Abstract
Background:
Data on STRIDE-II treatment target achievement in Middle Eastern inflammatory bowel disease (IBD) populations remain limited. We assessed the prevalence and predictors of deep remission at a tertiary IBD center in the United Arab Emirates.
Methods:
A cross-sectional analysis was conducted on 389 IBD patients (242 Crohn’s disease [CD], 147 ulcerative colitis [UC]) on stable treatment for ≥6 months. Deep remission required concurrent clinical, biochemical, and endoscopic remission. Predictors were identified using logistic regression.
Results:
Complete STRIDE-II assessment was available in 264 patients (67.9%). Deep remission was achieved in 164 patients (62.1% available-case; 42.2% conservative, treating incomplete assessments as failure). In the advanced therapy subgroup (n = 182), deep remission was 64.3% available-case and 43.8% conservative. Clinical remission was 78.7%, biochemical remission 72.4%, and endoscopic remission 69.2%. Rates were similar between CD and UC, and complicated CD phenotypes achieved equivalent deep remission to non-complicated disease (62.7% vs 63.9%, P = 0.85). Disease duration was the strongest overall predictor (OR 1.06 per year, 95% CI 1.02–1.10, P = 0.009). CD-specific predictors included B3 penetrating behavior (OR 5.49, P = 0.027) and male sex (OR 0.47, P = 0.039). In UC, older age and male sex were independently associated with remission. Higher advanced therapy exposure predicted lower remission odds in CD (adjusted OR 0.70, P = 0.034). No individual therapy demonstrated significant superiority in adjusted drug comparisons. Efficacy was preserved at second-line (67.4%) with decline at third-line (50.0%).
Conclusion:
Deep remission rates in this UAE tertiary center cohort were comparable to or numerically higher than international reports. Further validation in prospective, geographically diverse populations is warranted.
Keywords: Ulcerative colitis, Crohn’s disease, inflammatory bowel disease, remission induction, treatment outcome
INTRODUCTION
Inflammatory bowel disease (IBD) represents a growing global health challenge, with incidence rising across all epidemiologic transition stages from emergence to compounding.[1,2] The Global Burden of Disease Study documented over 3 million affected individuals in 2017.[3] In the Arabian Gulf region, IBD incidence and prevalence has increased substantially over the past two decades,[4,5,6] with evidence of aggressive phenotypes and younger age at diagnosis compared to Western populations.
This rising burden has coincided with an expansion of therapeutic options, with advanced therapies now available spanning multiple mechanisms of action.[7] Clinical trials and guidelines now advocate for risk-stratified top-down therapy and treat-to-target approaches, representing a paradigm shift from conventional step-up strategies.[8,9,10,11] The STRIDE-II consensus established treatment targets encompassing short-term (clinical remission), intermediate-term (biochemical remission), and long-term (endoscopic remission) goals.[12] However, real-world STRIDE-II implementation remains challenging. The multinational IBD-PODCAST study, spanning over 100 sites across 10 countries, revealed that approximately half of patients exhibited suboptimal disease control despite most receiving advanced therapies.[13] Regional cohorts from Spain, Italy, the United Kingdom, and Canada have replicated these findings, with impaired quality of life the predominant contributor to suboptimal control in over half of cases.[14,15,16,17]
The United Arab Emirates has witnessed substantial evolution in IBD clinical burden over the past two decades, with increasing case complexity, rising proportions of moderate-to-severe disease presentations, and particularly aggressive pediatric phenotypes characterized by extensive disease at diagnosis and high complication rates.[4,5] Despite the expanding therapeutic arsenal and defined treatment targets, substantial gaps persist in understanding real-world STRIDE-II achievement rates in Middle Eastern populations, limiting our ability to benchmark regional outcomes against international standards.[18] This study provides the first systematic STRIDE-II evaluation from a tertiary IBD center in the Gulf region. We assessed remission rates across clinical, biochemical, and endoscopic domains; compared outcomes between disease types and advanced therapy classes; and identified predictors of deep remission. Our findings provide regional benchmarks for treat-to-target strategies in an era where global data demonstrate that approximately half of patients fail to achieve optimal control despite advanced therapy use.
PATIENTS AND METHODS
Study design and population
This cross-sectional analysis used prospectively collected routine clinical data from the IBD Center of Sheikh Shakhbout Medical City (SSMC), Abu Dhabi, UAE. Patients were eligible if they had[1]: confirmed diagnosis of CD or UC according to established criteria[2]; diagnosis at least one year prior to enrolment[3]; prospectively collected remission data at clinic visits between October 2024 and December 2025; and[4] current treatment for at least six months or no active treatment, corresponding to the STRIDE-II long-term assessment timeframe. Patients with IBD-unclassified, prior proctocolectomy, or current enrolment in interventional trials were excluded. Two populations were defined: the primary cohort comprising all eligible patients, and the advanced therapy (AT) subgroup comprising patients receiving advanced therapy for at least six months. The study was approved by the SSMC Research Ethics Committee (reference: SSMCREC-585) on 02 March 2025.
The six-month minimum therapy duration was selected to ensure patients had completed induction and early maintenance phases, consistent with the STRIDE-II treatment phase framework and the IBD-PODCAST study design, which similarly focused on patients in the long-term treatment phase.[12,13] Assessment before 6 months may capture patients still responding to induction therapy or with active disease not yet optimally controlled, rather than reflecting established treatment outcomes.
Outcome definitions
Clinical remission was defined as Harvey-Bradshaw Index of 4 or less for CD and Partial Mayo Score of 1 or less for UC. Biochemical remission required CRP of 5 mg/L or less and/or faecal calprotectin below 250 micrograms per gram. These biochemical thresholds are based on STRIDE-II Recommendation 12,[12] which defines faecal calprotectin of 100–250 mg/g as an intermediate treatment target in both CD and UC. We adopted the less stringent end of this range (faecal calprotectin <250 mg/g). The STRIDE-II consensus notes that lower thresholds reflect deeper histological healing but are less universally achieved. Endoscopic remission was defined as SES-CD of 2 or less for CD or Mayo endoscopic subscore of 1 or less for UC. Deep remission required simultaneous clinical, biochemical, and endoscopic remission.
Disease phenotype classification
CD patients were categorized by Montreal classification. Complicated CD was defined as B2 structuring, B3 penetrating, or perianal disease. Non-complicated CD comprised B1 inflammatory behavior without perianal involvement. Advanced therapies were classified as anti-TNF (infliximab, adalimumab), anti-integrin (vedolizumab), anti-IL-12/23 (ustekinumab), anti-IL-23 (risankizumab, guselkumab), and JAK inhibitors (upadacitinib, tofacitinib). Treatment line was first-line (no prior AT), second-line (one prior), or third-line and beyond.
Statistical analysis
All analyses were conducted in R (version 4.4.2, R Foundation for Statistical Computing, Vienna, Austria) using RStudio (version 2024.12.1).[19] Remission rates were calculated with 95% Wilson confidence intervals. Univariable logistic regression identified predictors of deep remission. Drug comparisons were conducted separately for CD and UC, adjusting for disease duration, bio-experienced status, prior surgery, treatment duration, and disease-specific factors (complicated phenotype for CD; extensive disease for UC). Infliximab served as reference. Remission rates were compared between patients on established advanced therapy (≥6 months) and those not receiving advanced therapy using logistic regression, adjusted for disease type, age, disease duration, and prior surgery. Two-sided P < 0.05 was considered significant. Given the exploratory nature of subgroup analyses and multiple comparisons tested, results from CD, UC, and drug-specific subgroups should be interpreted cautiously and considered hypothesis-generating. No formal adjustment for multiple comparisons was applied; subgroup findings require confirmation in larger or prospective cohorts.
