Real-world effectiveness and safety of risankizumab in multirefractory Crohn’s disease: A multicenter AIRIS-Crohn registry analysis

Abstract

BACKGROUND

Many patients with Crohn’s disease (CD) remain uncontrolled despite multiple biologic therapies. Risankizumab, a selective interleukin-23p19 inhibitor, has shown efficacy in clinical trials, but real-world data in multirefractory CD are still scarce.

AIM

To evaluate the 12-month effectiveness and safety of risankizumab in a real-world cohort of patients with moderate-to-severe CD treated across multiple centers in Andalusia, Spain.

METHODS

Multicenter ambispective real-world study including adults with CD treated with risankizumab across 12 Andalusian hospitals (AIRIS-Crohn registry). Effectiveness outcomes were clinical remission (Harvey-Bradshaw index < 5), steroid-free remission (SFR), biochemical remission, and endoscopic response/remission at week 12, 6 months and 12 months. Modified non-responder imputation was applied to discontinuations.

RESULTS

Among 205 patients with highly refractory CD (median 2 prior failed advanced therapies; 81% prior ustekinumab exposure; 61% extraintestinal manifestations; 39% prior intestinal surgery), risankizumab rapidly improved clinical activity and maintained stable remission rates over 12 months. Clinical remission improved from 20% at baseline to 49% at week 12, 46% at 6 months and 49% at 12 months (P < 0.05 for all). SFR was maintained in 41%-44% throughout follow-up. Perianal disease response was observed in 65% at week 12 and 80% at 6 months. Endoscopic remission was achieved in 32% at 6 months. Treatment persistence exceeded 90% at one year. In multivariable analysis, prior vedolizumab exposure was related to lower odds of SFR (odds ratio = 0.41; 95% confidence interval: 0.17-0.99). Risankizumab demonstrated a reassuring safety profile: Only 3.4% of patients discontinued due to adverse events, and no serious infections, opportunistic infections, malignancies, or deaths occurred during follow-up.

CONCLUSION

In one of the largest real-world cohorts of multirefractory CD, risankizumab delivered rapid and sustained clinical benefit, meaningful SFR, robust treatment persistence, and a reassuring safety profile. These findings strengthen the role of interleukin-23 blockade as a key therapeutic strategy for patients with limited treatment options in everyday practice.

Key Words: Crohn’s disease; Inflammatory bowel disease; Risankizumab; Real-world evidence; Interleukin-12/23

Core Tip: Risankizumab, a selective interleukin-23p19 inhibitor, emerges as a promising therapeutic option for patients with multirefractory Crohn’s disease. This multicenter real-world study of 205 patients demonstrates that risankizumab rapidly achieves clinical remission (49% at week 12) and maintains steroid-free remission in over 40% of patients throughout one-year follow-up. The excellent safety profile and high treatment persistence (> 90%) establish interleukin-23 blockade as a key strategy for patients with limited biologic alternatives in routine clinical practice.

INTRODUCTION

Crohn’s disease (CD) is a chronic, relapsing inflammatory disorder of the gastrointestinal tract that is associated with significant physical and psychosocial burden[1]. Despite advances in therapeutic strategies, including anti-tumor necrosis factor (TNF) agents, vedolizumab, Janus Kinase inhibitors and the interleukin (IL)-12/23 inhibitor ustekinumab, a substantial proportion of patients either do not respond or lose response over time, with some experiencing adverse effects that limit long-term treatment efficacy[2,3].

CD is characterized by a complex and multifactorial pathogenesis involving genetic susceptibility, environmental factors, alterations in the gut microbiota, and dysregulated immune responses, leading to transmural inflammation and progressive bowel damage. Current therapeutic strategies follow a treat-to-target approach aimed at achieving sustained clinical and endoscopic remission through the use of conventional therapies and advanced treatments targeting key inflammatory pathways. However, management remains particularly challenging in patients with refractory disease and in those with complex phenotypes such as perianal fistulizing disease, which often requires a multidisciplinary approach combining optimized medical therapy and surgical interventions[4].

Risankizumab is a fully human IgG1 monoclonal antibody that selectively binds to the p19 subunit of IL-23, thereby inhibiting IL-23 from engaging its receptor and blocking downstream pro-inflammatory signaling, particularly within the IL-23/T helper 17 cell pathway[5]. This mechanism offers a more targeted approach compared to broader IL-12/23 inhibitors, potentially enhancing efficacy while maintaining a favorable safety profile[5].

