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

Timepoint	Baseline (n=142)	12 Weeks (n=124)	16 Weeks (n=87)	6 Months (n=87)	p¹
Harvey-Bradshaw Index (mean)	8.1	4.1 (<0.001)²	4.0 (<0.001)²	4.2 (<0.001)²	<0.001
CRP (mg/L, mean)	9.7	6.2 (0.031)²	6.1 (0.017)²	5.8 (0.017)²	0.021
Calprotectin (μg/g, mean)	1,323.3	1,099.8 (0.533)²	1,015.2 (0.164)²	1,055.6 (0.238)²	0.149
Clinical Remission (%)	16.7%	54.0% (<0.001)³	50.6% (<0.001)³	48.3% (<0.001)³	-
Clinical-Biochemical Remission (%)	2.1%	15.3% (<0.001)³	13.8% (0.001)³	16.1% (<0.001)³	-
Steroid-Free Remission (%)	-	13.7%	17.2% (0.025)³	18.4% (0.003)³	-
Treatment Discontinuation	-	11/142 (7.7%)	24/142 (16.9%)	31/142 (21.8%)	-

¹ Friedman test for related samples (two-way ANOVA by ranks).
² Pairwise comparisons using the Friedman test.
³ McNemar test for related samples.

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

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).

Effectivenessa	Any UPA dose
Time to first achievementb of clinical response per Daily pAMSb Events analysed – n/N (%) Median (IQR), days Clinical response per pAMSc at week 8 or 16 of induction, n/N (%) [95% CI]	364/373 (97.6) 4.0 (3.0-8.0) 258/324 (79.6) [75.2, 84.0]
Overall TEAEs, Week 26 of Therapy,d n (%) Any AE AE with a reasonable possibility of being related to study treatmente Severe TEAE Serious TEAE AE leading to discontinuation of the study drug AE resulting in deathf	Any UPA dose (N = 490) 251 (51.2) 171 (34.9) 25 (5.1) 27 (5.5) 34 (6.9) 1 (0.2)
Overview of TEAEs With Reasonable Possibility of Being Related to Study Treatment Through Week 26,d n (%) Any AEe Severe TEAE Serious TEAE AE leading to discontinuation of the study drug AE resulting in death	Any UPA dose (N = 490) 171 (34.9) 11 (2.2) 11 (2.2) 24 (4.9) 0
Table. Summary of PROFUNDUS Interim Effectiveness and Safety Results. FAS, full analysis set; IQR, interquartile range; pAMS, partial Adapted Mayo Score; RBS, rectal bleeding score; SF, stool frequency; TEAE, treatment-emergent adverse event; UPA, upadacitinib. aEffectiveness population included evaluable patients who took at least 1 dose of UPA and had available diary scores to define the corresponding outcome among the first 500 patients who provided informed consent and satisfied eligibility criteria. Patients who discontinued due to lack of effectiveness or intolerability were categorised as nonresponders, while those who discontinued due to other reasons were treated as missing data for the responder outcome and censored for the time-to-event outcome. bDefined as a decrease in daily pAMS ≥ 1 point and ≥ 30% from baseline, in addition to a decrease in daily RBS ≥ 1 or a daily RBS ≤ 1. Time to first achievement was based on the difference in time between the date of first achievement and first dose of UPA. Only patients with baseline daily pAMS > 0 with at least one post-baseline score are included. If a patient never achieved this outcome within 183 days (week 26), then that patient's time to first achievement was censored at day 183 (week 26), UPA discontinuation, study discontinuation, or cut-off date, whichever comes earlier. Kaplan-Meier nonparametric estimates were reported. cDefined as a decrease from baseline in pAMS ≥ 1 point and ≥ 30%, in addition to a decrease from baseline in the RBS ≥ 1 or absolute RBS ≤ 1. Patients with baseline score ≥1 and available score at end of induction are included. dIncluded patients with at least 1 dose of UPA among the first 500 patients who provided informed consent and satisfied eligibility criteria. Included events within 26 weeks (183 days) of starting study treatment. eAs assessed by study investigator. fThere was 1 death due to drowning that was determined to have no reasonable possibility of being related to the study drug. Data cut-off date was 28 Feb 2025.