RESULTS
Study population
Of 521 IBD patients identified, 389 (242 CD, 147 UC) met inclusion criteria [Supplementary Figure 1 (164.2KB, tif) ]. The AT subgroup comprised 267 patients (194 CD, 73 UC). Baseline characteristics are presented in Table 1. Mean age was 35.3 years (SD 13.7) with 60.2% male. Mean disease duration was 8.1 years (SD 6.9), and 63% had disease duration of five years or more. Advanced therapy was used by 68.6% overall, with higher utilization in CD (80.2%) than UC (49.7%). Among CD patients, 53.7% had complicated phenotype (B2 stricturing, B3 penetrating, or perianal disease). Mean AT duration was 33.6 months, and 47.2% of the AT subgroup were AT-experienced. Only six patients were on concurrent systemic corticosteroids.
Table 1.
Baseline characteristics
| Characteristic | Overall (n=389) | CD (n=242) | UC (n=147) | AT ≥6 mo (n=267) |
|---|---|---|---|---|
| n | 389 | 242 | 147 | 267 |
| Age, years, mean (SD) | 35.3 (13.7) | 34.4 (13.5) | 36.8 (13.8) | 34.3 (12.5) |
| Male, n (%) | 234 (60.2) | 161 (66.5) | 73 (49.7) | 167 (62.5) |
| Age at diagnosis, years, mean (SD) | 28.2 (13.1) | 27.0 (13.0) | 30.1 (13.1) | 26.6 (12.1) |
| Disease duration, years, mean (SD) | 8.1 (6.9) | 8.4 (7.0) | 7.6 (6.9) | 8.7 (6.6) |
| Disease duration ≥5 years, n (%) | 245 (63.0) | 156 (64.5) | 89 (60.5) | 189 (70.8) |
| Currently on AT, n (%) | 267 (68.6) | 194 (80.2) | 73 (49.7) | 267 (100) |
| AT naive, n (%) | 87 (22.4) | 27 (11.2) | 60 (40.8) | 0 (0) |
| 1 prior AT, n (%) | 166 (42.7) | 113 (46.7) | 53 (36.1) | 141 (52.8) |
| ≥2 prior AT, n (%) | 136 (35.0) | 102 (42.1) | 34 (23.1) | 126 (47.2) |
| ≥3 prior AT, n (%) | 61 (15.7) | 44 (18.2) | 17 (11.6) | 55 (20.6) |
| On immunomodulator, n (%) | 56 (14.4) | 39 (16.1) | 17 (11.6) | 48 (18.0) |
| Prior surgery, n (%) | 47 (12.1) | 37 (15.3) | 10 (6.8) | 35 (13.1) |
| Current smoker, n (%) | 38 (9.8) | 32 (13.2) | 6 (4.1) | 27 (10.1) |
| Complicated CD*, n (%) | 130 (53.7) | 130 (53.7) | - | 110 (56.7) |
| AT duration, months, mean (SD)** | 33.6 (33.2) | 33.6 (34.6) | 33.7 (29.5) | 33.6 (33.2) |
AT, advanced therapy; CD, Crohn’s disease; UC, ulcerative colitis; SD, standard deviation. *Among CD patients. **Among patients on AT
Of 389 patients in the primary cohort, clinical remission was assessable in all 389 (100%), biochemical remission in 344 (88.4%), and endoscopic remission in 279 (71.7%) patients. Incomplete biochemical assessment primarily reflected unavailable faecal calprotectin; incomplete endoscopic assessment reflected medical contraindication, patient refusal, or assessment not performed during the study window. Complete STRIDE-II assessment (all three components) was therefore available in 264 patients (67.9%). We present both available-case analysis (n = 264), and conservative sensitivity analysis treating incomplete assessments as remission failure.
Remission rates
Remission rates are presented in Table 2 and Figure 1. In the primary cohort, clinical remission was 78.7% (306/389, 95% CI 74.3–82.4%), biochemical remission 72.4% (249/344, 95% CI 67.4–76.8%), endoscopic remission 69.2% (193/279, 95% CI 63.5–74.3%), and deep remission 62.1% (164/264, 95% CI 56.1–67.8%). Deep remission rates were similar between CD at 61.0% (97/159) and UC at 63.8% (67/105). In the AT subgroup, remission rates were higher across all domains: clinical remission 84.3% (225/267, 95% CI 79.4–88.1%), biochemical remission 76.0% (184/242, 95% CI 70.3–81.0%), endoscopic remission 76.2% (144/189, 95% CI 69.6–81.7%), and deep remission 64.3% (117/182, 95% CI 57.1–70.9%). Deep remission was 63.3% (81/128) in CD and 66.7% (36/54) in UC. Notably, UC patients on AT achieved higher endoscopic remission (83.3%) compared to CD (73.3%), likely reflecting more accessible mucosal healing assessment in colonic disease. In a conservative sensitivity analysis treating all patients with incomplete assessments as not having achieved remission, deep remission was 42.2% (164/389) in the primary cohort, and 43.8% (117/267) in the AT subgroup.
Table 2.
Remission rates by study cohort and disease type
| Remission Outcome | Primary Cohort (n=389) | Advanced Therapy ≥6 Months (n=267) | ||||
|---|---|---|---|---|---|---|
|
|
|
|||||
| Overall | CD | UC | Overall | CD | UC | |
| Clinical Remission | 306/389 (78.7%) | 195/242 (80.6%) | 111/147 (75.5%) | 225/267 (84.3%) | 167/194 (86.1%) | 58/73 (79.5%) |
| Biochemical Remission | 249/344 (72.4%) | 154/211 (73.0%) | 95/133 (71.4%) | 184/242 (76.0%) | 131/174 (75.3%) | 53/68 (77.9%) |
| Endoscopic Remission | 193/279 (69.2%) | 117/169 (69.2%) | 76/110 (69.1%) | 144/189 (76.2%) | 99/135 (73.3%) | 45/54 (83.3%) |
| Deep Remission | 164/264 (62.1%) | 97/159 (61.0%) | 67/105 (63.8%) | 117/182 (64.3%) | 81/128 (63.3%) | 36/54 (66.7%) |
Data presented as n in remission/N assessed (%). Denominators reflect available-case analysis. Clinical: n=389/389 (100%). Biochemical: n=344/389 (88.4%; 45 missing). Endoscopic: n=279/389 (71.7%; 110 missing). Deep remission: n=264/389 (67.9%). Deep remission=clinical + biochemical + endoscopic remission among patients with all three assessments. Denominators differ across outcome domains as not all patients had biochemical markers or endoscopy performed within the assessment window. Deep remission calculated among patients with all three domains assessed. CD, Crohn’s disease; UC, ulcerative colitis
Figure 1.
Remission rates by outcome domain and disease type. Grouped bar chart showing clinical, biochemical, endoscopic, and deep remission rates with 95% confidence intervals. Rates calculated among patients assessed for each outcome. (a) Primary cohort (N = 389). (b) Advanced therapy ≥6 months subgroup (N = 267). Blue: overall; red: Crohn’s disease; cyan: ulcerative colitis
Deep remission by Crohn’s disease phenotype
Among CD patients in the AT subgroup, complicated phenotype achieved 62.7% deep remission (42/67) compared to 63.9% (39/61) for non-complicated CD (OR 0.94, 95% CI 0.50-1.78, P = 0.85). By Montreal behavior, B3 penetrating achieved the highest rate at 87.5% (14/16), followed by B1 inflammatory at 63.3% (50/79), and B2 stricturing at 51.5% (17/33). The high B3 remission rate likely reflects successful fistula healing with contemporary biologic therapy, while the lower B2 rate may reflect limited reversibility of fibrotic strictures. Patients with perianal disease achieved 60.0% (24/40) compared to 64.8% (57/88) without perianal involvement [Supplementary Table 1, Supplementary Figure 2 (104.7KB, tif) ]. Among UC patients in the AT subgroup, disease extent did not significantly predict deep remission. Neither left-sided colitis (E2; OR 1.48, P = 0.412), pancolitis (E3; OR 0.78, P = 0.555), nor extensive disease as a composite (OR 1.20, P = 0.792) were associated with outcomes, suggesting that disease extent may be less important than other factors in patients already selected for advanced therapy.