Clinical efficacy and safety in CD have been demonstrated in phase III induction and maintenance trials (ADVANCE, MOTIVATE and FORTIFY) where risankizumab induced early and maintained clinical response and remission in patients with moderately to severely active CD, including those with prior advanced therapy failures[6,7]. Furthermore, long-term data from open-label extension studies indicate that maintenance therapy with subcutaneous risankizumab (360 mg every 8 weeks) is well tolerated over multiple years, demonstrating sustained remission and endoscopic improvement, with no new safety signals observed[8,9].

Recent head-to-head comparison trials have positioned risankizumab favorably. In the SEQUENCE study, risankizumab demonstrated non-inferiority to ustekinumab in inducing clinical remission (CR) at 24 weeks and superiority in achieving endoscopic remission at 48 weeks, supporting its role in the management of CD[10]. Despite the robust therapeutic profile of risankizumab and ongoing unmet needs in CD patients inadequately responsive to current advanced therapies, real-world evidence regarding its use in heavily refractory populations remains limited. This study aimed to assess the effectiveness, safety, and predictors of steroid-free remission (SFR) with risankizumab at 6 months and 12 months in a highly refractory CD cohort.

MATERIALS AND METHODS

Study design and setting

We conducted a multicenter ambispective observational real-world study across 12 hospitals in Andalusia (Spain), using data from the AIRIS-Crohn registry, in the bosom of the Andalusian Digestive Diseases Society (SAPD). This registry collects comprehensive demographic, disease-related, clinical, endoscopic, and safety data from patients with CD undergoing advanced therapies. For the present analysis, we included patients who initiated risankizumab treatment from October 2022 onwards.

Study population

Eligible participants included adult patients (≥ 18 years) with a confirmed diagnosis of CD who received treatment with risankizumab (and completed the 12 weeks induction phase, at least). Patients were included regardless of prior advanced therapy exposure. Exclusion criteria included: Ulcerative colitis or indeterminate colitis; contraindications to risankizumab according to the product label; concurrent enrollment in experimental therapy trials; pregnancy or breastfeeding; inability to provide informed consent; and insufficient baseline demographic or disease-related data for analysis.

Outcomes

The following outcomes were analyzed. CR: Defined as a Harvey-Bradshaw index (HBI) ≤ 4, in accordance with commonly accepted clinical trial and real-world definitions of remission in CD[11]. Combined clinical and biochemical remission: Defined as HBI ≤ 4 plus C-reactive protein (CRP) < 5 mg/L and fecal calprotectin < 250 μg/g, consistent with treat-to-target recommendations[12]. SFR: Defined as CR (HBI ≤ 4) in the absence of systemic corticosteroid use from week 12 onwards[12]. Endoscopic remission: Defined as a Simplified Endoscopic Mucosal Assessment (SEMA)-CD < 2[13]. Endoscopic response: Defined as a ≥ 50% reduction in SEMA-CD from baseline[13]. Mucosal healing: Defined as SEMA < 2 with no visible ulceration[13].

Secondary outcomes included: Treatment persistence and reasons for discontinuation. Changes in inflammatory biomarkers (CRP, fecal calprotectin). Perianal disease response: Perianal disease was considered evaluable in patients with a documented history of perianal CD with baseline radiologic confirmation and at least one follow-up clinical assessment (and imaging when available). Clinical perianal response or remission was defined according to physician assessment based on improvement or resolution of drainage, pain, and local inflammatory signs, consistent with clinical practice recommendations[14].

Extraintestinal manifestation (EIM) improvement: EIMs were recorded according to European Crohn’s and Colitis Organisation definitions as inflammatory manifestations associated with inflammatory bowel disease[15]. Active EIMs were defined as clinically manifest and symptomatic at baseline, as judged by the treating physician. Activity during follow-up was assessed pragmatically through structured patient questioning (improvement, stability, or worsening) and physician global assessment.

Treatment protocol

Patients received risankizumab according to the approved dosing regimen for CD: Intravenous induction therapy at a dose of 600 mg at weeks 0, 4, and 8, followed by subcutaneous maintenance therapy at 360 mg every 8 weeks. This dosing schedule is based on the phase III ADVANCE, MOTIVATE, and FORTIFY trials and reflects the approved therapeutic regimen for moderate-to-severe CD[6,7,9].

