Introduction

The influence of environmental factors in the course of inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), is unclear.

Aims & Methods

We aimed to investigate the role of environmental factors in disease activity, severity, and initial course of IBD.
Since May 1^st, 2021, all adult and pediatric patients with incident IBD within a catchment area encompassing 20% of the Danish population were enrolled in the prospective population-based Copenhagen IBD Inception Cohort.¹ Upon diagnosis, all adult patients diagnosed between May 2021 and May 2023 were asked to report environmental factors using the International Organisation of IBD (IOIBD) and HeartDiet questionnaires.
A severe disease course was defined as a composite of a need for either oral glucocorticoids, immunomodulators, biologics, or intestinal resection within three months of disease. Severe disease activity was defined either endoscopically (UC: Mayo Endoscopic Score=3, CD: Simple Endoscopic Score-CD>16) or as a composite of biochemical activity (f-calprotectin>1800 μg/ g or C-reactive protein > 10 mg/L) and clinical activity (UC: Simple Clinical Colitis Activity Index (SCCAI)>10, CD: Harvey-Bradshaw Index (HBI)>7). Clinical remission was defined as SCCAI<3 or HBI<5 points. All findings were adjusted for gender, age, and disease phenotype in multivariable logistical analysis yielding adjusted odds ratios (aOR (95% confidence interval)).

Results

The population consisted of 208 and 128 patients with incident UC and CD (67.5% and 63.1% of the original cohort), respectively, who completed the questionnaires within a median of 1.3 months (IQR 0.4 – 3.4 months) from diagnosis. No clinical differences were between participants and non-participants. During six months of follow-up, 128 (61.5%) and 77 (60.2%) patients with UC and CD, respectively, achieved clinical remission.
In patients with UC, low intake of saturated fatty acids was associated with reduced probability of achieving clinical remission at follow-up (aOR= 0.42 [0.18;0.95]). In patients with CD, a high intake of whole meal bread was significantly associated with a reduced risk of severe activity (aOR=0.40 [0.16;0.98]), while high intake of fruits (aOR=0.27 [0.07;0.99]), vegetables (aOR=0.27 [0.09;0.80]), or fibers (aOR=0.30 [0.09;0.96]) were associated with lower risk of stricturing or penetrating phenotypes.
A severe disease course of UC was significantly and inversely associated with active smoking (aOR=0.28 [0.08;0.95]), intake of minced meat (aOR=0.38, [0.15;0.97]), and ultra-processed food (aOR=0.22 [0.06;0.78]). Conversely, minced meat was associated with elevated risk of a severe course of CD (aOR=3.59 [1.41;9.10]). In addition, active smoking was associated with increased risk of CD-related hospitalization (aOR=11.89 [2.53;55.92]) and stricturing phenotype (aOR=5.28 [1.76;15.85]). On the other hand, previous pregnancy (aOR=0.28 [0.09;0.93]) was associated with a reduced risk of a severe course of CD.
Among childhood factors, appendectomy was associated with increased risk of UC-related hospitalization (aOR=5.46 [1.05;28.34]), CD-related hospitalizations (aOR=11.89 [2.53;55.92]), and CD-related resections (aOR=19.48 [4.20;90.35]).

Conclusion

In conclusion, our prospective population-based study unveiled distinct environmental exposures to be associated with important clinical endpoints in UC and CD. These findings hold clinical value as they inform personalized patient counseling on lifestyle factors that might influence outcomes of IBD.

References

1. Attauabi M, Madsen GR, Bendtsen F, et al. Influence of Genetics, Immunity and the Microbiome on the Prognosis of Inflammatory Bowel Disease (IBD Prognosis Study): the protocol for a Copenhagen IBD Inception Cohort Study. BMJ Open. 2022;12(6):e055779. doi:10.1136/bmjopen-2021-055779

Disclosure

Mohamed Attauabi: None
Gorm Roager Madsen: Personal fees from Tillotts
Flemming Bendtsen: Tillotts, Ferring
Jakob Benedict Seidelin: has received research grants from Takeda, Janssen, the Danish Research Council, and the Capital Region Denmark, and is national coordinator of studies from AbbVie, Arena Pharmaceuticals, Ely Lilly, and Boehringer Ingelheim.
Johan Burisch: reports grants and personal fees from AbbVie, grants and personal fees from Janssen-Cilag, personal fees from Celgene, grants and personal fees from MSD, personal fees from Pfizer, grants and personal fees from Takeda, grants and personal fees from Tillots Pharma, personal fees from Samsung Bioepis, grants and personal fees from Bristol Myers Squibb, grants from Novo Nordisk, personal fees from Pharmacosmos, personal fees from Ferring, personal fees from Galapagos, outside the submitted work.