Supplementary Table 1.
Subgroup Analyses
| Panel A. Deep Remission by Crohn’s Disease Phenotype (AT ≥6 Months) | ||||
|---|---|---|---|---|
|
| ||||
| Phenotype | n | Assessed | Deep Remission | 95% CI |
| By Complicated Status | ||||
| Complicated CD | 110 | 67 | 42/67 (62.7%) | 50.7–73.3 |
| Non-complicated CD | 84 | 61 | 39/61 (63.9%) | 51.4–74.8 |
| By Montreal Behaviour | ||||
| B1 Inflammatory | 115 | 79 | 50/79 (63.3%) | 52.3–73.1 |
| B2 Stricturing | 45 | 33 | 17/33 (51.5%) | 35.2–67.5 |
| B3 Penetrating | 34 | 16 | 14/16 (87.5%) | 64.0–96.5 |
| By Perianal Disease | ||||
| No perianal disease | 127 | 88 | 57/88 (64.8%) | 54.4–73.9 |
| Perianal disease | 67 | 40 | 24/40 (60.0%) | 44.6–73.7 |
Data presented as n in remission/n assessed (%). Analysis among CD patients on AT ≥6 months with all three remission assessments. Complicated CD=B2 stricturing, B3 penetrating, or perianal disease. AT, advanced therapy; CD, Crohn’s disease; CI, confidence interval
| Panel B. Remission Rates by Treatment Line (AT ≥6 Months) | |||||
|---|---|---|---|---|---|
|
| |||||
| Treatment Line | n | Clinical | Biochemical | Endoscopic | Deep |
| Overall | |||||
| 1st line (bio-naive) | 141 | 87.9% (141) | 82.2% (129) | 81.1% (106) | 67.6% (102) |
| 2nd line | 71 | 84.5% (71) | 73.0% (63) | 77.1% (48) | 67.4% (46) |
| 3rd + line | 55 | 74.5% (55) | 64.0% (50) | 60.0% (35) | 50.0% (34) |
Data presented as rate % (n assessed). 1st line: bio-naive; 2nd line: one prior AT; 3rd + line: ≥2 prior ATs.
| Panel C. Remission Rates by Advanced Therapy Status | ||||
|---|---|---|---|---|
|
| ||||
| Remission Outcome | AT ≥6 Months (N=267) | Not on AT (N=122) | Adjusted OR (95% CI) | P |
| Clinical | 225/267 (84.3%) [79.3–88.4] | 81/122 (66.4%) [57.3–74.7] | 2.57 (1.47–4.52) | <0.001 |
| Biochemical | 184/242 (76.0%) [70.1–81.3] | 65/102 (63.7%) [53.6–73.0] | 1.98 (1.13–3.45) | 0.02 |
| Endoscopic | 144/189 (76.2%) [69.5–82.1] | 49/90 (54.4%) [43.6–65.0] | 3.13 (1.74–5.74) | <0.001 |
| Deep | 117/182 (64.3%) [56.9–71.2] | 47/82 (57.3%) [45.9–68.2] | 1.47 (0.82–2.66) | 0.20 |
Data presented as n/N (%) [95% CI]. *Adjusted for disease type, age, disease duration, and prior surgery. Abbreviations: AT, advanced therapy; CI, confidence interval; OR, odds ratio.
Advanced therapy and treatment line analysis
Drug comparisons were conducted separately for CD and UC [Supplementary Table 2]. These exploratory analyses are limited by small subgroup sizes and should be considered hypothesis-generating. Infliximab achieved 70.6% (24/34), with numerically similar rates for adalimumab (72.2%), vedolizumab (83.3%), risankizumab (60.6%), ustekinumab (56%), and upadacitinib (50%). In UC, vedolizumab achieved 87.5% deep remission (14/16) and showed a trend toward superiority over infliximab at 58.8% (adjusted OR 6.39, 95% CI 1.02–58.83, P = 0.064). No other drugs differed significantly from infliximab. Pairwise comparisons are in Supplementary Table 2.
Supplementary Table 2.
Drug Comparisons (Exploratory Analysis)
| Panel A. Remission Rates by Drug | |||||||
|---|---|---|---|---|---|---|---|
|
| |||||||
| Drug | n | Clinical | Biochemical | Endoscopic | Deep | Adj OR (95% CI) | P |
| Crohn’s Disease | |||||||
| Infliximab | 56 | 51/56 (91.1%) | 39/51 (76.5%) | 27/34 (79.4%) | 24/34 (70.6%) | 1.00 (ref) | — |
| Adalimumab | 24 | 22/24 (91.7%) | 19/21 (90.5%) | 13/20 (65.0%) | 13/18 (72.2%) | 0.92 (0.24–3.73) | 0.904 |
| Vedolizumab | 7 | 7/7 (100%) | 5/7 (71.4%) | 5/6 (83.3%) | 5/6 (83.3%) | 2.59 (0.32–55.77) | 0.429 |
| Ustekinumab | 35 | 29/35 (82.9%) | 24/32 (75.0%) | 20/27 (74.1%) | 14/25 (56.0%) | 0.44 (0.14–1.36) | 0.158 |
| Risankizumab | 52 | 45/52 (86.5%) | 34/44 (77.3%) | 27/36 (75.0%) | 20/33 (60.6%) | 0.83 (0.26–2.63) | 0.744 |
| Guselkumab | 10 | 7/10 (70.0%) | 4/9 (44.4%) | N/A | N/A | N/A | — |
| Upadacitinib | 10 | 6/10 (60.0%) | 6/10 (60.0%) | 6/8 (75.0%) | 4/8 (50.0%) | 0.77 (0.14–4.42) | 0.770 |
| Ulcerative Colitis | |||||||
| Infliximab | 22 | 17/22 (77.3%) | 15/20 (75.0%) | 15/17 (88.2%) | 10/17 (58.8%) | 1.00 (ref) | — |
| Vedolizumab | 22 | 18/22 (81.8%) | 18/21 (85.7%) | 15/16 (93.8%) | 14/16 (87.5%) | 6.39 (1.02–58.83) | 0.064 |
| Ustekinumab | 10 | 9/10 (90.0%) | 8/10 (80.0%) | 6/8 (75.0%) | 5/8 (62.5%) | 0.89 (0.10–7.68) | 0.915 |
| Upadacitinib | 11 | 9/11 (81.8%) | 10/11 (90.9%) | 8/10 (80.0%) | 7/10 (70.0%) | 2.08 (0.14–56.26) | 0.605 |
Adj OR, adjusted odds ratio; CI, confidence interval. Data presented as n in remission/N assessed (%). Exploratory analysis with small sample sizes; interpret with caution. Adjusted ORs from logistic regression with infliximab as reference
Deep remission declined with successive treatment lines: first-line 67.6% (69/102), second-line 67.4% (31/46), and third-line or beyond 50.0% (17/34) as shown in Supplementary Table 1. The most notable attenuation occurred in endoscopic remission, dropping from 81.1% in first-line to 60% in third-line or beyond. Drug-specific performance varied by treatment setting; notably, risankizumab achieved 76.5% deep remission in bio-naïve CD patients but 43.8% in bio-experienced patients, while vedolizumab maintained high efficacy in UC across treatment lines (81.8% first-line, 100% bio-experienced). Detailed breakdowns are in Supplementary Table 2.
