Introduction

Filgotinib (FIL) is an oral, JAK1 preferential inhibitor approved for the treatment of ulcerative colitis (UC). Although the clinical efficacy of FIL in UC has been demonstrated in the SELECTION trial,¹ real-world data are limited.

Aims & Methods

In total, 600 adult patients with moderately to severely active UC who initiate FIL treatment in routine clinical care will be enrolled in GALOCEAN (NCT05817942), an ongoing, European, multi-site, prospective, observational study. Here, we report baseline characteristics of the first 100 enrolled patients and effectiveness data from patients who reached week 10. Baseline demographics, disease characteristics, prior UC-related treatment and reasons for starting FIL were collected. At week 10, mean changes from baseline (CFBs) in the partial Mayo Clinic Score (pMCS) and the PRO-2 score, and the proportions of patients in pMCS remission (pMCS of ≤2) or PRO-2 remission (rectal bleeding subscore of 0 and stool frequency subscore of ≤1) were assessed. Mean CFBs at week 10 in patient-reported outcomes (Short Inflammatory Bowel Disease Questionnaire [SIBDQ], Urgency Numerical Rating Scale [NRS] and Functional Assessment of Chronic Illness Therapy-Fatigue [FACIT-Fatigue] scores) were also calculated. Safety was evaluated by documenting adverse events.

Results

As of January 2024, 100 patients (FIL 200 mg, 97% [97/100]; FIL 100 mg, 3% [3/100]) were enrolled, and had baseline data available; out of which 55 reached week 10. Baseline characteristics are shown in the Table. In total, 70% of patients (67/96) had up to moderate disease activity (pMCS of ≤6) and 30% (29/96) had severe disease activity (pMCS of ≥7) at baseline; 42% (42/100) were biologic-naive. The most common cardiovascular risk factor was active or prior smoking (37% [37/100]). FIL was used as monotherapy in 47% of patients (47/100). At week 10, the mean (standard deviation [SD]) CFB in the pMCS was –2.7 (2.5; n=43), and 58% of patients (25/43) achieved pMCS remission. The mean (SD) CFB in the PRO-2 score at week 10 was –1.8 (1.7; n=46), and 72% of patients (33/46) achieved PRO-2 remission. Mean (SD) CFBs in patient-reported outcomes at week 10 were 10.1 (12.4; n=42) for the SIBDQ score, –1.3 (2.8; n=38) for the Urgency NRS score and 4.0 (9.3; n=42) for the FACIT-Fatigue score. Overall, 10 patients discontinued FIL because of adverse events, lack of effectiveness or physician decision. No new safety signals were identified.

Conclusion

In this first interim report of GALOCEAN, week 10 data show that FIL improves symptoms in patients with UC in real-world clinical practice and has beneficial effects on health-related quality of life and fatigue. GALOCEAN is ongoing and long-term data with higher patient numbers will be evaluated to further characterize the real-world effectiveness of FIL in UC.

Table. Baseline characteristics.

Characteristic	Totala (N=100)
Age, years, median (min­–max)	37.0 (19–67)
Female, n (%)	52 (52)
UC duration, years, median (min­–max)	5.9 (0–26)
UC type, n (%) Proctitis Left-sided colitis Pancolitis Unknown	13 (13) 49 (49) 34 (34) 3 (3)
Disease activity and patient-reported outcomes, mean (SD) pMCS PRO-2 score SIBDQ score Urgency NRS score FACIT-Fatigue score	5.3 (2.0) 3.3 (1.6) 38.0 (11.5) 4.5 (2.6) 28.6 (11.7)
CRP, mg/L, median (min­–max)	3.3 (0–50)
Prior biologic therapy, n (%)	58 (58)
Number of prior biologic therapies, n (%)b 0 1 2 3 ≥4	42 (42) 23 (23) 23 (23) 7 (7) 5 (5)
aThe number of patients with missing data was n=1 for UC duration and UC type,n=4 forpMCS and PRO-2 score, n=11 for SIBDQ score, n=16 for urgency NRS score, n=11 for FACIT-Fatigue score and n=43 for CRP. bMultiple uses of the same therapy were counted once. CRP, C-reactive protein; FACIT-Fatigue, Functional Assessment of Chronic Illness Therapy-Fatigue; pMCS, partial Mayo Clinic Score; NRS, Numerical Rating Scale; PRO-2, patient-reported outcome-2; SIBDQ, Short Inflammatory Bowel Disease Questionnaire; UC, ulcerative colitis.