Introduction

Active inflammatory bowel disease in pregnancy is associated with an increased risk of adverse maternal and neonatal outcomes. Understanding patterns of disease activity may inform strategies for improving outcomes.

Aims & Methods

A retrospective cohort study was conducted of pregnancies managed through an IBD–antenatal clinic between August 2020 and January 2025. Patients were stratified into 2 groups based on disease activity during pregnancy. Active disease was defined using the Physician Global Assessment, symptoms, and biomarkers (CRP and/or FCP). Disease flare was defined by an increase in symptoms and/or biomarkers from their baseline. Disease activity was assessed pre-conception (within 6 months before pregnancy) during pregnancy and post-partum (up to 6 months post birth).

Results

Of 209 pregnancies (Table 1), 76.3% (n=158) were in remission and 23.7% (n=49) had active disease pre-conception. Among those with active disease, 81.6% (n=40) remained active into pregnancy, while 18.4% (n=9) achieved remission. Of those in remission at pre-conception, 73.4% (n=116) stayed in remission during pregnancy, and 24.7% (n=39) flared. 2 patients with no pre-conception data were active in pregnancy.
Of 125 patients in remission during pregnancy, 73.6% (n=92) stayed in remission post-partum and 12.0% (n=15) flared. Among 81 patients with active disease in pregnancy, 39.5% (n=32) remained active, and 53.0% (n=43) achieved remission post-partum.
Patients in remission through pregnancy had a higher mean BMI (24.5 vs 23.0 kg/m², p=0.027), were more likely to be of white ethnicity compared to minority ethnic groups (61.0% vs 38.4% p=0.0026), have a diagnosis of Crohn’s disease (58.6% vs 37.0%, p=0.0088), and be nulliparous (51.2% vs 35.0%, p=0.0414).
At conception, approximately 30% of patients in both groups were not receiving any treatment. During pregnancy, this proportion fell to 8.6% in the active group, reflecting therapy escalation. Use of biologics increased from 22.2% to 38.2% in the active group and remained stable at 36.0% in the remission group. Corticosteroid use was exclusive to the active disease cohort (6.2% at conception; 23.5% during pregnancy).
Active disease in pregnancy was associated with higher rates of adverse outcomes: gestational diabetes (12.3% vs 8.0%, p=0.001), fetal growth restriction (4.9% vs 0%, p=0.044), and low birth weight (<2500g: 14.6% vs 2.4%, p=0.015). While rates of small for gestational age infants were higher in the active group (9.9% vs 4.0%), this was not statistically significant.
Emergency c-sections were more common in the active group (29.9% vs 15.0%, p=0.03), while elective c-sections were more frequent in the remission group (27.5% vs 13.4%, p = 0.03). Women in remission more often had an intact perineum (63.6% vs 54.7%), while episiotomy was more frequent in those with active disease (18.8% vs 11.7%); both did not reach statistical significance.

Conclusion

This study underscores the impact of active IBD on maternal and neonatal outcomes.
Nearly 1 in 4 women in remission at preconception flared during pregnancy. This highlights the need for effective pre-conception counselling, access to disease monitoring tools, multidisciplinary management and timely treatment optimisation to sustain remission during pregnancy.

Disclosure

No disclosures

Introduction

Upadacitinib (UPA) is an oral, reversible Janus kinase inhibitor (JAKi) approved for the treatment of patients with moderate-to-severe ulcerative colitis (UC).^1-2 Despite substantial evidence from clinical trials supporting the use of UPA for treating UC, real-world (RW) data on its effectiveness and safety remain limited.³ The Prospective Real-World Study of UPA in UC (PROFUNDUS) is an ongoing multi-country, open-label, noninterventional, observational study aimed to evaluate the effectiveness and safety of UPA in patients with moderate-to-severe UC in RW practice (initiated 15 Aug 2022).