| Panel B. Pairwise Drug Comparisons for Deep Remission | ||||||
|---|---|---|---|---|---|---|
|
| ||||||
| Comparison | N 1 | N 2 | Rate1 | Rate2 | Adj OR (95% CI) | P |
| Crohn’s Disease | ||||||
| Infliximab vs Adalimumab | 34 | 18 | 70.6% | 72.2% | 1.25 (0.29–5.27) | 0.756 |
| Infliximab vs Vedolizumab | 34 | 6 | 70.6% | 83.3% | 0.40 (0.02–4.06) | 0.477 |
| Infliximab vs Ustekinumab | 34 | 25 | 70.6% | 56.0% | 2.42 (0.76–8.38) | 0.145 |
| Infliximab vs Risankizumab | 34 | 33 | 70.6% | 60.6% | 1.23 (0.35–4.27) | 0.746 |
| Adalimumab vs Vedolizumab | 18 | 6 | 72.2% | 83.3% | 0.50 (0.02–7.18) | 0.616 |
| Ustekinumab vs Risankizumab | 25 | 33 | 56.0% | 60.6% | 0.49 (0.11–2.03) | 0.332 |
| Ulcerative Colitis | ||||||
| Vedolizumab vs Infliximab | 16 | 17 | 87.5% | 58.8% | 5.65 (0.97–48.82) | 0.072 |
| Vedolizumab vs Ustekinumab | 16 | 8 | 87.5% | 62.5% | 38.41 (1.22–125484) | 0.147 |
| Vedolizumab vs Upadacitinib | 16 | 10 | 87.5% | 70.0% | 4.70 (0.11–340) | 0.397 |
| Infliximab vs Ustekinumab | 17 | 8 | 58.8% | 62.5% | 0.94 (0.12–7.60) | 0.951 |
| Infliximab vs Upadacitinib | 17 | 10 | 58.8% | 70.0% | 0.42 (0.02–5.52) | 0.520 |
| Ustekinumab vs Upadacitinib | 8 | 10 | 62.5% | 70.0% | 0.48 (0.01–39.27) | 0.714 |
CD adjusted for disease duration, bio-experienced status, prior surgery, treatment duration, and complicated phenotype. UC adjusted for disease duration, bio-experienced status, prior surgery, treatment duration, and extensive disease (E2/E3). Deep remission among patients on AT ≥6 months with all three assessments. N₁ and Rate₁ refer to first drug in comparison; N₂ and Rate₂ refer to second drug
| Panel C. Deep Remission by Drug and Treatment Line | ||||
|---|---|---|---|---|
|
| ||||
| Drug | N | First-Line | N | Bio-Experienced |
| Crohn’s Disease | ||||
| Risankizumab | 17 | 76.5% (13/17) | 16 | 43.8% (7/16) |
| Infliximab | 23 | 73.9% (17/23) | 11 | 63.6% (7/11) |
| Adalimumab | 11 | 72.7% (8/11) | 7 | 71.4% (5/7) |
| Ustekinumab | 16 | 56.2% (9/16) | 9 | 55.6% (5/9) |
| Vedolizumab | — | — | 4 | 75.0% (3/4) |
| Upadacitinib | — | — | 6 | 50.0% (3/6) |
| Guselkumab | — | — | 4 | 25.0% (1/4) |
| Ulcerative Colitis | ||||
| Vedolizumab | 11 | 81.8% (9/11) | 5 | 100% (5/5) |
| Upadacitinib | 3 | 66.7% (2/3) | 7 | 71.4% (5/7) |
| Infliximab | 12 | 50.0% (6/12) | 5 | 80.0% (4/5) |
| Ustekinumab | 5 | 40.0% (2/5) | 3 | 100% (3/3) |
Deep remission rates among patients on AT ≥6 months with all three assessments. First-line: bio-naive. Bio-experienced: ≥1 prior AT. Indicates insufficient data
Predictors of deep remission
Univariable predictors are presented in Figure 2. In the primary cohort (n = 264), disease duration was the strongest predictor (OR 1.06 per year, 95% CI 1.02–1.10, P = 0.009), with age also significant (OR 1.02 per year, 95% CI 1.00–1.04, P = 0.040). Prior surgery showed a trend toward improved outcomes (OR 2.17, 95% CI 0.98–5.31, P = 0.07). In CD (n = 159), B3 penetrating behavior was the strongest positive predictor (OR 5.49, 95% CI 1.47–35.66, P = 0.027), while male sex was associated with lower odds (OR 0.47, 95% CI 0.23–0.95, P = 0.039). Multiple prior AT exposure showed a trend toward worse outcomes (OR 0.44, P = 0.057). Complicated phenotype was not significant (OR 0.94, 95% CI 0.50–1.78, P = 0.85). In UC (n = 105), age (OR 1.06 per year, 95% CI 1.02–1.11, P = 0.003), disease duration (OR 1.12 per year, 95% CI 1.04–1.23, P = 0.010), and disease duration of 5 years or more (OR 2.43, 95% CI 1.08–5.59, P = 0.033) were significant predictors. Male sex showed a trend toward improved outcomes in UC (OR 2.17, P = 0.061), contrasting with CD.
Figure 2.
Univariable logistic regression, exploratory subgroup analyses. Forest plot of unadjusted odds ratios with 95% confidence intervals. These findings are exploratory and should not be interpreted as independent predictors. Dashed vertical line indicates OR = 1.0 (no effect). Filled squares indicate statistically significant predictors (P < 0.05). (a) Primary cohort (N = 264). (b) Crohn’s disease (N = 159). (c) Ulcerative colitis (N = 105). *P < 0.05, **P < 0.01. See Supplementary Table 3 for multivariable regression results
| Panel B: Univariable Logistic Regression | ||||
|---|---|---|---|---|
|
| ||||
| Predictor | n | OR (95% CI) | P | Sig |
| Primary Cohort (n=264) | ||||
| Disease duration (per year) | 264 | 1.06 (1.02–1.10) | 0.009 | ** |
| Age (per year) | 264 | 1.02 (1.00–1.04) | 0.040 | * |
| Prior surgery | 264 | 2.17 (0.98–5.31) | 0.070 | |
| Disease duration ≥5 years | 264 | 1.47 (0.89–2.46) | 0.135 | |
| Male sex | 264 | 0.89 (0.53–1.49) | 0.670 | |
| Crohn’s Disease (n=159) | ||||
| B3 Penetrating behaviour | 159 | 5.49 (1.47–35.66) | 0.027 | * |
| Male sex | 159 | 0.47 (0.23–0.95) | 0.039 | * |
| B2 Stricturing behaviour | 159 | 0.51 (0.25–1.04) | 0.065 | |
| Upper GI involvement (L4) | 159 | 2.65 (0.91–9.67) | 0.097 | |
| Prior surgery | 159 | 2.27 (0.90–6.57) | 0.100 | |
| Complicated phenotype | 159 | 0.94 (0.50–1.78) | 0.849 | |
| Ulcerative Colitis (n=105) | ||||
| Age (per year) | 105 | 1.06 (1.02–1.11) | 0.003 | ** |
| Disease duration (per year) | 105 | 1.12 (1.04–1.23) | 0.010 | ** |
| Disease duration ≥5 years | 105 | 2.43 (1.08–5.59) | 0.033 | * |
| Male sex | 105 | 2.17 (0.97–4.94) | 0.061 | |
| Bio-experienced (≥2 AT) | 105 | 2.27 (0.86–6.77) | 0.114 | |
| Extensive disease (E2/E3) | 105 | 1.20 (0.29–4.48) | 0.792 | |
Univariable logistic regression. *P<0.05, **P<0.01. Primary cohort includes patients with all three remission assessments. Complicated phenotype=B2/B3/Perianal. OR, odds ratio; CI, confidence interval; AT, advanced therapy
Multivariable logistic regression [Supplementary Table 3, Supplementary Figure 4 (115KB, tif) ] identified disease duration as a significant independent predictor in the overall cohort (adjusted OR 1.05 per year, 95% CI 1.01–1.11, P = 0.038). In the CD subgroup, higher total advanced therapy exposure (per additional prior therapy) was associated with lower odds of deep remission (adjusted OR 0.70, 95% CI 0.50–0.96, P = 0.034). In UC, age (adjusted OR 1.06, 95% CI 1.02–1.11, P = 0.011) and male sex (adjusted OR 2.68, 95% CI 1.08–6.90, P = 0.036) were independently associated with remission.