References

1. Feagan BG et al. Lancet 2021;397:2372–84.

Disclosure

The GALOCEAN study was sponsored by Galapagos NV (Mechelen, Belgium), who funded these analyses.
Medical writing support for the development of this abstract was provided by Risha Bulusu, MBiochem, of PharmaGenesis London, London, UK, and was funded by Alfasigma S.p.A.
WS, AM, MZ are employees of Alfasigma S.p.A at the time of abstract submission.
AA reports consulting and/or advisory board fees from AbbVie, Allergan, Amgen, Arena Pharmaceuticals, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Celltrion, Eli Lilly, Ferring Pharmaceuticals, Galapagos, Gilead Sciences, Janssen Pharmaceuticals, Lionhealth, MSD, Mylan, Nestlé, Pfizer, Roche, Samsung Bioepis, Sandoz and Takeda; lecture and/or speaker bureau fees from AbbVie, Amgen, Biogen, Bristol Myers Squibb, Celltrion, Eli Lilly, Ferring Pharmaceuticals, Galapagos, Gilead Sciences, Janssen Pharmaceuticals, Mitsubishi Tanabe Pharma Corporation, MSD, Novartis, Pfizer, Roche, Samsung Bioepis, Sandoz, Takeda and Teva Pharmaceuticals; and research grants from Biogen, MSD, Pfizer and Takeda.
CGdSJ reports speaker and/or consultancy fees from AbbVie, Alfasigma, Amgen, Celltrion, Janssen, Galapagos, MSD, Pfizer and Takeda.
ER reports speaker fees from AbbVie, Faes Farma, Ferring Pharmaceuticals, Galapagos, Janssen Pharmaceuticals, Kern Pharma, MSD, Pfizer and Takeda; and consulting fees from AbbVie, Eli Lilly, Fresenius Kabi, Galapagos, Janssen Pharmaceuticals, MSD and Pfizer.
GD reports research/educational grants from Abbott, AbbVie, Celltrion, Genuity, Janssen Pharmaceuticals, MSD, Pfizer, Takeda and Tillotts Pharma; and speaker/personal fees from AbbVie, Amgen, Bristol Myers Squibb, Celltrion, Dr Falk Pharma, Galapagos, Gilead Sciences, Janssen Pharmaceuticals, MSD, Pfizer, Takeda/Shire and Tillotts Pharma.
JPS reports speaker fees from AbbVie, Fresenius Kabi, Galapagos, Janssen-Cilag, Pharmacosmos, Takeda and Tillotts Pharma; and advisory board fees from AbbVie, Bristol Myers Squibb, Dr Falk Pharma and Galapagos.
ML reports consultancy/lecture fees from AbbVie, Bristol Myers Squibb, Eli Lilly, Galapagos, Janssen-Cilag, Johnson & Johnson, Medtronic, Pfizer, Takeda, and Tillotts, grants from
Galapagos and NFU and central reading services for Alimentiv.
MLH reports research grants from Ferring, Janssen, Pfizer, Tilllotts, and Takeda, speaker fees from AbbVie, Ferring, Galapagos, Meda, MSD, Tilllotts and Takeda; and advisory board fees from AbbVie, Eli Lilly, Galapagos, Janssen, MSD, Pfizer and Takeda.
RS reports no financial disclosures or conflicts of interest.
SV reports financial support for research from AbbVie, Galapagos, Johnson & Johnson, Pfizer and Takeda; speaker and/or consultancy fees from AbbVie, Abivax, AbolerIS Pharma, AgomAb Therapeutics, Alimentiv, Arena Pharmaceuticals, AstraZeneca, Bior Therapeutics (formerly Progenity), Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Cytoki Pharma, Dr Falk Pharma, Eli Lilly, Ferring Pharmaceuticals, Galapagos, Genentech-Roche, Gilead Sciences, GSK, Hospira, IMIDomics, Janssen Pharmaceuticals, Johnson & Johnson, Materia Prima, Mestag Therapeutics, MiroBio, Morphic Therapeutic, MRM Health, MSD, Mundipharma, Pfizer, ProDigest, Prometheus Biosciences, Robarts Clinical Trials, Surrozen, Takeda, Theravance Biopharma, Tillotts Pharma AG, VectivBio, Ventyx Biosciences and Zealand Pharma.
SS reports personal fees from AbbVie, Amgen, Arena Pharmaceuticals, Biogen, Bristol Myers Squibb, Celgene, Celltrion, Dr Falk Pharma, Eli Lilly, Ferring Pharmaceuticals, Fresenius Kabi, Galapagos/Gilead Sciences, Hikma Pharmaceuticals, I-Mab, Janssen Pharmaceuticals, Morphic Therapeutic, MSD, Mylan, Pfizer, Protagonist Therapeutics, Provention Bio, Sandoz/Hexal, Takeda, Theravance Biopharma and Ventyx Biosciences.
WR reports speaker fees from AbbVie, Celltrion, Ferring Pharmaceuticals, Galapagos, Janssen Pharmaceuticals, MEDICE, MSD, Pfizer, Roche, Sobi and Takeda; consulting fees from AbbVie, Amgen, AOP Health (formerly AOP Orphan), Boehringer Ingelheim, Bristol Myers Squibb, Calyx, Celltrion, Eli Lilly, Galapagos, Gilead Sciences, InDex Pharmaceuticals, Janssen Pharmaceuticals, MedAhead, Microbiotica, Pfizer and Takeda; advisory board fees from AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celltrion, Galapagos, Janssen Pharmaceuticals and Pfizer; and research funding from AbbVie, Janssen Pharmaceuticals, Sandoz, Sanofi and Takeda.
AJ and WS were employees of Galapagos NV (former study sponsor), and are now employees of Alfasigma S.p.A (current study sponsor).
MZ was an employee and shareholder of Galapagos NV (former study sponsor), and is now an employee of Alfasigma S.p.A (current study sponsor).

