELEVATE UC 52 trial, primary and key secondary efficacy endpoints at Week 52 were evaluated among all patients randomised at baseline. The efficacy of etrasimod can be further characterised by evaluating efficacy endpoints at Week 52 among the subset of patients who met each efficacy endpoint at the end of the induction period (Week 12).

Aims & Methods

Here, we report proportions of patients receiving etrasimod that sustained induction efficacy endpoints at Week 52. In ELEVATE UC 52 (NCT03945188), patients (16–80 years) with moderately to severely active UC (defined as modified Mayo Score 4–9, endoscopic subscore ≥2 and rectal bleeding subscore [RBS] ≥1) were randomised 2:1 to once-daily etrasimod 2 mg or placebo. The ELEVATE UC 52 clinical trial comprised a 12-week induction period followed by a 40-week maintenance period with a treat-through design. This post hoc analysis assessed efficacy endpoints at Week 52 among the subset of patients who met the following efficacy endpoints at Week 12: clinical remission, endoscopic improvement, endoscopic improvement-histologic remission, symptomatic remission and RBS of 0.

Results

In ELEVATE UC 52, 81/289 (28.0%) patients treated with etrasimod achieved clinical remission at Week 12; of these, 66.7% (54/81) sustained clinical remission at Week 52 (Table). Among the 108/289 (37.4%) patients who achieved endoscopic improvement at Week 12, 72.2% (78/108) sustained the endpoint at Week 52; of 66/289 (22.8%) who achieved endoscopic improvement-histologic remission at Week 12, 63.6% (42/66) sustained the endpoint at Week 52; of 134/289 (46.4%) patients who achieved symptomatic remission at Week 12, 74.6% (100/134) sustained the endpoint at Week 52; of 166/289 (57.4%) patients who achieved an RBS of 0 at Week 12, 75.3% (125/166) sustained the endpoint at Week 52.

Table. Proportions of patients receiving etrasimod who sustained Week 12 induction efficacy endpoints at Week 52 (full analysis set)
	Maintained response at Week 52	Loss of response/discontinued treatment
Clinical remissiona n/N (%)	54/81 (66.7)	27/81 (33.3)
Endoscopic improvementb n/N (%)	78/108 (72.2)	30/108 (27.8)
Endoscopic improvement-histologic remissionc n/N (%)	42/66 (63.6)	24/66 (36.4)
Symptomatic remissiond n/N (%)	100/134 (74.6)	34/134 (25.4)
RBS=0 n/N (%)	125/166 (75.3)	41/166 (24.7)
aClinical remission is defined as an SFS=0 (or =1 with a ≥1-point decrease from baseline), RBS=0 and ES ≤1 (excluding friability) bEndoscopic improvement is defined as an ES ≤1 (excluding friability) cEndoscopic improvement-histologic remission is defined as an ES ≤1 (excluding friability) with histologic remission measured by a Geboes Index score <2 dSymptomatic remission is defined as an SFS=0 (or =1 with a ≥1-point decrease from baseline) and RBS=0 ES, endoscopic subscore; RBS, rectal bleeding subscore; SFS, stool frequency subscore.

Conclusion

These findings suggest efficacy endpoints achieved at Week 12 were sustained by large proportions of etrasimod-treated patients at Week 52 based on both subjective and objective measures including clinical, endoscopic and histologic efficacy responses. Further analyses of larger samples sizes with longer follow-up are needed to evaluate long-term efficacy of etrasimod in patients with moderately to severely active UC.