Supplementary Table 3.
Predictors of Deep Remission
| Panel A. Multivariable Logistic Regression | ||||
|---|---|---|---|---|
|
| ||||
| Predictor | Adj OR | 95% CI | P | Sig |
| Overall (n=264) | ||||
| Age (per year) | 1.01 | 0.99-1.03 | 0.3552 | |
| Male sex | 0.99 | 0.58-1.71 | 0.9766 | |
| Disease duration (per year) | 1.05 | 1.01-1.11 | 0.0375 | * |
| Total AT exposure (per prior therapy) | 0.86 | 0.68-1.09 | 0.2101 | |
| Prior surgery | 2.08 | 0.88-5.4 | 0.1096 | |
| On immunomodulator | 0.84 | 0.4-1.8 | 0.648 | |
| Current smoker | 0.7 | 0.29-1.72 | 0.4339 | |
| Crohn’s Disease (n=159) | ||||
| Age (per year) | 0.99 | 0.97-1.02 | 0.5898 | |
| Male sex | 0.48 | 0.22-1 | 0.0551 | . |
| Disease duration (per year) | 1.05 | 0.99-1.12 | 0.1339 | |
| Total AT exposure (per prior therapy) | 0.7 | 0.5-0.96 | 0.0338 | * |
| Complicated CD (B2/B3) | 0.81 | 0.36-1.8 | 0.6039 | |
| Perianal disease | 0.8 | 0.36-1.77 | 0.5798 | |
| Upper GI involvement | 2.86 | 0.93-10.89 | 0.0867 | . |
| Prior surgery | 2.94 | 0.93-10.56 | 0.0783 | . |
| On immunomodulator | 1.08 | 0.43-2.79 | 0.8732 | |
| Ulcerative Colitis (n=105) | ||||
| Age (per year) | 1.06 | 1.02-1.11 | 0.0105 | * |
| Male sex | 2.68 | 1.08-6.9 | 0.036 | * |
| Disease duration (per year) | 1.07 | 0.98-1.19 | 0.2027 | |
| Total AT exposure (per prior therapy) | 1.29 | 0.84-2.11 | 0.2678 | |
| Extensive UC (E3) | 0.62 | 0.12-2.94 | 0.5494 | |
| Prior surgery | 1.36 | 0.25-10.54 | 0.7328 | |
| On immunomodulator | 0.19 | 0.03-1.01 | 0.0637 | . |
Adj OR, adjusted odds ratio; AT, advanced therapy; CI, confidence interval; IMM, immunomodulator. Multivariable logistic regression for predictors of STRIDE-II deep remission. Models adjusted for all covariates shown. *P<0.05
Remission rates by advanced therapy status
To describe differences in remission rates by advanced therapy status, we compared patients on established advanced therapy (n = 267) and those not receiving advanced therapy (n = 122). Patients on advanced therapy demonstrated significantly higher remission rates across clinical, biochemical, and endoscopic outcomes [Supplementary Figure 3 (86.9KB, tif) ]. Clinical remission was achieved in 84.3% (225/267) of patients on advanced therapy compared with 66.4% (81/122) of those not on advanced therapy (adjusted OR 2.57, 95% CI 1.47–4.52; P < 0.001). Similarly, biochemical remission rates were higher in the advanced therapy group (76.0% vs 63.7%; adjusted OR 1.98, 95% CI 1.13–3.45; P = 0.02), as were endoscopic remission rates (76.2% vs 54.4%; adjusted OR 3.13, 95% CI 1.74–5.74; P < 0.001). Deep remission showed a numerical advantage for advanced therapy (64.3% vs 57.3%) that did not reach statistical significance after adjustment for disease type, age, disease duration, and prior surgery (adjusted OR 1.47, 95% CI 0.82–2.66; P = 0.20). The magnitude of difference was most pronounced for endoscopic remission, with patients on advanced therapy demonstrating three-fold higher odds of achieving mucosal healing compared with those managed without advanced therapy.
DISCUSSION
This study provides the first systematic evaluation of STRIDE-II treatment target achievement from a tertiary center in the Gulf region. We assessed deep remission rates in patients on established advanced therapy, examined outcomes across disease phenotypes and therapeutic classes, and identified predictors of treatment success in this Middle Eastern cohort.
Our principal finding was that approximately two-thirds of patients on established advanced therapy achieved deep remission, a rate comparable to or numerically higher than contemporary international reports. The IBD-PODCAST study reported suboptimal disease control in over half of patients across predominantly European sites despite advanced therapy use in 77% of CD and 65% of UC cases.[13] Other Western cohorts have validated these findings: Spain (53.1% CD, 41.5% UC with suboptimal control),[14] Italy (53.4% CD, 49.0% UC),[15] the United Kingdom (52.4% CD, 45.3% UC),[16] and Canada.[17] In our cohort, 79% of the total IBD population was receiving advanced therapy for ≥6 months, comparable to IBD-PODCAST rates. Across all these cohorts, impaired quality of life (SIBDQ <50) emerged as the predominant contributor to suboptimal disease control in 56–72% of cases, followed by failure to achieve endoscopic remission and presence of extraintestinal manifestations. Our cohort’s achievement of deep remission in approximately two-thirds of patients therefore represents performance comparable to or numerically higher than global real-world benchmarks.
Direct comparison with IBD-PODCAST, which employed SIBDQ-based definitions of suboptimal control, is limited, as this represents a fundamentally different construct from STRIDE-II deep remission based on integrated clinical, biochemical, and endoscopic criteria. Several factors may explain our cohort’s favorable outcomes. First, high advanced therapy utilization reflects contemporary treatment paradigms emphasizing early intervention and risk-stratified therapy selection. The landmark PROFILE trial demonstrated that top-down treatment with combination biologic and immunomodulator therapy achieved substantially higher rates of symptom control, inflammatory marker normalization, and endoscopic remission compared with conventional step-up approaches, while markedly reducing the need for urgent surgery.[11] These paradigm-shifting findings underscore that contemporary treatment strategies, including judicious use of early intensive therapy and, in select cases, upfront surgical intervention, can fundamentally alter disease trajectories. Second, our single-center design ensures uniform assessment protocols, consistent treatment algorithms, and cohesive multidisciplinary care delivery. The IBD-PODCAST investigators noted that endoscopy was performed in fewer than expected patients, faecal calprotectin analyses in less than half, and imaging in fewer than 15% of cases across participating sites,[20] suggesting incomplete STRIDE-II implementation in routine practice. Third, these findings demonstrate that dedicated IBD services with comprehensive advanced therapy access can achieve outcomes comparable to Western benchmarks, even in populations with aggressive disease phenotypes.[21,22] This contradicts assumptions that Middle Eastern populations might experience inferior outcomes due to genetic, environmental, or healthcare system factors. The higher remission rates in patients on advanced therapy likely reflect both therapeutic efficacy and more intensive monitoring protocols, reinforcing the value of structured assessment in achieving STRIDE-II targets.