Clinical Case Summary

A 24-year-old male presented with jaundice and mild vertigo after a 10-day prodrome (asthenia, nausea, headache, fever). Ibuprofen (1200 mg/d) was taken for these symptoms only during the first 5 days. Labs revealed acute hepatocellular injury and elevated cholestasis (AST 215, ALT 862, FA 134, GGT 126 IU/L), marked mixed hyperbilirubinemia (Total 13.5 mg/dL, Direct 7.58 mg/dL) and coagulopathy (INR 1.59). Ultrasound showed hepatosplenomegaly. Viral hepatitis (HAV/HBV/HCV/CMV) and autoimmune/metabolic causes were excluded. Epstein-Barr Virus (EBV) serology showed low-titer positive VCA IgM but negative VCA IgG, EBNA IgG, and serum EBV DNA PCR, indicating recent non-active infection. Given ibuprofen timing and high RUCAM score, drug-induced liver injury (DILI) with a hepatocellular pattern was suspected. Liver biopsy confirmed acute hepatitis with lymphomonocytic infiltrate, necrosis and canalicular cholestasis. Despite improving liver function tests post-ibuprofen cessation, he developed worsening vertigo, severe ataxia, nausea, vomiting, hypophonia, necessitating nasogastric feeding/bed confinement. Cerebrospinal fluid (CSF) showed mild mononuclear pleocytosis (16 cells/mm³); a multiplex PCR pathogen panel (including EBV) was negative. Brain MRI/EEG were normal. Post-infectious EBV acute cerebellar ataxia was diagnosed concurrently with DILI, based on timing post-recent EBV, exclusion of active neurological infection (negative CSF PCR, normal imaging), mild pleocytosis, and supported by later IgG seroconversion. IV methylprednisolone treatment, chosen for clinical severity, led to significant neurological improvement within days and eventual recovery after physiotherapy. This case highlights the significant challenges of diagnosis and management of concomitant DILI and recent EBV infection with neurological sequelae, requiring careful differentiation of liver damage patterns (hepatocellular DILI vs cholestatic EBV) and optimal management of neurological symptoms.