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

The need for effective therapies in moderate to severe Crohn's disease (CD) drives the comparative evaluation of biologic treatments. The current work uses an anchored Matching-Adjusted Indirect Comparison (MAIC) to assess the efficacy of guselkumab (GUS) relative to risankizumab (RZB) during the treatment induction phase. This MAIC is using data from five phase 3 placebo-controlled blinded clinical trials (GRAVITI, GALAXI 2, GALAXI 3, ADVANCE, MOTIVATE).

Aims & Methods

Adult patients with moderate to severe CD, as defined in GRAVITI, GALAXI 2/3, ADVANCE and MOTIVATE trials were included. An anchored MAIC was utilized, leveraging placebo as common comparator and following guidance from the National Institute for Health Care Excellence in UK. The analysis aligned pooled individual patient data for GUS with published data for RZB by matching exclusion criteria and patient baseline characteristics that could be treatment effect modifiers (eg Age, Sex, BMI, CDAI, disease location or prior biologic treatment failure). During induction, patients received GUS 200 mg intravenous or 400 mg subcutaneous at weeks 0, 4, and 8 or RZB 600 mg intravenous at weeks 0, 4, and 8. The endpoints of interest were symptomatic endpoints such as clinical remission, PRO-2 remission, clinical response, abdominal pain and stool frequency remission, as well as endoscopic response at week 12, which marks the end of the induction period.

Results

After matching, baseline characteristics were balanced between the GUS and RZB cohorts. In a mixed population of bio-naïve and bio-experienced patients, GUS demonstrated statistically significant results in comparison to RZB for PRO-2 remission, clinical response and abdominal pain remission (table 1). Clinical remission showed a trend in favor of GUS, endoscopic response and stool frequence remission were comparable to RZB. In patients with biologic treatment failure versus the MOTIVATE trial, results had been generally more in favor of GUS, while maintaining positive outcomes seen across mixed populations (ADVANCE & MOTIVATE). Results were also mostly consistent whether analyzing pooled GUS data or individual trials, eg from GRAVITI, against RZB.

Table 1: Results of GUS from pooled GRAVITI, GALAXI 2/3 vs. RZB for induction period at week 12

Endpoint	RE measure	Mixed population (ADVANCE & MOTIVATE)		Bio-failure population (MOTIVATE)
		BC	SA	BC	SA
Clinical response	OR [95%CI]	1.78* [1.06; 2.99]	1.42 [0.76; 2.64]	1.71 [0.82; 3.57]	1.23 [0.49; 3.04]
Endoscopic response	OR [95%CI]	1.05 [0.56; 1.97]	1.05 [0.53; 2.09]	1.57 [0.59; 4.18]	1.56 [0.49; 5.01]
Clinical remission	OR [95%CI]	1.51 [0.84; 2.70]	1.22 [0.60; 2.46]	1.52 [0.65; 3.51]	1.08 [0.39; 3.01]
PRO-2 remission	OR [95%CI]	1.96* [1.13; 3.38]	1.85* [1.03; 3.33]	2.89* [1.29; 6.49]	2.97* [1.11; 7.94]
AP score remission	OR [95%CI]	1.68 [1.00; 2.82]	1.37 [0.75; 2.52]	2.02 [0.97; 4.20]	1.68 [0.69; 4.09]
SF score remission	OR [95%CI]	0.99 [0.62; 1.59]	0.93 [0.55; 1.58]	1.14 [0.59; 2.19]	1.04 [0.48; 2.26]

Footnotes: clinical response= ≥100-point reduction from baseline in CDAI OR CDAI <150; endoscopic response= ≥50% improvement from baseline in SES-CD OR SES-CD ≤2; clinical remission= CDAI <150; PRO-2 remission=AP mean daily score at or below 1 [AP≤1] AND SF mean daily score at or below 3 [SF≤3], and no worsening of AP or SF from baseline; AP score remission=Abdominal Pain mean daily score at or below 1 [AP≤1];
SF score remission= number of liquid or very soft stools mean daily score at or below 3 [SF≤3];
BC=baseline risk-adjusted; SA=sensitivity analysis; *p<0,05

Conclusion

The anchored MAIC analysis demonstrates comparable to even superior efficacy of guselkumab over risankizumab in inducing symptomatic improvements in Crohn's disease patients. It also suggests that subcutaneous induction seems to be preferential over iv induction.