The equivalent remission rates between complicated and non-complicated CD phenotypes challenge traditional assumptions about prognostic stratification by disease behavior.[23] However, patients with complicated phenotypes in our cohort likely received earlier and more intensive treatment, reflecting appropriate risk stratification that may mitigate baseline phenotypic disadvantages. The behavior-specific analysis revealed important heterogeneity warranting nuanced interpretation. The high remission observed in penetrating disease likely reflects confounding by surgical resection, as patients with penetrating complications frequently undergo definitive surgery prior to reassessment.[24] Our penetrating disease subgroup’s outcomes must therefore be interpreted in this surgical context. Conversely, the lower remission in stricturing disease aligns with emerging mechanistic understanding of intestinal fibrosis which remains one of the largest unmet needs in IBD, affecting approximately 35% of CD patients within 10 years of diagnosis.[25] These findings support treatment approaches individualized by specific disease behavior rather than composite phenotype classifications.
In CD, no agent demonstrated statistical superiority, with wide confidence intervals reflecting sample size limitations. These findings are hypothesis-generating and cannot exclude either substantial efficacy differences or therapeutic equivalence. Contemporary head-to-head trials comparing newer biologics and network meta-analyses provide important context, establishing efficacy benchmarks for IL-23 inhibitors in bio-experienced patients while demonstrating comparable performance between anti-TNF and anti-IL-12/23 agents in bio-naïve populations.[26,27,28,29] In UC, our observation of vedolizumab’s trend toward superiority aligns with the VARSITY trial, the EVOLVE real-world study demonstrating superior treatment persistence and fewer disease exacerbations with vedolizumab versus anti-TNF in bio-naïve UC patients, and recent network meta-analyses demonstrating vedolizumab among the most effective and best-tolerated advanced therapies, particularly for biologic-naïve patients.[30,31,32,33,34,35,36,37,38] Importantly, our study was not designed or powered for definitive drug comparisons, and the observational design introduces confounding by indication. Drug selection in CD likely reflected disease behavior considerations, with anti-TNF agents preferentially used for penetrating phenotypes based on superior fistula closure rates, while vedolizumab was reserved for inflammatory phenotypes or patients with contraindications to anti-TNF therapy. These analyses therefore remain hypothesis-generating and require validation in larger regional cohorts or registry data.
The preservation of efficacy at second-line with decline at third-line observed in our cohort aligns with contemporary evidence demonstrating diminishing returns with sequential therapy failures. Large real-world studies support mechanistic switching after first-line failure rather than cycling within the same drug class, with certain agents (notably vedolizumab in CD) showing reduced effectiveness when used later in treatment sequences.[34,35] Predictor profiles differed between CD and UC in our cohort, reflecting disease-specific pathophysiology. In CD, the association of penetrating behavior with higher remission likely reflects surgical confounding as discussed above. The association of male sex with lower remission in CD lacks clear mechanistic explanation and requires replication. In UC, older age and longer disease duration predicted higher remission, a counterintuitive finding potentially reflecting survivor bias, as patients with aggressive disease may have undergone colectomy earlier, leaving a cohort enriched for treatment-responsive phenotypes. The heterogeneity in predictors across studies underscores the need for larger regional cohorts to validate these patterns.
Our study has several important limitations. First, this is a single-center cross-sectional analysis from a tertiary IBD referral center, which may not represent broader IBD populations or primary care settings. Second, selection bias is introduced by the inclusion criteria requiring at least six months of stable therapy, which enriches our cohort for patients with established, well-controlled disease. Third, we employed an available-case analysis including only 264 of 389 patients with complete STRIDE-II assessment; the conservative sensitivity analysis yielded 42.2% deep remission (compared to 62.1%). Fourth, biochemical thresholds (faecal calprotectin <250 mg/g) represent an intermediate target; stricter thresholds would yield lower proportions. Fifth, subgroup analyses are exploratory without formal multiplicity adjustment. Sixth, the AT vs non-AT comparison is subject to confounding by indication. Finally, categorical clinical remission assessments were available rather than Harvey-Bradshaw Index or Partial Mayo Score continuous scores. The absence of histological remission assessment represents a limitation given emerging evidence for “disease clearance” (simultaneous clinical, endoscopic, and histologic remission) as an optimal treatment target and is being systematically explored in the VERDICT study.[36,37,38,39] Histological data were not systematically recorded in our cohort as pathology reporting lacked consistency, and we opted to exclude incomplete data to avoid bias. Future iterations of STRIDE may incorporate histological endpoints as standardized assessment tools and reporting practices become established. The absence of comprehensive patient-reported outcome (PRO) data beyond clinical remission assessment represents another limitation. Given that impaired quality of life was the predominant driver of suboptimal disease control in IBD-PODCAST cohorts, systematic PRO assessment using validated instruments would enhance characterization of treatment success from patient perspectives.[13,14,15,16] Objective remission measures may not fully capture patients’ disease burden and functional status. Additionally, the lack of transmural healing assessment via intestinal ultrasound or magnetic resonance enterography represents a limitation, as emerging evidence suggests discordance between endoscopic and transmural remission in a subset of patients.[40]
In conclusion, in this single-center tertiary IBD cohort, 62.1% of patients with complete STRIDE-II assessment achieved deep remission, comparable to or numerically higher than international reports. However, a conservative sensitivity analysis yielded a more conservative 42.2% rate. These findings are from a single tertiary center with exploratory subgroup analyses; prospective, multicenter studies are warranted to validate STRIDE-II achievement across diverse IBD populations
Conflicts of interest
MNQ has received speaker fees from Johnson and Johnson, Takeda, AbbVie, Hikma and Lilly and consultancy fees from AbbVie, Johnson and Johnson and Lilly.
Study flowchart showing patient identification, exclusion criteria, and final study populations for the primary cohort (N=389) and advanced therapy subgroup (N=267). Abbreviations: AT, advanced therapy; CD, Crohn’s disease; IBD, inflammatory bowel disease; UC, ulcerative colitis
Deep remission by Crohn’s disease phenotype. Deep remission rates among CD patients on advanced therapy ≥6 months with all three remission assessments. Left panel: Montreal behaviour (B1 inflammatory, B2 stricturing, B3 penetrating). Middle panel: complicated status. Right panel: perianal disease status
Remission rates by advanced therapy status. Comparison of clinical, biochemical, endoscopic, and deep remission rates between patients on established advanced therapy (≥6 months; N=267; blue) and patients not on advanced therapy (N=122; purple). Error bars represent 95% confidence intervals. Patients on advanced therapy demonstrated significantly higher rates of clinical (84.3% vs 66.4%, p<0.001), biochemical (76.0% vs 63.7%, p=0.02), and endoscopic remission (76.2% vs 54.4%, p<0.001). Deep remission showed a numerical but non-significant advantage (64.3% vs 57.3%, p=0.20)
Multivariable logistic regression forest plot for predictors of STRIDE-II deep remission. Three-panel display showing overall cohort, Crohn’s disease subgroup, and ulcerative colitis subgroup. Points represent adjusted odds ratios; horizontal lines represent 95% confidence intervals. Models adjusted for all covariates shown. Dashed vertical line indicates OR=1 (no effect)
Funding Statement
Nil.