Follow-up

Clinical, biochemical, endoscopic, and safety assessments were conducted at week 12, 6 months, and 12 months following risankizumab initiation. All patients who continued risankizumab completed 12 months of follow-up; those who discontinued earlier were considered non-responders.

Statistical analysis

Study variables were described using medians and interquartile ranges (IQRs) for continuous variables, and n (%) for categorical variables. To assess changes over time in continuous variables, the Friedman test for related samples was applied, followed by post-hoc analyses when appropriate. Categorical variables were analyzed using McNemar’s test, suitable for comparing proportions in paired samples. Comparisons between categorical and continuous variables were performed using the Mann-Whitney U test. Finally, logistic regression analysis was used to simultaneously assess the independent effect of prognostic factors. Variables with a P value < 0.200 in the univariate analysis were entered into the multivariable model. For variables that remained statistically significant, odds ratios were calculated as measures of association. The modified non-responder imputation method was applied, considering patients who discontinued treatment prior to the analysis timepoint as “non-responders”, thus preserving the robustness of the estimates. Statistical analyses were performed using IBM SPSS Statistics version 27, with a 95% confidence interval level.

RESULTS

A total of 205 patients with CD were included, with a median age of 49 (IQR: 38-61) years and a balanced sex distribution, 52% (107/205) women. 49% of the cohort presented with ileal involvement (100/205). EIMs were common, affecting 61% (125/205) of patients, while perianal disease was present in 18% (36/205). Prior intestinal surgery had been performed in 39% (n = 80) of patients. The population was highly refractory, with a median of two failed prior advanced therapies. More than 80% (167/205) had previously been treated with ustekinumab, 71% (145/205) with adalimumab, and 61% (125/205) with infliximab. Concomitant corticosteroids were used in 28% (57/205) at baseline, while immunomodulators were infrequently used, 2.5% (5/205). The median disease duration of the 205 patients was 13 years (Table 1).

Table 1 Baseline characteristics and disease features, n (%).

Baseline characteristic	Patients (n = 205)
Mean (years), median (interquartile range)	49.2 (38-61)
Sex
Female	107 (52.2)
Male	98 (47.8)
Smoking status
Active	49 (23.9)
Former	56 (27.3)
Never	100 (48.8)
Disease location
Ileal	100 (48.8)
Colonic	16 (7.8)
Ileocolonic	88 (42.9)
Upper gastrointestinal	14 (6.9)
Extraintestinal manifestations	125 (61.0)
Perianal disease	36 (17.6)
Prior intestinal resection	80 (39.4)
Previous biologics failed
Infliximab	125 (61.0)
Adalimumab	145 (70.7)
Vedolizumab	47 (22.9)
Ustekinumab	167 (81.5)
Certolizumab	7 (3.4)
Upadacitinib	21 (10.2)
Concomitant corticosteroids	57 (28.4)
Concomitant immunomodulators	5 (2.5)
Herpes zoster vaccination	87 (44.2)

Clinical activity improved rapidly after risankizumab induction. The median HBI decreased from 8 (IQR: 5-11) at baseline to 4 (IQR: 3-8) at week 12 and remained stable at 5 (IQR: 3-8) and 4 (IQR: 2-8) at 6 months and 12 months, respectively (P < 0.001) (Figure 1). In parallel, CR rates increased from 20% at baseline (mainly attributable to recent surgery, residual effects of previous advanced therapies, or concomitant corticosteroid use at treatment initiation) to 49% at week 12 (P < 0.001), 46% at 6 months (P < 0.001), and 49% at 12 months (P = 0.016). SFR was achieved in 41%-44% of patients across follow-up, while clinical-biochemical remission remained modest (7%-9%), not statistically significant (Table 2; Figure 2).

Figure 1 Distribution of Harvey-Bradshaw index across baseline, 12 weeks, 6 months, and 12 months (boxplots represent median, interquartile range, and min-max).

Figure 2 Remission rates in risankizumab-treated Crohn’s disease patients. CD: Crohn’s disease.

Table 2 Clinical and biochemical remission, median (interquartile range)/n (%).