Disclosure

van Sanden S, Trevisan M, Strobl A and Wirth D are employees of J&J Innovative Medicines

Introduction

​​​​​PSC is chronic infammatory disease of bile ducts leading to strictures of bile duct and eventually to liver cirrhosis. Chronic inflammation is associated with markedly increased risk of cholangiocancer (CCA). In addition, gall bladder abnormalities are common in patients with PSC¹ such as cholecystitis, gallstones, polys and gallbladder carcinoma (GBCA). Increased fasting gallbladder volume has been reported with normal gallbladder emptying². Due to the increased risk of GBCA³ cholecystectomy is recommended in PSC with gallbladder polyps ≥8 mm and smaller polyps growing⁴. However, cholecystectomy has been associated with impaired PSC outcome. A study consisting of 11 PSC patients with cholecystectomy suggested protective role of gallbladder based on MRCP changes and elevated AST levels in patients with cholecystectomy. No significant difference in serum bile acids was observed in patients with or w/o cholecystectomy⁵. Another small study including five PSC patients with cholecystectomy showed that cholecystectomy was associated with worse Mayo scores and an elevated FIB4⁶. More than 50% of PSC have enlarged gallbladder which is suspected to be caused by hyperpressure in the biliary tract⁵. Cholecystectomy may thus eliminate this reserve function and lead to progression of bile duct strictures.

Aims & Methods

To evaluate the impact of cholecystectomy on liver enzyme levels, biliary bile acid composition, bile duct disease progression, and overall outcomes in a large PSC patient cohort, we analyzed data from 1,009 individuals enrolled in the prospective Helsinki PSC registry. Of these, 114 patients (11.3%) had undergone cholecystectomy—34 prior to and 80 following the PSC diagnosis. Patients with gallbladder cancer were excluded. Clinical and laboratory parameters were collected, along with data on disease progression based on sequential ERC examinations scored by the Helsinki ERC score⁷. Additionally, bile composition was analyzed in a subgroup of 157 patients receiving UDCA therapy, 32 of whom had undergone cholecystectomy.

Results

Demographics, liver function tests, and outcomes stratified by cholecystectomy, are presented in the table. We found no differences between the three groups (no cholecystectomy, cholecystectomy done prior or after PSC dg) regarding the progression of bile duct disease or its severity, liver function tests, development of biliary dysplasia or need for dilatation, Mayo- and MELD-scores. The cumulative incidence of the composite end point (= transplantation, liver related death, HCC or CCA) did not differ between groups. The molar-% of phospholipids were lower and cholic acid and deoxycholic acid (mg) elevated in bile in patients with cholecystectomy, whereas no differences were found in UDCA content.

Variable	No cholecystectomy, n=895	Cholecystectomy before PSC dg, n=34	Cholecystectomy after PSC dg, n=80	P-value**
Men, n(%)	537(60)	12(35)	39(49)	0.003
Age, mean (SD)	37(13)	46(12)	43(13)	<0.001
BMI, mean(SD)	25.6(4.5)	26.5(4.2)	26.4(4.5)	0.22
ERC-score, mean (SD)	5.8(3.5)	6.4(3.7)	6.4(3.5)	0.16
Need for dilatation	398(44)	18(53)	42(53)	0.26
P-AST, U/l, median (IQR)	36(25,58)	37(28,52)	34(26,51)	0.83
P-ALP, U/l, median (IQR)	132(96,222)	130(88,191)	113(84,179)	0.082
Mayo Score, mean (SD)	-0.29(0.84)	-0.10(0.63)	-0.10(0.78)	0.079
Composite end point, n [Incidence (95% CI:)]*	142 [16.4 (13.8 -19.3)]	6 [13.31 (4.88 - 28.97)]	14 [14.16 (7.74 - 23.76)]	0.66

