Front. Immunol.Frontiers in ImmunologyFront. Immunol.1664-3224Frontiers Media S.A.10.3389/fimmu.2026.1762379Original ResearchIncreased risk of inflammatory bowel disease in ankylosing spondylitis compared to psoriasisHeZhen1†Writing – original draftWriting – review & editingZhangYi-Nan1†Writing – original draftWeiJames Cheng-Chung234*‡Project administrationResourcesSupervisionWriting – review & editingDaiSheng-Ming1*‡ConceptualizationProject administrationSupervisionWriting – review & editingDepartment of Rheumatology and Immunology, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaInstitute of Medicine, College of Medicine, Chung Shan Medical University, Taichung, TaiwanDepartment of Allergy, Immunology and Rheumatology, Chung Shan Medical University Hospital, Taichung, TaiwanGraduate Institute of Integrated Medicine, China Medical University, Taichung, TaiwanCorrespondence: James Cheng-Chung Wei, jccwei@gmail.com; Sheng-Ming Dai, shengmingdai@163.com
While ankylosing spondylitis (AS) and psoriatic arthritis (PsA) share similar immune dysregulation, their relative risks for inflammatory bowel disease (IBD), including definitive subtypes (Crohn’s disease [CD] and ulcerative colitis [UC]) and possible subtypes (indeterminate colitis [IC] and microscopic colitis [MC]), remain unquantified. We aimed to establish comparative IBD risk gradients among AS, psoriasis (PSO), and PsA cohorts.
Methods
The study utilized a long-term retrospective cohort design by analyzing an electronic health record database. Propensity score matching (PSM) was used to adjust multiple confounders. Cox proportional hazards models and log rank test were employed to evaluate the risk of IBD development.
Results
The study included 26,610 patients with AS and 322,317 with PSO (2005–2023). After PSM, 26,569 matched pairs were analyzed. Compared to PSO, AS was associated with a significantly higher risk of definite IBD [hazard ratio (HR) = 2.96, 95% CI: 2.64–3.33], CD (HR = 3.38, 95% CI: 2.90–3.94), UC (HR = 2.43, 95% CI: 2.07–2.85), and IC (HR = 2.45, 95% CI: 1.33–4.51), but not MC. Subgroup analyses confirmed a consistently higher IBD risk in AS across all ages, sexes, races, BMI categories, and comorbidity profiles. Compared to the general population, AS conferred the highest independent risk for definite IBD (HR = 4.22, 95% CI: 3.60–4.94), followed by PsA (HR = 1.52) and PSO (HR = 1.37). AS also showed a 2.60-fold higher definite IBD risk than PsA (95% CI: 2.32–2.92).
Conclusions
AS is the phenotype most strongly associated with IBD among the studied spectrum. Compared to PSO, AS confers a significantly higher risk of CD, UC, and IC, and it carries a greater burden of definite IBD than PsA or the general population.
ankylosing spondylitisepidemiologyinflammatory bowel diseasepsoriatic diseaserisk factorThe author(s) declared that financial support was received for this work and/or its publication. This work was supported by the National Natural Science Foundation of China (grant numbers 82271837, 82071809).section-at-acceptanceAutoimmune and Autoinflammatory Disorders : Autoimmune DisordersIntroduction
Spondyloarthritis (SpA) encompasses a spectrum of chronic inflammatory disorders targeting the axial skeleton and peripheral joints, with systemic manifestations frequently involving the skin, eyes, and gastrointestinal tract. Key subtypes include ankylosing spondylitis (AS), reactive arthritis, inflammatory bowel disease (IBD)-associated arthritis, and psoriatic arthritis (PsA) (1). These subtypes share common immunogenetic pathways (2), such as the dysregulation of the interleukin (IL)-23/T helper 17 (Th17) axis (3–6). Notably, AS and psoriatic disease exhibit distinct tissue tropisms. AS is characterized by axial skeletal damage, while psoriatic disease is mainly manifested as cutaneous and peripheral joint inflammation. Both conditions are associated with a high prevalence of extra-musculoskeletal and peripheral manifestations, particularly IBD (7–10).