Disclosure

BES: research/grants, e.g. Grant/Research Support: Arena, Janssen. Lecture fees/Speakers Bureau: BMS, Janssen, Lilly, Pfizer, Takeda. Consultancy, Advisory Committee/Board Member: AbbVie, Alimentiv, Amgen, Arena, AstraZeneca, Boehringer-Ingelheim, BMS, Celltrion, Fresenius Kabi, Genentech, GSK, Janssen, Lilly, Merck, Pfizer, Prometheus Biosciences, Sun Pharma Global, Takeda Pharmaceuticals International, Teva Branded Pharmaceutical Products R&D. Shareholder/Stock Options: Ventyx Biosciences. Other non-financial support: Janssen, Lilly, Pfizer, Takeda.
SV: grant/research support: AbbVie, MSD, Pfizer, Galapagos, Takeda; consultancy/advisory: AbbVie, AbolerIS, Alimentiv, Arena, AstraZeneca, Avaxia, Bristol-Myers Squibb, Boehringer Ingelheim, Celgene, CVasThera, Dr. Falk, Eli Lilly, Ferring, Galapagos, Genentech/Roche, Gilead, Hospira, Imidomics, Janssen, Johnson & Johnson, Materia Prima, MiroBio, Morphic, MrMHealth, MSD, Mundipharma, Pfizer, Prodigest, Progenity, Prometheus, Robarts Clinical Trials, Second Genome, Shire, Surrozen, Takeda, Theravance, Tillotts, Zealand; lecture/speaker: AbbVie, Dr. Falk, Ferring, Hospira, MSD, Takeda, Tillotts.
MCD: grant/research support: Janssen; consultancy: AbbVie, Arena, Bristol-Myers Squibb, Celgene, Eli Lilly, Galapagos, Genentech, Gilead, Janssen, Pfizer, Prometheus, Takeda, Trellus Health, UCB; shares/royalties: Trellus; directorship/ownership interests: Trellus.
BGF: consultant/on advisory board: AbbVie, AbolerIS, AgomAB, AllianThera, Amgen, AnaptysBio, Applied Molecular Transport, Arena, Avoro Capital, Atomwise, BIOJAMP, Biora, Boehringer Ingelheim, Boxer, Celsius, Celgene/Bristol-Myers Squibb, Connect, Cytoki, Disc Medicine, Duality, EcoR1, Eli Lilly, Equillium, Ermium, First Wave, FirstWord, Galapagos, Galen Atlantica, Genentech/Roche, Gilead, Gossamer, GSK, Hinge, HotSpot, InDex, Imhotex, Immunic, JAK, Janssen, Japan Tobacco., Kaleido, Landos, Leadiant, L.E.K., Lenczner Slaght, LifeSci, Lument AB, Millennium, MiroBio, Morgan Lewis, Morphic, Mylan, OM, Origo, Orphagen, Pandion, Pendopharm, Pfizer, Prometheus, Diagnostics, Play to Know AG, Progenity, Protagonist, PTM, Q32, Rebiotix, REDX, Roche, Sandoz, Sanofi, Seres, Silverback, Surrozen., Takeda, Teva, Thelium, TiGenix, Tillotts, Ventyx, VHSquared Ltd., Viatris, Ysios, YSOPIA, Zealand; speaker: AbbVie, Janssen, Takeda; Alimentiv Senior Scientific Director, provides central reading services; not a company employee, no equity stake; shareholder: Gossamer.
RP: research support: AbbVie, Janssen, Takeda, Pfizer; consultancy: Abbott, AbbVie, Abivax, Alimentiv, Amgen, Arena, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Celltrion, Cosmos, Eisai, Elan, Eli Lilly, Ferring, Galapagos, Fresenius Kabi, Genentech, Gilead, GSK, BIOJAMP, Janssen, Merck, Mylan, Novartis, Oppilan, Organon, Pandion, Pendopharm, Pfizer, Progenity, Prometheus, Protagonist, Roche, Sandoz, Satisfai, Shire, Sublimity, Takeda, Theravance, Trellus, Viatris, Ventyx, UCB; speaker: AbbVie, Amgen, Arena, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Gilead, Janssen, Merck, Organon, Pfizer, Roche, Sandoz, Shire, Takeda; member of advisory boards: AbbVie, Alimentiv, Amgen, Arena, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Genentech, Gilead, GSK, BIOJAMP, Janssen, Merck, Mylan, Novartis, Oppilan, Organon, Pandion, Pfizer, Progenity, Protagonist, Roche, SandozShire, Sublimity, Takeda, Ventyx.
VJ: financial support: Celgene/Bristol-Myers Squibb, Pfizer, AbbVie, Boehringer Ingelheim, Eli Lilly, Janssen, Takeda, Gilead and TiGenix; consultancy: AbbVie, Alimentiv, Amgen, Anokion, Applied Strategic, Arena, Asahi Kasei, Asieris, AstraZeneca, BIOJAMP, Celgene/Bristol-Myers Squibb, Celltrion, Eli Lilly, Ferring, F Hoffmann La Roche, Flagship Pioneering, Fresenius Kabi, Fusion MD, Galapagos, Genentech, Gilead, GSK, Janssen, Knightslab, Organon, Landos, McKesson, Metacrine, Mylan, Pandion, Pendopharm, Pfizer, Prometheus, Protagonist, Reistone, Roche, Sandoz, Second Genome, Sorriso, Takeda, Teva, Topivert, Ventyx, Viatris, Vividion; lecture: AbbVie, Ferring, Galapagos, Janssen, Pfizer, Takeda, Bristol-Myers Squibb.
AJY: consultancy: Pfizer, Arena, Takeda, Bristol-Myers Squibb; lecture/speaker: Bristol-Myers Squibb.
MVC: grant support: Pfizer, Janssen, Novartis, Bristol-Myers Squibb; consultancy: AbbVie, Arena, Bristol-Myers Squibb, Medtronic, Pfizer, Prometheus, Eli Lilly, Janssen and Takeda; speaker: AbbVie, Janssen, Medtronic, Pfizer, Bristol-Myers Squibb, Takeda.
JP: personal: AbbVie, Arena, Athos, Atomwise, Boehringer Ingelheim, Celgene, Celltrion, Ferring, Galapagos, Genentech/Roche, GSK, Immunic, Janssen, Mirum, Morphic, Nestlé, Origo, Pandion, Pfizer, Progenity, Revolo, Takeda, Theravance and Wassermann; grant support: AbbVie, Pfizer.
MG: employee & shareholder of Pfizer AG.
CJR, PS, JW: employees & shareholders of Pfizer.
SG: financial support/grants: GSK; speaker: Janssen, AbbVie, Pfizer, Takeda, Eli Lilly, Celltrion; advisory board: Janssen, AbbVie, Takeda, Pfizer, Bristol-Myers Squibb, Gilead, Galapagos, Ferring; Steering Committee member: Janssen, Bristol-Myers Squibb, AbbVie; Drug Monitoring Committee member: Janssen.