* Per 1 000 person years
** Adjusted for sex and PSC age

Conclusion

In this large study investigating the impact of cholecystectomy on PSC outcomes, we found no effect on liver enzyme levels, prognostic indices, bile duct disease progression, or overall prognosis, regardless of whether the procedure was performed before or after the PSC diagnosis.

References

1. Said K, eta al. Journal of Hepatology 2008; 48:598–605
2. Said K, et al. World J Gastroenterol 2009; 15: 3498-3503
3. van Erp LW, et al. Liver Int 2020; 40:382–92.
4. Chazouilleres O et al. EASL Clinical Practice Guidelines on sclerosing cholangitis. J Hepatol 2022; 77:761–806
5. Cazzagon N, et al. JHEP Reports 2023. https://doi.org/10.1016/j.jhepr.2022.100649
6. Miyake N, et al. Cureus 17(3): e80184. DOI 10.7759/cureus.80184
7. Boyd S, et al. Endoscopy. 2016;48:432-9.

Introduction

Perianal Crohn’s disease (pCD) represents a challenging phenotype of Crohn's disease (CD). While risankizumab (RZB) has demonstrated efficacy in luminal CD, its role in pCD remains unknown. We aimed to evaluate the effectiveness of RZB in pCD and compare the outcomes with other biologics including anti-TNF, ustekinumab (UST), and vedolizumab (VDZ).

Aims & Methods

This retrospective multicenter study performed at nine international centers included adult patients with pCD who initiated RZB as advanced-line (second or more) therapy between 2020 and 2024. Historical controls included pairwise propensity-scored matched pCD patients treated with anti-TNF, UST, or VDZ as second- or third-line therapies. The primary outcome was clinical remission in patients with active pCD, defined as complete resolution of perianal symptoms. Secondary outcomes included clinical response (any symptomatic improvement) in active perianal disease, and relapse rates among patients with inactive pCD at baseline, defined as new or recurrent signs or symptoms of perianal disease.

Results

A total of 214 patients with active pCD were included: 59 (27.6%) received RZB, 62 (29.0%) anti-TNF, 57 (26.6%) UST, and 36 (16.8%) VDZ. Clinical remission was achieved in 58% of patients treated with RZB, compared to 32.9% of those receiving non-RZB therapies (p = 0.01), including 27% for anti-TNF, 44% for UST, and 25% for VDZ. Clinical pCD response rates were 81% for RZB, compared to 71% for anti-TNF, 88% for UST, and 44% for VDZ; p < 0.001. In propensity score–matched comparisons, remission rates with RZB were numerically higher than anti-TNF (56% vs. 31%, p = 0.056) and VDZ (58% vs. 29%, p = 0.08), and comparable to UST (53% vs. 43%, p = 0.5). The median time to clinical response with RZB was three months [IQR: 2–3.5], comparable to anti-TNF (3 [IQR: 2–4], p = 0.4), but significantly shorter than UST (5 [IQR: 4–6], p < 0.001) and VDZ (6.5 [IQR: 4–8], p < 0.001).
Among 160 patients with inactive pCD at baseline, matched analysis showed significantly lower relapse rates with RZB compared to anti-TNF (2% vs. 22%, p = 0.004) and VDZ (0% vs. 28%, p = 0.004), with no significant difference compared to UST (3% vs. 15%, p = 0.2).

Conclusion

Risankizumab demonstrates favorable clinical response, faster time to response, and higher remission rates in active pCD, along with the lowest relapse rates in inactive disease. These results support RZB as an effective therapeutic option for pCD, warranting prospective validation.

Disclosure

No conflicts of interest were declared in relation to this study.