Aims & Methods

PROFUNDUS recruited 785 adult patients (18 to 75 years [yrs] of age) with moderate-to-severe UC initiating UPA in 16 countries worldwide. UPA was administered in accordance with the terms of the local marketing authorization, with patient treatment determined by the investigator, and patients followed for up to 3 yrs (156 weeks [wk]). This analysis represents data available after the first 500 patients completed 6 months of treatment or discontinued before 6 months, with a data cut-off of 28 Feb 2025. Of the first 500 patients who provided informed consent and met the inclusion criteria, the full analysis set (FAS) included 490 patients who initiated a once-daily UPA dosing regimen. This analysis reported baseline demographics and disease characteristics among FAS; the time to achievement of first clinical response per daily Partial Adapted Mayo Score (pAMS) and the percentage of patients achieving clinical response per pAMS at the end of UPA induction (wk 8) or extended induction (wk 16) were reported among evaluable patients who took at least 1 dose of UPA and had available scores to define the outcomes, a subset of FAS. Safety outcomes were analysed through week 26 (6 months), with treatment-emergent adverse events (TEAEs) presented as patient numbers and percentages.

Results

Among FAS, the patient age range was 18 to 79 yrs; 43.3% were female. At baseline (defined as the last available assessment on or before the first dose date of UPA), pAMS were as follows: < 2: 26.5%; 2-4: 48.1%; > 4-5: 18.8%; > 5-6: 6.6%; with score 0 indicative of inactive disease, while a score of 6 indicates active disease and spontaneous bleeding.⁴ At baseline, 51.3% of patients had a history of intolerance or inadequate response (IR) to advanced therapies (AT-IR), with 13.1% of patients who failed ≥ 1 JAKi. Among evaluable patients, the median (IQR) time to achieve the first clinical response per daily pAMS was 4 (3.0-8.0) days (N = 373; Table). By the end of induction treatment (wk 8 or 16), 79.6% (258/324) of the evaluable UPA-treated patients achieved clinical response per pAMS (Table). Among UPA-treated patients, the occurrence rates of any treatment-emergent adverse events (TEAEs) and TEAEs possibly related to the study treatment were as follows: any adverse event (AE) (51.2%; 34.9%), serious AEs (5.5%; 2.2%), and severe AEs (5.1%; 2.2%) (Table).

Conclusion

In this interim analysis of the PROFUNDUS study, UPA demonstrated rapid effectiveness in achieving clinical response in patients with moderate-to-severe UC in RW practice, in a wide variety of age ranges, consistent with the efficacy observed in the UPA UC clinical trials.¹ Overall, UPA was well-tolerated, with few serious AEs reported, and most of these were assessed as unrelated to UPA by the investigator.

References

1. AbbVie Inc. RINVOQ (Upadacitinib) [package insert] U.S. Food and Drug Administration website. https://www.rxabbvie.com/pdf/rinvoq_pi.pdf. Revised May 2023. Accessed 25 Feb 2025.
2. AbbVie DG& CoK. RINVOQ. Summary of Product Characteristics. European Medicine Agency website. https://www.ema.europa.eu/en/documents/product-information/rinvoq-epar-product-information_en.pdf. Revised Feb 2025. Accessed 25 Feb 2025.
3. Seidelin J, et al. J Crohn’s Colitis. 2025;19(1):i1260-i1262. [Abstract].
4. Louis E, et al. JAMA. 2024;332(11):881-897.