References

Illustrative Material References:
- Liver biopsy histology slides (highlighting lymphomonocytic infiltrate, necrosis, and canalicular cholestasis characteristic of DILI).
- Table/Graph showing serial Liver Function Tests (AST, ALT, Bilirubin) over time, depicting injury peak and recovery trend.
- Table summarizing sequential Epstein-Barr Virus (EBV) serology results (VCA IgM, VCA IgG, EBNA IgG) demonstrating seroconversion.
- Table summarizing Cerebrospinal fluid (CSF) analysis results (cell count, protein, glucose, negative multiplex PCR).
- Representative Brain MRI images (axial/sagittal views) confirming absence of structural lesions or encephalitis signs.

Introduction

Active ulcerative colitis (UC) is typically assessed through clinical manifestations, laboratory examinations, and colonoscopy, which also determine the disease's severity.
An easy-to-use and patient-friendly technique for early clinical suspicion confirmation is intestinal ultrasonography (IUS). Ancillary technologies such as elastographic techniques have recently become available and can be used in conjunction with traditional IUS.

Aims & Methods

The study aim was to assess the accuracy and reproducibility of intestinal 2D-shear Wave Elastography (2D-SWE) as a predictor of disease’s activity and mucosal healing (MH). 2D-SWE was performed in 34 consecutive patients with active disease confirmed by colonoscopy. The 2D-SWE measurements (n. 10 with IQR/Med < 30%) was taken in the sigmoid colon by two independent operators at basal and 3 months after the starting of a new treatment regimen. The correlation between 2D-SWE and the Mayo endoscopic score (MES) was investigated along with clinical and conventional ultrasound parameters such as Bowel Wall Thickness (BWT) and Limberg score (LS).

Results

2D-SWE values (kPa) positively correlated with MES with a statistically significant difference between mucosal healing (MH) and active disease groups (p = 0.003). The AUROC (95% CI) for assessing mucosal healing by 2D-SWE was 0.84 (95% CI: 0.70-0.97). Using a cut off value of 21.5 kPa, sensibility and the specificity for mucosal healing were 0.62 and 0.99, respectively. The median 2D-SWE values obtained by the two independent operators were 19.7 kPa (IQR 16.2-26.8) and 17.7 kPa (IQR 14.4-23.7) respectively. 2D-SWE was also positively correlated with rectal bleeding, LS and BWT (r 0.38 p=0.027; r 0.43 p=0.014; r 0.33 p=0.057) but not with fecal calprotectin and C-reactive protein. No significant correlation was found between 2D-SWE values and clinical remission (Partial Mayo Score ≤ 2) after 3 months of a new treatment regimen (p = 0.491).

Conclusion

This study demonstrated the feasibility of 2D-SWE technique with an excellent inter-observer repeatability. The technique showed good accuracy in predicting mucosal healing, with increasing values correlating with disease severity. In the future, 2D-SWE could help reduce the number of colonoscopies and improve clinical decision making.

Disclosure

No discosure to declare

Introduction

Inflammatory bowel disease (IBD) is associated with an increased risk of cerebrovascular disease (CVD) and coronary heart disease (CHD). It has been suggested that chronic inflammation may be the mechanism. Previous studies have primarily assessed IBD as a group and not ulcerative colitis (UC) or Crohn’s disease (CD) separately.

Aims & Methods

This study aims to determine the relationship between UC and CD and CVD and CHD risk factors/outcomes in a large UK population. General practice electronic medical records were sourced from the United Kingdom (UK) via The Health Improvement Network (THIN). UC and CD risk factors and disease outcomes were identified through Read codes.

Results

Factors	UC Prevalence, n (%) n=3,432	UC Odds Ratio, 95% CI	CD Prevalence, n (%) n=2,831	CD Odds Ratio, 95% CI
Female Sex	1,796 (52.3%)	1.16, 1.09-1.25	1,689 (59.7%)	2.71, 2.08-3.62
Age	43.95 ± 14.4	0.99, 0.99-0.99	45.7 ± 15.7	0.95, 0.94-0.96
Diabetes Type II	417 (12.2%)	1.50, 1.35-1.66	265 (9.4%)	1.12, 0.98-1.27
Dyslipidemia	176 (5.1%)	1.26, 1.08-1.47	112 (4.0%)	0.96, 0.79-1.16
Obesity	7 (0.2%)	0.99, 0.47-2.10	7 (0.3%)	1.21, 0.58-2.55
AMI	113 (3.3%)	1.57, 1.30-1.89	57 (2.0%)	0.95, 0.73-1.23
Ischemic Stroke	47 (1.4%)	1.46, 1.09-1.95	23 (0.8%)	0.86, 0.57-1.30
Intracranial Hemorrhage	15 (0.4%)	1.67, 1.01-2.78	10 (0.4%)	1.35, 0.72-2.51
COPD	31 (0.9%)	1.85, 1.30-2.64	24 (0.9%)	1.74, 1.16-2.59

A total of 1,062,022 unique adult patients were available for analysis. There were 3,432 UC (mean age: 43.95 years, SD=14.4 years; 52% female) and 2,831 CD cases (mean age: 40.9 years, SD=14.06 years; 60% female).