IBD comprises a wide range of chronic immune-mediated intestinal disorders, which have traditionally been classified into Crohn’s disease (CD) and ulcerative colitis (UC) (11). Epidemiological studies confirm an elevated IBD risk in patients with AS, PsA, or psoriasis (PSO) compared to the general population (12–20). Emerging data collectively suggest that this risk may follow a gradient across these related phenotypes—for instance, some studies comparing AS and PsA suggest a higher risk in AS, while analyses within the psoriatic disease spectrum indicate that risk increases from PSO to PsA (13, 14, 21–24). However, these evidence streams have not been integrated within a single, methodologically consistent framework. Thus, while a risk hierarchy is biologically plausible, a unified analysis providing directly comparable risk estimates for AS, PSO, and PsA is scarce.
Beyond CD and UC, emerging entities like indeterminate colitis (IC) and microscopic colitis (MC) challenge traditional classification (25–27). IC, a provisional diagnosis with overlapping CD/UC features, may represent a transitional gut inflammation state (28). To date, however, epidemiological and mechanistic studies investigating the association between IC and other immune−mediated diseases remain notably scarce. MC, an immune-mediated disorder linked to autoimmunity (29, 30), has reported associations with both PSO and AS (31, 32), but its comparative risk across these cohorts is undefined.
Furthermore, meaningful interpretation of such comparative studies is complicated by significant heterogeneity in environmental exposures (e.g., smoking) (33), therapeutic interventions (e.g., TNF inhibitors) (34), and ethnic factors, all of which can obscure disease-specific risk estimates (8). Consequently, there is a lack of comprehensive studies that simultaneously directly compare the risk of definitive IBD (CD, UC) and possible IBD (IC, MC) across AS, PSO, and PsA and rigorously adjust for this broad range of potential confounders.
To address these gaps, we conducted a large-scale, propensity score-matched (PSM) cohort study. Our primary objectives were (1) to perform a direct, adjusted comparison of overall IBD and subtype risk between AS and PSO patients and (2) to establish and compare the independent IBD risk associated with AS, PSO, and PsA by deriving standardized hazard ratios (HR) relative to matched general population cohorts. This approach aims to delineate a risk gradient to inform tailored clinical surveillance.
MethodsData sources
The database was from a collaborative electronic health record database (https://trinetx.com), a federated health program which provides real-time updates of data from electronic healthcare records, including demographics, vital statuses, laboratory results, diagnoses, and treatments (35). The personal identification is protected. The International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM) codes were used to classify diseases. In addition, the study was approved under the authority of the Institutional Review Board of Chung Shan Medical University Hospital (no.: CS2-21176).
Study design and patient selection
We select patients aged 20 or older from the database who had been diagnosed with PSO, PSA, and AS in accordance with the ICD-10-CM code during the period from January 1, 2005 to December 31, 2023 (Supplementary Table S1). The AS cohort, defined by ICD-10 codes, primarily represents patients with radiographic axial spondyloarthritis (axSpA). In these cohorts, patients diagnosed with IBD were designated as the primary outcome of this study. Those patients who had been diagnosed with IBD prior to the index date were excluded from the analysis. Some covariates, namely, age, sex, body mass index (BMI), race, medical utilization, comorbidities, and medication usage, were analyzed (Supplementary Table S2). To mitigate the impact of confounding factors, we employed the PSM method with a 1:1 ratio matching based on the aforementioned covariates. All covariates listed in Supplementary Table S2 were included in the PSM model. Comparisons between the AS and PSO cohorts both before and after matching were investigated using a standardized mean difference (SMD). It was considered as well matched if the SMD was lower than 0.1. Subgroup analyses were further carried out to examine whether the risk of IBD in PSO and AS patients varied according to each covariate.
Statistical analysis
The baseline characteristics of the participants were expressed as numbers and percentages for categorical variables and means ± standard deviations for continuous variables. Chi-square and Student’s t-tests were applied to examine the categorical and continuous variables between the two cohorts. A Cox proportional hazards survival model was used to compare event rates over time between diagnostic groups. The HR and 95% confidence interval (CI) were calculated using univariate Cox proportional hazard model. The results were graphically inspected via Kaplan–Meier plots to validate the model assumptions. Log-rank tests were done to assess whether the survival curves differed between different cohorts.