Disclosure

Funding: AbbVie funded this study (PROFUNDUS; NCT05494606) and participated in the study design, research, analysis, data collection, interpretation of data, reviewing, and approval of the publication. All authors had access to relevant data and participated in the drafting, review, and approval of this publication. No honoraria or payments were made for authorship.
Acknowledgments: AbbVie and the authors thank the participants, study sites, and investigators who participated in this clinical trial. Paulette A. Krishack, PhD, of AbbVie, provided medical writing support.
Disclosures: Remo Panaccione has received consulting fees, speaker fees, and research support from Abbott, AbbVie, Abbivax, Alimentiv Amgen, AnaptysBio, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene Corporation, Celltrion, Cosmos Pharmaceuticals, Eisai, Elan, Eli Lilly, Ferring Pharmaceuticals, Galapagos, Fresenius Kabi, Genentech, Gilead Sciences, GlaxoSmithKline, JAMP Bio, Janssen Pharmaceuticals, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pendopharm, Pfizer, Progenity, Prometheus Biosciences, Protagonist Therapeutics, Roche, Sandoz, Sanofi, Satisfai Health, Sublimity Therapeutics, Takeda Pharmaceuticals, Theravance Biopharma, Trellus, Viatris, Ventyx, and UCB.
Gareth Parkesreports personal payments, honoraria, speaker fees, travel grants and/or fellowships from AbbVie, Allergan, Bristol Myers Squibb, Celltrion, Ferring, Galapagos, Janssen, Napp, Takeda, and Tillotts, and directorship and shareholding with Ampersand Health. TR reports personal grants from AbbVie; personal consulting fees from AbbVie, Arena, Aslan, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Eli Lilly, Ferring, Galapagos, Gilead, GSK, Heptares, LabGenius, Janssen, MonteRosa, Mylan, MSD, Novartis, Numab, Pfizer, Roche, Sandoz, Takeda, UCB and XAP; membership of the ECCO Scientific Committee, and membership in the UEG Scientific Committee; director of Endoread.
Mathurin Fumery has received lecture and consulting fees from AbbVie, Amgen, Biogen, BI, BMS, Celgene, Celltrion, CTMA, Ferring, Fresenius, Galapagos, Gilead, Janssen, Pfizer, Lilly, MSD, Sandoz, Takeda, Tillots, and Viatris.
Dominik Bettenworth is on the advisory board or consultant for Amgen, AbbVie, Dr. Falk Foundation, Ferring, MSD, Pfizer, Pharmacosmos, Roche, Takeda, Tillotts Pharma, and Vifor. Silvio Danese has served as a speaker, consultant, and advisory board member for Schering-Plough, AbbVie, Actelion, Alphawasserman, AstraZeneca, Cellerix, Cosmo Pharmaceuticals, Ferring, Genentech, Grünenthal, Johnson and Johnson, Millenium Takeda, MSD, Nikkiso Europe GmbH, Novo Nordisk, Nycomed, Pfizer, Pharmacosmos, UCB Pharma and Vifor.
Pierre A Morisset, Madhuja Mallick, Shirley H. Chen, and Smitha Suravaram are employees of AbbVie and may own stock options.

Introduction

Upadacitinib, a selective JAK inhibitor, is approved for moderate-to-severe Crohn’s disease (CD). However, real-world data on its effectiveness and safety, particularly in highly refractory populations, remain scarce. The UPITA-Crohn registry was established to evaluate the outcomes of upadacitinib in clinical practice across multiple centers in Andalusia, Spain.

Aims & Methods

This ambispective, multicenter registry included 142 patients with refractory CD treated with upadacitinib in 12 Andalusian hospitals. Clinical and biochemical data were collected at baseline, weeks 12 and 16, and at 6 months. Clinical remission (CR) was defined as a Harvey-Bradshaw Index (HBI) <5; clinical-biochemical remission (CBR) as HBI <5, CRP <5 mg/L, and fecal calprotectin <250 μg/g; and steroid-free remission (SFR) as HBI <5 without corticosteroids from week 12. Outcomes were also analyzed overall and according to prior exposure to advanced therapies.

Results

The UPITA-Crohn registry cohort included 142 patients with refractory Crohn’s disease. The mean age was 40.8 years (range 18–76), with 40% male. The mean disease duration at the time of upadacitinib initiation was 13.3 years (range 1–42), with a mean of 2.7 failed advanced therapies, highlighting a population with longstanding and complex disease. Most patients had ileocolonic involvement (50%), 22% had perianal disease, and 32% had previously undergone resective surgery.
The majority (74.4%) received induction with upadacitinib 45 mg for 12 weeks. At week 12, clinical remission was achieved by 54% of patients, with 15% reaching clinical-biochemical remission. At 6 months, among those still on treatment, 48.3% maintained clinical remission, 16.1% achieved clinical-biochemical remission, and 18.4% achieved steroid-free remission (Table 1).
When stratified by prior therapy, 6-month clinical remission was similar between patients with ≥2 prior advanced therapies (48.5%) and those with only 1 prior therapy (47.4%), with no significant difference. Steroid-free and clinical-biochemical remission rates were also slightly higher among less refractory patients, but differences were modest.
A total of 31 patients (21.8%) discontinued upadacitinib before 6 months, mainly due to primary non-response (70.9%). Adverse events were reported in 21.1% of patients, most commonly infections (9 cases), acne (7), transient transaminase elevation (5), and herpes zoster (2). Seven discontinuations were due to serious adverse events, including thrombosis, stroke, myocardial infarction, fever, and severe infections.