Outcome	Baseline	12 weeks	6 months	12 months	P value
HBI	8 (5-11)	4 (3-8) (< 0.001)1	5 (3-8) (0.003)1	4 (3-8) (< 0.001)1	< 0.001
CRP (mg/L)	4.8 (2.9-12.1)	4.0 (2.0-8.2)	4.0 (2-10)	3.9 (1.6-7.4)	0.268
FC (μg/g)	1113.5 (437-2200)	807.5 (274.0-1500.3)	840.0 (336.5-1488.0)	1063.5 (341.3-2200.0)	0.103
Clinical remission	41 (20.2)	89 (48.6) (< 0.001)2	56 (46.3) (< 0.001)2	22 (48.9) (0.016)2
Clinical-biochemical remission	9 (4.4)	16 (8.7)	8 (6.6)	3 (6.7)
Steroid-free remission		75 (41.0)	53 (43.8)	19 (42.2)

¹Pairwise comparisons of the Friedman test.

²McNemar test for related samples.

HBI: Harvey-Bradshaw index; CRP: C-reactive protein; FC: Fecal calprotectin.

Biomarker trends were consistent with clinical outcomes. Median CRP decreased from 4.8 mg/L (IQR: 2.9-12.1) at baseline to 3.9 mg/L (IQR: 1.6-7.4) at 12 months, although differences did not reach statistical significance (P = 0.268; Figure 3A). Fecal calprotectin showed a marked initial reduction, from 1113.5 μg/g (IQR: 437-2200) to 807.5 μg/g (IQR: 274-1500.3) at week 12, but values increased again by month 12 with a median of 1063.5 μg/g (IQR: 341.5-2200), without significant differences compared to baseline (Figure 3B).

Figure 3 Distribution across baseline, 12 weeks, 6 months, and 12 months (boxplots represent median, interquartile range, and min-max). A: C-reactive protein (mg/L); B: Fecal calprotectin (μg/g). CRP: C-reactive protein.

Clinical evaluation of perianal disease demonstrated a substantial benefit, with CR or response documented in 65% (15/23) of evaluable patients at week 12 and 80% (12/15) at month 6 (P = 0.134). Regarding response assessed by imaging, only 4 patients were evaluated, of whom half showed a radiological response in perianal disease.

With respect to EIMs, 125 patients (61%) presented a history or presence of extraintestinal involvement at baseline. However, only 21 patients had active and evaluable EIMs during follow-up. Among them, 47% (10/21) experienced clinical improvement with risankizumab after six months and 33% (7/21) after one year (P = 0.450), while 62% (13/21) remained unchanged. Only one patient experienced worsening of extraintestinal symptoms. By EIM type, musculoskeletal manifestations improved in 7/8 patients at 6 months and 12 months, cutaneous in 5/5 at 12 weeks and 3/5 at 6 months, and ocular in 2/2 at 12 weeks. Endoscopic disease activity was also assessed. At baseline colonoscopy, 75% (76/102) of patients presented with moderate-to-severe endoscopic activity (SEMA-CD ≥ 7). At 6 months, endoscopic improvement was observed, with 29% (10/35) showing mild endoscopic activity and 32% (11/35) achieving endoscopic remission (SEMA-CD < 2).

Treatment persistence was high (Figure 4). By week 12, 6% of patients had discontinued risankizumab, increasing to 8% at 6 months and 13% at 12 months. Discontinuations were mainly due to primary non-response, with a smaller proportion related to adverse events or treatment intolerance. Survival analyses confirmed favorable persistence, particularly in patients exposed to fewer prior biologics. Indeed, CR rates at 6 months were highest among patients using risankizumab as first advanced therapy (82%), compared to 55% in second-line and 39% in ≥ third-line therapy (P = 0.021). SFR showed a similar gradient, with 83% of first-line patients in remission at 12 months vs 43% in later lines (Table 3). When stratified by prior biologic failure, SFR at 6 months was achieved in 41.5% of patients who had failed ustekinumab, 30.3% in those with prior vedolizumab exposure, and 26.7% after upadacitinib. Persistence of benefit was maintained at 12 months (Table 4).

Figure 4 Probability of risankizumab drug survival expressed as a Kaplan-Meier curve with 95% confidence interval.

Table 3 Clinical remission by line of therapy, n (%).

Line of therapy1	Baseline	6 months	12 months	P value
First line (n = 30)	7 (24.1)	9 (81.8)	5 (83.3)	0.021 at 6 months
Second line (n = 72)	19 (26.4)	23 (54.8)	9 (56.3)
Third line (n = 96)	15 (15.6)	26 (39.4)	9 (42.9)

¹Clinical remission rates at baseline, 6 and 12 months, stratified by line of therapy.

Table 4 Steroid-free remission by prior biologic failure, median (interquartile range)/n (%).