ResultsComparison of baseline characteristics in AS and PSO patients
During the study period within the database, a total of 42,717 adults with AS and 385,749 adults with PSO, all aged 20 or older, were identified. Subsequent to the application of exclusion criteria and the removal of patients diagnosed with IBD, 26,610 individuals with AS and 322,317 individuals with PSO were singled out (Figure 1). The baseline characteristics, including age, sex, race, social economic status, BMI, medical utilization, comorbidities, and medication intake, were compared between the AS and PSO groups (Supplementary Table S2). Before propensity matching, the AS group was mainly composed of male patients (58.60%) and was marginally younger than the PSO group (49.76 ± 16.39 years versus 51.44 ± 15.70 years). The AS group had a relatively higher proportion of Asian, Black or African Americans, and American Indian or Alaska native compared to the PSO group. PSO patients exhibited higher rates of comorbidities, such as hypertensive diseases (18.87% versus 15.36%), dyslipidemia (15.85% versus 12.36%), diabetes mellitus (9.56% versus 6.79%), liver diseases (3.29% versus 2.19%), cerebrovascular diseases (2.51% versus 2%), and nicotine dependence (5.34% versus 3.62%). In terms of medical usage, a greater number of PSO patients were treated with corticosteroids (21.23% versus 19.86%) and cyclosporine (0.36% versus 0.26%), while AS patients tended to receive methotrexate (1.75% versus 1.44%). Regarding the application of anti-tumor necrosis factor (TNF) antibodies and anti-interleukin (IL)-17 antibodies, more AS patients received etanercept, infliximab, adalimumab, golimumab, certolizumab Pegol, and secukinumab (Supplementary Table S2). After PSM, 26,569 patients were selected for each group, with all baseline features well balanced (Supplementary Table S2).
Flow chart of subject selection.
Flowchart detailing patient selection from a research network of 117,794,290 individuals. Two groups: ankylosing spondylitis (AS) with 26,569 individuals and psoriasis with 26,569 individuals, both aged 20 or older with diagnosis between 2005 and 2023. Exclusions include history of autoimmune diseases, psoriasis, ankylosing spondylitis, and inflammatory bowel disease before index date. Propensity score matching used for 1:1 matching by age, sex, race, socioeconomic status, BMI, medical utilization, comorbidities, and medication.Overall risk of IBD in AS compared to PSO
Following PSM analysis based on age, sex, race, social economic status, BMI, medical utilization, comorbidities, and medication intake, the risk of definite and possible IBD in AS and PSO patients was evaluated. Herein CD and UC were defined as definite IBD, while IC and MC were defined as possible IBD. The cumulative incidence of CD, UC, and IC was higher in the AS group than in the PSO group (7.13% versus 2.15% for CD, 5.64% versus 3.14% for UC, and 0.4% versus 0.16% for IC), whereas no difference was observed in the incidence rate of MC between the two groups (0.9% versus 0.93%). AS was associated with a substantially higher risk of definite IBD in comparison to PSO, with a HR of 2.96 (95% CI: 2.64–3.33; log-rank test, P < 0.001) (Table 1, Figure 2). For possible IBD, patients with AS had a stronger association with IC (HR = 2.45, 95% CI: 1.33–4.51; log-rank test, P = 0.003) (Table 1, Figure 2), but not for MC (HR = 1.27, 95% CI: 0.95–1.70; log rank test, P = 0.106) (Table 1, Figure 2). Sensitivity analysis across different network databases corroborated these results (Supplementary Table S3).
Risk of inflammatory bowel disease exposed to ankylosing spondylitis compared to psoriasis.
Kaplan–Meier plots and log-rank tests for risk of inflammatory bowel disease exposed to ankylosing spondylitis compared to psoriasis. (A–F) Separately indicated definite inflammatory bowel disease, Crohn’s disease, ulcerative colitis, possible inflammatory bowel disease, indeterminate colitis, and microscopic colitis. The orange straight line denoted ankylosing spondylitis, while the gray straight line indicated psoriasis. P < 0.05 was considered statistically significant.