Table 1: Effectiveness Outcomes

Conclusion

Upadacitinib demonstrated meaningful effectiveness and a manageable safety profile in a real-world cohort of refractory Crohn’s disease patients. Notably, clinical remission rates remained stable even in those with multiple prior advanced therapies, suggesting upadacitinib may be a valuable option for patients with limited alternatives.

Introduction

Treatment options for patients with mild-to-moderate ulcerative colitis (UC) failing 5-ASA are limited. MH002 is an optimized live biotherapeutic product consisting of 6 non-pathogenic, well‑characterized commensal bacteria. Its anticipated mechanism in UC is reversion of dysregulated host inflammatory mechanisms and interactions with gut microbiota, and induction of mucosal healing.

Aims & Methods

In this 2:1-randomized, double-blind, placebo-controlled frist-in-disease study (EudraCT 2020-001355-33), 45 patients with mild-to-moderate active UC (Modified Mayo Score [MMS] =4-8 and centrally assessed Mayo Endoscopic Sub-score [MES] ≥2) received treatment with 400mg MH002 or placebo (PBO) once daily for 8wks, followed by an 8-wk extension with MH002 (same dose) unless responding to PBO. All patients were on stable 5-ASA for ≥4wks prior and during the study. Full colonoscopies with biopsies were performed at baseline and wk8. The primary endpoint was the rate of treatment-emergent adverse events. Exploratory efficacy endpoints included clinical remission (MMS≤2 with all sub-scores ≤1 and rectal bleeding =0), endoscopic improvement (MES≤1), clinical response (reduction of MMS of ≥3 points or a reduction of ≥1 point of the Mayo sub-scores for stool frequency and rectal bleeding), biomarker normalisation, and mechanistic effects of MH002. Here, changes in faecal microbiome (shotgun metagenomics) and gene expression of colonic mucosal biopsies (whole transcriptome RNAseq) are reported.

Results

MH002 treatment was safe and well tolerated, and resulted in clinically meaningful improvements in disease activity and inflammatory parameters¹. At wk8, endoscopic improvement was achieved in 6/28 (21%) and 2/14 (14%) patients treated with MH002 and PBO, respectively. In this MH002-treated subgroup, α-diversity (Pielou eveness, Shannon diversity) increased significantly as compared to baseline whereas the relative abundance of Enterobacterales decreased significantly over time (1-sided Wilcoxon p<0.05). Similar but less pronounced changes were observed in MH002-treated patients achieving clinical response or even no response.
Furthermore, a total of 1496 significantly differentially expressed genes (DEGs) at wk8 vs. baseline were found in the MH002-treated patients with endoscopic improvement (p<0.05; lnFC>1.5). Among the most significantly downregulated DEGs are the regenerating islet-derived (REG) genes (REG1α, REG1β, REG3α) and serum amyloid A (SAA) genes (SAA1, SAA2, SAA4). Since REG proteins have bactericidal, anti-inflammatory, and tissue repair functions, and SAA are acute-phase proteins induced by inflammatory stimuli, this could result from a state of lower inflammation and activation by bacterial components, from the resolution of tissue injury, and from lower local gut inflammation following treatment. Lastly, when intersecting these DEGs with UC-associated DEGs reported in 3 independent studies^2,3, 16-21% of intersecting DEGs showed fold changes in opposite polarity to UC vs. healthy individuals whereas 0-3% showed similar fold changes.

Conclusion

These observations suggest that MH002-treated patients had positive changes in gut microbial diversity and overall microbiome composition, coinciding with clinical improvement and downregulation of genes involved in immune and inflammatory responses, antimicrobial defense mechanisms, and resulting in dampening of immune cells’ activity, and associated with UC. MH002, therefore, represents a promising new treatment for mild-to-moderate UC patients insufficiently controlled with 5‑ASA. These results warrant further development in a phase 2/3 study.