Prior biologic failed1	Number of prior therapies	Steroid-free remission 6 months	Steroid-free remission 12 months
Vedolizumab	4 (3-4)	10 (30.3)	4 (30.8)
Ustekinumab	3 (2-3)	43 (41.5)	14 (36.8)
Upadacitinib	4 (3-5)	4 (26.7)	1 (16.7)

¹Steroid-free remission rates according to prior biologic therapy exposure.

In univariate analysis, most baseline characteristics (including sex, smoking status, disease location, perianal disease, and concomitant corticosteroid use) were not significantly associated with SFR at 6 months. A trend towards higher remission rates was observed among patients with fewer prior biologic exposures. In the multivariate model, prior treatment with vedolizumab was independently associated with a lower likelihood of achieving SFR at 6 months (odds ratio = 0.41, 95% confidence interval: 0.17-0.99, P = 0.046). No other clinical or biochemical variables retained statistical significance after adjustment (Supplementary Table 1).

Risankizumab was generally well tolerated throughout the follow-up period. At week 12, the most frequently reported adverse events were mild upper respiratory tract infections (pharyngitis or rhinitis) (n = 3), transient liver enzyme elevations (n = 3), arthralgia (n = 3), headache (n = 2), and transient cutaneous eruptions (n = 2). Five patients (2.4%) discontinued treatment within the first 12 weeks due to adverse events, including hepatotoxicity (n = 1), hypersensitivity reactions (n = 1), treatment intolerance (n = 1), or moderate cutaneous reactions (n = 2). Between week 12 and 6 months, additional adverse events were documented: Paraesthesia (n = 1), arthralgia (n = 1), fungal infection (n = 1), cutaneous reaction (n = 1), and alopecia (n = 1). One patient discontinued therapy specifically due to alopecia. At month 12, one patient reported asthenia, and one further patient discontinued risankizumab because of a localized fungal infection of the feet. Cumulative adverse events leading to discontinuation by 12 months totaled 7 patients (3.4%). No serious infections, malignancies, or deaths were observed during follow-up.

DISCUSSION

This multicenter real-world study provides valuable evidence on the effectiveness and safety of risankizumab in a highly refractory CD population. The findings are consistent with pivotal phase III trials, such as ADVANCE, MOTIVATE and FORTIFY, which demonstrated significant induction and maintenance of remission in moderate-to-severe CD, including patients with prior biologic failures[6,7,9]. Importantly, our cohort, which comprised predominantly multirefractory patients with extensive exposure to prior advanced therapies (median 2 failed biologic agents), demonstrates that risankizumab efficacy observed in controlled trials translates effectively into routine clinical practice.

When compared with previously published real-world cohorts, our findings are highly consistent while reflecting an even more refractory population. In a Belgian multicenter study including heavily pretreated patients, risankizumab achieved steroid-free clinical response in 58.2% and remission in 27.3% at week 52[16], despite a high rate of prior biologic exposure. Similarly, data from the French GETAID registry reported steroid-free CR rates of approximately 47% at week 26, which were maintained at around 46%-48% at one year, together with high treatment persistence[17]. Notably, a large United States multicenter cohort described week-12 CR rates exceeding 49% and endoscopic remission approaching 49.5% at 12 months, closely mirroring the early and sustained effectiveness observed in our study[18]. Taken together, these data reinforce that risankizumab is effective not only in controlled trial settings but also in heterogeneous and highly refractory real-life populations. A recent single-center study evaluated risankizumab in 135 patients with CD, of whom 52% (n = 70) had prior ustekinumab experience[19]. In that cohort, CR rates were 69% at week 12, 64% at week 26, and 54% at week 52. Notably, remission rates were not significantly different between ustekinumab-experienced and ustekinumab-naive patients, and prior ustekinumab exposure was not independently associated with lower odds of SFR at 1 year. These results in the ustekinumab group are similar to ours, the SFR rate after 6 months and 12 months is 41.5% and 36,8%, respectively. Based on this, it is important to note that risankizumab could be a good option also in patients previously treated with ustekinumab.