REFERENCES
- 1.Ng SC, Shi HY, Hamidi N, Underwood FE, Tang W, Benchimol EI, et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: A systematic review of population-based studies. Lancet. 2017;390:2769–78. doi: 10.1016/S0140-6736(17)32448-0. [DOI] [PubMed] [Google Scholar]
- 2.Hracs L, Windsor JW, Gorospe J, Cummings M, Coward S, Buie MJ, et al. Global evolution of inflammatory bowel disease across epidemiologic stages. Nature. 2025;642:458–66. doi: 10.1038/s41586-025-08940-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Alatab S, Sepanlou SG, Ikuta K, Vahedi H, Bisignano C, Safiri S, et al. The global, regional, and national burden of inflammatory bowel disease in 195 countries and territories, 1990–2017: A systematic analysis for the Global Burden of Disease Study 2017. Lancet Gastroenterol Hepatol. 2020;5:17–30. doi: 10.1016/S2468-1253(19)30333-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Ahmed HA, Alzaabi MN, Swaid TK, Khan SW, Ali ABAA, Tenaiji KA, et al. Evolving clinical burden of inflammatory bowel disease in the United Arab Emirates: A two-decade analysis of diagnoses and disease severity. Frontline Gastroenterol. 2025 doi: 10.1136/flgastro-2025-103345. [Google Scholar]
- 5.Al Atrash E, Mohammad SM, Mohammad S, Al Ghafli H, Miqdady M, Quraishi MN. Accelerating burden of paediatric IBD in UAE: Phenotypes and treatment patterns at a single center (2012-2024) Frontline Gastroenterol. 2026:1–9. doi: 10.1136/flgastro-2025-103397. [Google Scholar]
- 6.Mosli M, Alawadhi S, Hasan F, Abou Rached A, Sanai F, Danese S. Incidence, prevalence, and clinical epidemiology of inflammatory bowel disease in the Arab World: A systematic review and meta-analysis. Inflamm Intest Dis. 2021;6:123–31. doi: 10.1159/000518003. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Vieujean S, Jairath V, Peyrin-Biroulet L, Dubinsky M, Iacucci M, Magro F, et al. Understanding the therapeutic toolkit for inflammatory bowel disease. Nat Rev Gastroenterol Hepatol. 2025;22:455. doi: 10.1038/s41575-025-01047-x. [DOI] [PubMed] [Google Scholar]
- 8.Al Awadhi S, Al Hassani A, El Ouali S, Alam MB, Azar C, Georgopoulos F, et al. Second United Arab Emirates consensus guidance on the diagnosis and management of inflammatory bowel disease. World J Gastroenterol. 2025;31:109882. doi: 10.3748/wjg.v31.i35.109882. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Moran GW, Gordon M, Sinopolou V, Radford SJ, Darie AM, Vuyyuru SK, et al. British Society of Gastroenterology guidelines on inflammatory bowel disease in adults: Gut. 2025;2025;74((Suppl 2)):s1–101. doi: 10.1136/gutjnl-2024-334395. [DOI] [PubMed] [Google Scholar]
- 10.Colombel JF, Panaccione R, Bossuyt P, Lukas M, Baert F, Vaňásek T, et al. Effect of tight control management on Crohn's disease (CALM): A multicenter, randomised, controlled phase 3 trial. Lancet Lond Engl. 2017;390:2779–89. doi: 10.1016/S0140-6736(17)32641-7. [DOI] [PubMed] [Google Scholar]
- 11.Noor NM, Lee JC, Bond S, Dowling F, Brezina B, Patel KV, et al. A biomarker-stratified comparison of top-down versus accelerated step-up treatment strategies for patients with newly diagnosed Crohn's disease (PROFILE): A multicenter, open-label randomised controlled trial. Lancet Gastroenterol Hepatol. 2024;9:415–27. doi: 10.1016/S2468-1253(24)00034-7. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Turner D, Ricciuto A, Lewis A, D’Amico F, Dhaliwal J, Griffiths AM, et al. STRIDE-II: An update on the selecting therapeutic targets in inflammatory bowel disease (STRIDE) initiative of the international organization for the study of IBD (IOIBD): Determining therapeutic goals for treat-to-target strategies in IBD. Gastroenterology. 2021;160:1570–83. doi: 10.1053/j.gastro.2020.12.031. [DOI] [PubMed] [Google Scholar]
- 13.D’Amico F, Parigi TL, Yarur A, Allocca M, Estevinho MM, Zilli A, et al. Suboptimal disease control assessed by STRIDE-II criteria in patients with inflammatory bowel disease treated with advanced therapies: A multinational study. United Eur Gastroenterol J. 2024;12:1243–54. [Google Scholar]
- 14.Vega P, Huguet JM, Gómez E, Rubio S, Suarez P, Vera MI, et al. IBD-PODCAST Spain: A close look at current daily clinical practice in IBD management. Dig Dis Sci. 2024;69:749–65. doi: 10.1007/s10620-023-08220-9. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Calabrese E, Onali S, Variola A, Ribaldone DG, Savarino EV, Viola A, et al. Suboptimal disease control and contributing factors in Italian IBD patients: The IBD-PODCAST study. Dig Liver Dis. 2025;57:241–50. doi: 10.1016/j.dld.2024.08.040. [DOI] [PubMed] [Google Scholar]
- 16.de Silva S, Steed H, Allen PB, Vegad C, Crooks J, Jaulim A, et al. Assessing disease control in inflammatory bowel disease: A real world cross-sectional study in the UK (PODCAST-IBD) Curr Med Res Opin. 2024;40:1847–54. doi: 10.1080/03007995.2024.2410928. [DOI] [PubMed] [Google Scholar]
- 17.Siffledeen J, Singh S, Shulman SM, Igoe J, Heatta-Speicher T, Leitner C, et al. Effect of suboptimal disease control on patient quality of life: Real-world data from the observational IBD-PODCAST Canada trial. Dig Dis Sci. 2024;69:1636–48. doi: 10.1007/s10620-024-08313-z. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Alzaabi MN, Swaid TK, Ahmed HA, Alahmed MA, Omar NM, Kumar KKC, et al. Effectiveness of risankizumab in an Emirati Crohn's disease cohort: Real-world insights on induction, maintenance, and dose intensification outcomes. J Crohns Colitis. 2025 doi: 10.1093/ecco-jcc/jjae190.1168. [Google Scholar]
- 19.R Core Team. R: A Language and Environment for Statistical Computing. Vienna, Austria: R Foundation for Statistical Computing; 2025. Available from: https://www.R-project.org/ [Google Scholar]
- 20.Stallmach A, Grunert PC. Taking IBD treatment in STRIDE: How objective disease assessment is essential for the successful implementation of treat-to-target strategies. Dig Dis Sci. 2024;69:657–9. doi: 10.1007/s10620-023-08221-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Siegel CA, Yang F, Eslava S, Cai Z. Treatment pathways leading to biologic therapies for ulcerative colitis and Crohn's disease in the United States. Clin Transl Gastroenterol. 2020;11:e00128. doi: 10.14309/ctg.0000000000000128. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22.Teeple A, Sah J, Mallampati R, Adams C, Waters D, Muser E. Persistence, dosing, and other treatment patterns among Crohn's disease patients initiating biologics in United States. Crohns Colitis 360. 2021;3:otab076. doi: 10.1093/crocol/otab076. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Bernstein CN, Panaccione R, Nugent Z, Marshall DA, Kaplan GG, Vanner S, et al. Crohn's Disease phenotypes and associations with comorbidities, surgery risk, medications and nonmedication approaches: The MAGIC in IMAGINE study. Inflamm Bowel Dis. 2025;31:113–22. doi: 10.1093/ibd/izae055. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 24.McCurdy JD, Stwalley D, Olsen MA, Deepak P. Comparative effectiveness of biologic therapies in preventing penetrating complications in patients with Crohn's disease. Clin Gastroenterol Hepatol Off Clin Pract J Am Gastroenterol Assoc. 2024;22:377–85.e5. doi: 10.1016/j.cgh.2023.08.017. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25.Rieder F, Mukherjee PK, Massey WJ, Wang Y, Fiocchi C. Fibrosis in IBD: From pathogenesis to therapeutic targets. Gut. 2024;73:854–66. doi: 10.1136/gutjnl-2023-329963. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Peyrin-Biroulet L, Chapman JC, Colombel JF, Caprioli F, D’Haens G, Ferrante M, et al. Risankizumab versus ustekinumab for moderate-to-severe Crohn's disease. N Engl J Med. 2024;391:213–23. doi: 10.1056/NEJMoa2314585. [DOI] [PubMed] [Google Scholar]