References

1) Vermeire et al. JCC 2024 (S1)
2) Lloyd-Price et al. Nature 2019
3) Haberman et al. Nat Commun 2019

Disclosure

SB, MD, MdL, IP, KC, SP & LH: employee, paid consultant and/or shareholder of MRM Health
SV: financial support for research from AbbVie, J&J, Pfizer, Takeda and Galapagos; speakers’ and/or consultancy fees from AbbVie, Abivax, AbolerISPharma, AgomAb, Alimentiv, Arena Pharmaceuticals, AstraZeneca, BMS, Boehringer Ingelheim, Celgene, Cytoki Pharma, Dr Falk Pharma, Ferring, Galapagos, Genentech-Roche, Gilead, GSK, Hospira, Imidomics, Janssen, J&J, Lilly, Materia Prima, Mestag Therapeutics, MiroBio, Morphic, MRM Health, Mundipharma, MSD, Pfizer, Prodigest, Progenity, Prometheus, Robarts Clinical Trials, Surrozen, Takeda, Theravance, Tillots Pharma AG, VectivBio, Ventyx, Zealand Pharma

Introduction

Ozanimod (OZA) is approved for the treatment of moderately to severely active ulcerative colitis (UC) in adults. In the phase 3 True North (TN; NCT02435992) study, patient (pt) responses to OZA were heterogenous at Week (W) 52. Group-based trajectory modeling (GBTM) can be used to identify patterns of therapeutic responses in patient subpopulations.

Aims & Methods

This TN post hoc analysis employed GBTM to identify patterns of OZA response trajectories during the TN maintenance period (MP) in W10 OZA clinical responders who were rerandomized to continue OZA (OZA/OZA arm; n=230) in MP. Change from baseline (BL; TN W0) in partial Mayo score (PMS) was used as a variable for identifying pt clusters with various OZA response patterns. GBTM, a specialized application of finite mixture models,¹ was used to estimate OZA response trajectories. GBTM was determined by maximum likelihood estimation, and the optimal model was selected using the Bayesian information criterion. The last observation carried forward imputation method was used for handling missing data. After modeling, clinical and mucosal outcomes at W52 were compared in the GBTM-identified pt clusters.

Results

Of the 230 pts in the MP OZA/OZA arm, 1 pt did not have postbaseline PMS data available and was excluded from this analysis. Five distinct groups of pt-response patterns to OZA therapy were identified during MP. At W10, a PMS response was observed in all 5 trajectory groups. Over the 42 weeks during MP, trajectory groups diverged into fast sustained improvement (Group 1; n=38 [16.6%, 38/229]); slow sustained improvement (Group 2; n=85 [37.1%, 85/229]); gradual improvement (Group 3; n=60 [26.2%, 60/229]); fast rebound (Group 4; n=25 [10.9%, 25/229]); and slow rebound (Group 5; n=21 [9.2%, 21/229]). Although all pts entering the MP were OZA clinical responders, 20% of pts did not demonstrate sustained improvement from BL in PMS (Groups 4 and 5), but 80% did demonstrate sustained improved from BL in PMS (Groups 1–3). From W10 onward, 26.2%, 37.1%, and 16.6% of pts achieved and maintained PMS reductions of at least 3.98, 5.27, and 6.71 points, respectively. Pts in Groups 4 and 5 had a slightly younger age at diagnosis and a higher W10 Geboes histologic index score than the other trajectory groups; notably, pts in Group 4 had the most corticosteroid use at screening (Table). At W52, more pts in Groups 1–3 combined achieved clinical response (74%) and clinical remission (46%) than those in Groups 4 and 5 combined (7% and 2%, respectively). Furthermore, Groups 1–3 combined had more pts with endoscopic improvement (56%) and mucosal healing (37%) at W52 than Groups 4 and 5 combined (7% and 2%, respectively).

Conclusion

Five groups of pt-response trajectories to OZA therapy were identified, with approximately 80% of pts in Groups 1–3 classified as having sustained response to OZA treatment. This analysis indicates that GBTM identifies clinically meaningful pt subgroups by pt-response patterns to OZA treatment. This approach needs to be validated in prospective studies.