Ulcerative Colitis: Univariate analysis in Table 1. Multiple logistic regression (MLR) of CHD risk factors and outcomes (adjusted in all models for age, sex, diabetes, COPD, dyslipidaemia, obesity, and statins) revealed statistically significant independent CHD risk factors: female sex (OR: 1.19, 95%CI: 1.11-1.28), younger age (OR: 0.98, 95%CI: 0.98-0.99), type 2 diabetes (OR: 1.22, 95%CI: 1.09-1.37), and increased risk of acute myocardial infarction (AMI) (OR: 1.35, 95%CI: 1.11-1.64).
MLR of CVD risk factors and outcomes (adjusted as above plus thrombolytic agents) found statistically significant independent CVD risk factors: female sex (OR: 1.19, 95%CI: 1.10-1.27), younger age (OR: 0.99, 95%CI: 0.98-0.99), diabetes type 2 (OR: 1.20, 95%CI: 1.07-1.34), statin use (OR: 1.13, 95%CI: 1.03-1.25), and any anti-thrombolytic agents (OR: 1.37, 95%CI: 1.25-1.51).
Crohn’s Disease: Univariate analysis in Table 1. MLR of CHD risk factors and outcomes (adjusted) revealed statistically significant independent CHD risk factors: female sex (OR: 0.92, 95%CI: 0.85-0.99), younger age (OR: 0.98, 95%CI: 0.97-0.99), statin use (OR: 1.23, 95%CI: 1.11-1.36), and an increased likelihood of death (OR: 1.28, 95%CI: 1.12-1.47).
MLR of CVD risk factors and outcomes (adjusted) revealed statistically significant independent CVD risk factors: female sex (OR: 0.91, 95%CI: 0.84-0.98), younger age (OR: 0.97, 95%CI: 0.96-0.98), anti-thrombolytic agents (OR: 1.71, 95%CI: 1.55-1.90), and an increased likelihood of death (OR: 1.18, 95%CI: 1.03-1.35).

Conclusion

UC cases are more likely to be female, have diabetes, be taking statins, and anti-thrombolytic agents, and have an increased risk of AMI and death. CD cases are less likely to be female, but more likely to be taking statins, anti-thrombolytic agents, and more likely to die.

Disclosure

Guy D. Eslick and Michael P. Jones have nothing to disclose. Nicholas J. Talley Disclosures: GutSee Ltd (consulting microbiome, 2025), Brown University, Agency for Health Care Research and Quality (fiber and laxation) (2024), Rome Foundation (member gastroduodenal committee) (present) Biocodex (FD diagnostic tool) (present) Microba (consulting microbiome - commencing 2025) Comvita Manuka Honey (FD trial consulting) (2025), BluMaiden outside the submitted work. In addition, Dr. Talley has a patent Nepean Dyspepsia Index (NDI) 1998, a patent Licensing Questionnaires Talley Bowel Disease Questionnaire licensed to Mayo/Talley, “Diagnostic marker for functional gastrointestinal disorders” Australian Provisional Patent Application 2021901692, ”Methods and compositions for treating age-related neurodegenerative disease associated with dysbiosis” US Patent Application No. 63/537,725.
Boards: The Gut Foundation Board (2025-present), Asia Pacific Association of Medical Editors (APAME) Board (President 2023-2025), Doctors for the Environment (Chair 2024-present), Luminal Faculty GESA (Chair) (2023-2025)
Editorial: UptoDate (Section Editor), Mayo Clinic Proceeding Associate Editor (2023-present)
Financial support: Dr. Talley is supported by funding from the National Health and Medical Research Council (NHMRC) to the Centre for Research Excellence in Digestive Health and he holds an NHMRC Investigator grant.