A key strength of our study lies in the challenging baseline profile of included patients, characterized by long-standing disease, multiple prior biologic failures, and high rates of surgery and EIMs. Notably, the cohort included a small subgroup of patients with isolated upper gastrointestinal CD (n = 14), in whom no significant differences were observed in CR, SFR, or biomarker response compared with the rest of the cohort. Despite this, risankizumab achieved meaningful clinical and endoscopic outcomes over 12 months, including improvements in perianal disease, EIMs, and endoscopic activity, an integrative assessment not addressed in previous studies. From a mechanistic perspective, selective IL-23 blockade may contribute to improvement in perianal fistulizing disease by downregulating the IL-23/T helper 17 cell axis, which plays a central role in chronic transmural inflammation and fistula tract persistence in CD. Unlike TNF-α inhibitors, which exert a rapid anti-inflammatory effect and promote fistula closure through broad cytokine suppression and tissue remodeling, risankizumab targets upstream pathogenic pathways involved in granulomatous inflammation and epithelial-mesenchymal transition, potentially supporting sustained fistula healing in selected patients. This complementary mechanism may explain why clinical benefit in perianal disease can still be observed in highly refractory populations, even after prior anti-TNF exposure[20]. CR or response in perianal disease was observed in the majority of evaluable patients, and endoscopic remission was achieved in nearly one-third of those assessed at 6 months. Interestingly, fecal calprotectin levels showed a rebound towards baseline values at 12 months despite sustained CR. This discrepancy may be partly explained by the high proportion of ileal involvement in our cohort (49%), as fecal calprotectin has lower sensitivity in isolated or predominant ileal CD, potentially underestimating biological response despite clinical improvement. Treatment persistence was high, with only a small proportion discontinuing therapy, mainly due to primary non-response. Importantly, patients with fewer prior biologic failures demonstrated the highest rates of clinical and SFR, highlighting risankizumab’s potential as a valuable option for difficult-to-treat populations. Compared with prior French and Belgian cohorts, our population had even greater prior exposure to advanced therapies, underscoring the robustness of these outcomes.

In terms of safety, our findings are consistent with both clinical trial data and other real-world reports. Risankizumab was generally well tolerated, with only 3.4% of patients discontinuing treatment due to adverse events. Most adverse events were mild and transient, the most common being upper respiratory tract infections, arthralgia, headache, and transient cutaneous eruptions. No serious infections, malignancies, or deaths were observed during follow-up. These results support the notion that selective IL-23 blockade can provide efficacy advantages without compromising safety, distinguishing risankizumab from broader IL-12/23 inhibition[2].

Nonetheless, some limitations must be acknowledged. First, its ambispective observational design, although reflective of real-world practice, is inherently susceptible to selection bias, channeling bias, and residual confounding. Second, endoscopic follow-up was incomplete, and procedures were performed and interpreted locally without centralized review, which may introduce both selection bias and inter-observer variability in the assessment of mucosal healing. Third, fecal calprotectin has limited sensitivity in isolated ileal disease. Fourth, sample sizes in several key subgroups, particularly those with endoscopic follow-up, perianal disease, and active extraintestinal or immune-mediated manifestations, were relatively small, limiting statistical power and the generalizability of subgroup findings. This relatively low rate of endoscopic reassessment (35/205 patients at 6 months) is inherent to the real-world observational design of the study, as no protocol-mandated endoscopic schedule was established. In routine clinical practice, follow-up endoscopy was mainly performed based on clinical indication, patient acceptance, or disease activity, with some patients in CR or declining invasive reassessment, which may have contributed to attrition. Additionally, a modified non-responder imputation approach was applied across all effectiveness outcomes, including CR, SFR, endoscopic outcomes, and EIM response, to provide a conservative estimation of treatment effectiveness in the presence of missing data. Finally, the clinical evaluation of perianal disease and EIMs was partly subjective and not based on formal scoring systems, which may introduce measurement variability in these domains.

Future prospective studies and registry-based analyses with endoscopic endpoints will be crucial to validate these findings and to position risankizumab against other therapeutic alternatives, including ustekinumab and newer IL-23 inhibitors. In conclusion, our results add to the growing body of real-world evidence supporting the effectiveness and safety of risankizumab in CD. Taken together with data from other European and United States cohorts, they reinforce the role of IL-23 blockade as a key therapeutic strategy for multirefractory patients and support the integration of risankizumab into the treatment algorithm of CD.

CONCLUSION

In conclusion, our results add to the growing body of real-world evidence supporting the effectiveness and safety of risankizumab in CD. Taken together with data from other European and United States cohorts, they reinforce the role of IL-23 blockade as a key therapeutic strategy for multirefractory patients and support the integration of risankizumab into the treatment algorithm of CD.