- 27.Danese S, Panaccione R, Feagan BG, Afzali A, Rubin DT, Sands BE, et al. Efficacy and safety of 48 weeks of guselkumab for patients with Crohn's disease: Maintenance results from the phase 2, randomised, double-blind GALAXI-1 trial. Lancet Gastroenterol Hepatol. 2024;9:133–46. doi: 10.1016/S2468-1253(23)00318-7. [DOI] [PubMed] [Google Scholar]
- 28.Ferrante M, D’Haens G, Jairath V, Danese S, Chen M, Ghosh S, et al. Efficacy and safety of mirikizumab in patients with moderately-to-severely active Crohn's disease: A phase 3, multicenter, randomised, double-blind, placebo-controlled and active-controlled, treat-through study. Lancet. 2024;404:2423–36. doi: 10.1016/S0140-6736(24)01762-8. [DOI] [PubMed] [Google Scholar]
- 29.Shehab M, Alrashed F, Alrashidi A, Hassan A, Ma C, Narula N, et al. Network meta-analysis: Comparative efficacy of biologics and small molecules in the induction and maintenance of remission in Crohn's disease. Aliment Pharmacol Ther. 2025;62:472–82. doi: 10.1111/apt.70295. [DOI] [PubMed] [Google Scholar]
- 30.Sands BE, Peyrin-Biroulet L, Loftus EV, Danese S, Colombel JF, Törüner M, et al. Vedolizumab versus adalimumab for moderate-to-severe ulcerative colitis. N Engl J Med. 2019;381:1215–26. doi: 10.1056/NEJMoa1905725. [DOI] [PubMed] [Google Scholar]
- 31.Ananthakrishnan AN, Murad MH, Scott FI, Agrawal M, Haydek JP, Limketkai BN, et al. Comparative efficacy of advanced therapies for management of moderate-to-severe ulcerative Colitis: 2024 American Gastroenterological Association Evidence Synthesis. Gastroenterology. 2024;167:1460–82. doi: 10.1053/j.gastro.2024.07.046. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 32.Shehab M, Alrashed F, Alsayegh A, Aldallal U, Ma C, Narula N, et al. Comparative efficacy of biologics and small molecule in ulcerative colitis: A systematic review and network meta-analysis. Clin Gastroenterol Hepatol. 2025;23:250–62. doi: 10.1016/j.cgh.2024.07.033. [DOI] [PubMed] [Google Scholar]
- 33.Bressler B, Yarur A, Silverberg MS, Bassel M, Bellaguarda E, Fourment C, et al. Vedolizumab and anti-tumour necrosis factor ? real-world outcomes in biologic-naïve inflammatory bowel disease patients: Results from the EVOLVE study. J Crohns Colitis. 2021;15:1694–706. doi: 10.1093/ecco-jcc/jjab058. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 34.Kapizioni C, Desoki R, Lam D, Balendran K, Al-Sulais E, Subramanian S, et al. Biologic therapy for inflammatory bowel disease: Real-world comparative effectiveness and impact of drug sequencing in 13 222 patients within the UK IBD BioResource. J Crohns Colitis. 2024;18:790–800. doi: 10.1093/ecco-jcc/jjad203. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 35.Chanchlani N, Lin S, Bewshea C, Hamilton B, Thomas A, Smith R, et al. Mechanisms and management of loss of response to anti-TNF therapy for patients with Crohn's disease: 3-year data from the prospective, multicenter PANTS cohort study. Lancet Gastroenterol Hepatol. 2024;9:521–38. doi: 10.1016/S2468-1253(24)00044-X. [DOI] [PubMed] [Google Scholar]
- 36.Jairath V, Zou G, Wang Z, Adsul S, Colombel JF, D’Haens GR, et al. Determining the optimal treatment target in patients with ulcerative colitis: rationale, design, protocol and interim analysis for the randomised controlled VERDICT trial. BMJ Open Gastroenterol. 2024;11:e001218. doi: 10.1136/bmjgast-2023-001218. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 37.Feakins R, Borralho Nunes P, Driessen A, Gordon IO, Zidar N, Baldin P, et al. Definitions of Histological Abnormalities in Inflammatory Bowel Disease: an ECCO Position Paper. J Crohns Colitis. 2024;18:175–91. doi: 10.1093/ecco-jcc/jjad142. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 38.D’Amico F, Magro F, Siegmund B, Kobayashi T, Kotze PG, Solitano V, et al. Disease Clearance as a New Outcome in Ulcerative Colitis: a Systematic Review and Expert Consensus. Inflamm Bowel Dis. 2024;30:1009–17. doi: 10.1093/ibd/izad159. [DOI] [PubMed] [Google Scholar]
- 39.Bryant RV, Winer S, Travis SPL, Riddell RH. Systematic review: histological remission in inflammatory bowel disease. Is complete remission the new treatment paradigm? An IOIBD initiative. J Crohns Colitis. 2014;8:1582–97. doi: 10.1016/j.crohns.2014.08.011. [DOI] [PubMed] [Google Scholar]
- 40.Fernandes SR, Rodrigues RV, Bernardo S, Cortez-Pinto J, Rosa I, da Silva JP, et al. Transmural Healing Is Associated with Improved Long-term Outcomes of Patients with Crohn's Disease. Inflamm Bowel Dis. 2017;23:1403–9. doi: 10.1097/MIB.0000000000001143. [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Study flowchart showing patient identification, exclusion criteria, and final study populations for the primary cohort (N=389) and advanced therapy subgroup (N=267). Abbreviations: AT, advanced therapy; CD, Crohn’s disease; IBD, inflammatory bowel disease; UC, ulcerative colitis
Deep remission by Crohn’s disease phenotype. Deep remission rates among CD patients on advanced therapy ≥6 months with all three remission assessments. Left panel: Montreal behaviour (B1 inflammatory, B2 stricturing, B3 penetrating). Middle panel: complicated status. Right panel: perianal disease status
Remission rates by advanced therapy status. Comparison of clinical, biochemical, endoscopic, and deep remission rates between patients on established advanced therapy (≥6 months; N=267; blue) and patients not on advanced therapy (N=122; purple). Error bars represent 95% confidence intervals. Patients on advanced therapy demonstrated significantly higher rates of clinical (84.3% vs 66.4%, p<0.001), biochemical (76.0% vs 63.7%, p=0.02), and endoscopic remission (76.2% vs 54.4%, p<0.001). Deep remission showed a numerical but non-significant advantage (64.3% vs 57.3%, p=0.20)
Multivariable logistic regression forest plot for predictors of STRIDE-II deep remission. Three-panel display showing overall cohort, Crohn’s disease subgroup, and ulcerative colitis subgroup. Points represent adjusted odds ratios; horizontal lines represent 95% confidence intervals. Models adjusted for all covariates shown. Dashed vertical line indicates OR=1 (no effect)