References

1. Nagin D. Group-based trajectory modeling: an overview. Ann Nutr Metab. 2014;65:205-210.

Disclosure

The study was funded by Bristol Myers Squibb, Princeton, NJ, USA.
SS: received speaker fees from and consulted for AbbVie, Amgen, Bristol Myers Squibb, Eli Lilly, Falk Pharma, Galapagos/Gilead, Genentech/Roche, Hikma, Janssen, MSD, Pfizer, and Takeda.
BGF: consulted for AbbVie, ActoGeniX, Albireo, Amgen, AstraZeneca, Avaxia Biologics, Baxter, Biogen Idec, Boehringer Ingelheim, Bristol Myers Squibb, Calypso, Celgene, Elan, Eli Lilly, enGene, Ferring Pharmaceuticals, Genentech/Roche, gIcare, Gilead, Given Imaging, GlaxoSmithKline, Ironwood, Janssen, Johnson & Johnson, Lexicon, Merck, Millennium, Nektar, Novo Nordisk, Pfizer, Prometheus, Protagonist, Sanofi, and UCB; director for Robarts Clinical Trials.
BES: received speaker fees from and consulted for Abivax, Bristol Myers Squibb, Eli Lilly, Janssen, Pfizer, and Takeda; received consulting fees from AbbVie, Adiso Therapeutics, Alimentiv, Amgen, Arena, Artizan Biosciences, Artugen, AstraZeneca, Bacainn Therapeutics, Boehringer Ingelheim, Boston Pharmaceuticals, Calibr, Celltrion, ClostraBio, Cytoki Pharma, Connect Biopharma, Entera, Evommune, Fresenius Kabi, Galapagos, Genentech, Gilead Sciences, GlaxoSmithKline, Gossamer Bio, Imhotex, Immunic, InDex Pharmaceuticals, Innovation Therapeutics, Inotrem, Ironwood Pharmaceuticals, Kaleido Biosciences, Kallyope, MiroBio, Morphic Therapeutics, MRM Health, OSE Immunotherapeutics, Progenity, Prometheus Biosciences, Protagonist Therapeutics, Q32 Bio, RedHill Biopharma, Sun Pharma, Surrozen, Synlogic, Target RWE, Teva, Theravance Biopharma, TLL Pharmaceutical, USWM Enterprises, Viela Bio, and VTA Labs; received personal fees and stock options for consulting from Thelium Therapeutics and Ventyx.
FR: consulted or participated in advisory board for 89Bio, AbbVie, Adnovate, Agomab, Allergan, Arena, Boehringer Ingelheim, Celgene/Bristol Myers Squibb, CDISC, Ferring, Galapagos, Galmed Pharmaceuticals, Genentech, Gilead, Gossamer, Guidepoint, Helmsley, Horizon Therapeutics, Image Analysis Limited, InDex Pharmaceuticals, Janssen, Koutif Therapeutics, Mestag Therapeutics, Metacrine, Morphic Therapeutic, Organovo, Origo, Pfizer, Pliant, Prometheus Biosciences, Receptos, REDX, Roche, Samsung, Surmodics, Surrozen, Takeda, TD Cowen, Techlab, Theravance, Thetis Pharmaceuticals, UCB, and Ysios Capital.
JT: received advisory board or speaker fees from AbbVie, Bristol Myers Squibb, Janssen, and Pfizer; received grant support from AbbVie.
ZL, AJ, HW, and MTO: employees and/or shareholders of Bristol Myers Squibb.
MTA: consulted or participated in advisory board for AbbVie, Amgen, Arena, Bristol Myers Squibb, Celsius Therapeutics, Eli Lilly, Gilead Sciences, Janssen, Microba Life Sciences, Pfizer, Prometheus Biosciences, UCB Biopharma, and WebMD Global; reported teaching, lecturing, or speaking for Alimentiv, Amgen, Janssen, and Takeda.
PD: received research support from Bristol Myers Squibb, Pfizer, and Takeda; consulted for Abivax, Adiso, Bristol Myers Squibb, Eli Lilly, Gilead, GlaxoSmithKline, Janssen, Novartis, Pfizer, and Takeda.