Six line graphs compare the incidence of various bowel diseases over 20 years between ankylosing spondylitis (orange line) and psoriasis (grey line). Graphs A to F show increasing incidences in ankylosing spondylitis across all conditions compared to psoriasis. Significant differences with log-rank p-values are noted: A (p < 0.001), B (p < 0.001), C (p < 0.001), D (p = 0.008), E (p = 0.003), and F (p = 0.106). Conditions covered are inflammatory bowel disease, Crohn’s disease, ulcerative colitis, possible inflammatory bowel disease, indeterminate colitis, and microscopic colitis.Subgroup analysis of IBD risk in AS compared to PSO
To further illustrate the elevated risk of IBD associated with AS in contrast to PSO, we carried out subgroup analysis based on age, sex, BMI, race, and comorbidities (Table 2). In general, among the 20–40, 41–64, and ≥65 age groups, the presence of IBD patients was observed in 349/7,873 (4.43%), 438/11,078 (3.95%), and 168/5675 (5.92%) of AS patients, respectively, while in the PSO population, the corresponding figures were 109/7873 (1.38%), 143/11,078 (1.29%), and 72/5675 (1.27%). When stratified by gender, the incident rates of IBD were persistently higher in AS patients regardless of gender (Table 2). Additionally, differences in IBD incidence were consistently detected between the AS and PSO groups across diverse BMI categories (Table 2). With regard to race, White patients with AS (HR = 3.01, 95% CI: 2.64–3.44), Black or African American patients with AS (HR = 5.48, 95% CI: 3.03–9.94), and Asian patients with AS (HR = 2.14, 95% CI: 1.03–4.43) exhibited a higher susceptibility to developing IBD when compared to their counterparts with PSO. Moreover, the risk of IBD in AS patients remained higher than that in PSO patients, irrespective of whether they were complicated by hypertensive diseases (HR = 1.75, 95% CI: 1.29–2.37) and dyslipidemia (HR = 1.59, 95% CI: 1.12–2.23) (Table 2).
Subgroup analysis of risk of inflammatory bowel disease exposed to ankylosing spondylitis compared to psoriasis.
Variable
Ankylosing spondylitis
Psoriasis
N
No. of events
N
No. of events
HR (95% CI)
Age, years
20–40
7,873
349
7,873
109
3.53 (2.84–4.37)a
41–64
11,078
438
11,078
143
3.34 (2.77–4.04)a
≥65
5,675
168
5,675
72
2.73 (2.07–3.60)a
Sex
Female
9,265
341
9,265
149
2.58 (2.13–3.13)a
Male
15,157
620
15,157
197
3.47 (2.95–4.07)a
Race
White
19,572
795
19,572
295
3.01 (2.64–3.44)a
Black or African American
1,590
67
1,590
13
5.48 (3.03–9.94)a
Asian
951
21
951
11
2.14 (1.03–4.43)a
BMI (kg/m2)
<30
4,588
172
4,588
85
2.30 (1.77–2.98)a
≥30
2,582
73
2,582
37
2.34 (1.57–3.48)a
Comorbidities
Hypertensive diseases
3,965
106
3,965
71
1.75 (1.29–2.37)a
Dyslipidemia
3,180
77
3,180
57
1.59 (1.12–2.23)a
Cerebrovascular diseases
519
11
519
12
1.12 (0.49–2.54)
If the patient’s count is 1–10, the results indicate a count of 10.
CI, confidence interval; BMI, body mass index.
Considered statistically significant.
Analysis of IBD risk among different groups
Subsequently, we assessed the risk of IBD among different groups. We discovered that in the general population, the cumulative incidence of definite IBD ranged from 2.18% to 2.85%. In contrast, it was approximately 11% in patients with AS, 4.08% in those with PSO, and around 5% in patients with PsA, respectively (Table 3). A continuously elevated risk of developing IBD was observed in patients with AS (HR = 4.22, 95% CI: 3.6–4.94), PSO (HR = 1.37, 95% CI: 1.31–1.45), and PsA (HR = 1.52, 95% CI: 1.36–1.70) in comparison to the general population. Further comparison with PsA showed that AS was associated with a considerably higher risk of definite IBD, with a HR of 2.60 (95% CI: 2.32–2.92) (Table 3).
Risk of inflammatory bowel disease among different groups.
Group
N
No. of events
HR (95% CI)
Cumulative incidence (%)
Group
Psoriatic arthritis
25,377
408
Reference
5.52
Ankylosing spondylitis
25,377
989
2.60 (2.32–2.92)a
11.14
Group
General population
24,276
187
Reference
2.18
Ankylosing spondylitis
24,276
948
4.22 (3.61–4.94)a
10.68
Group
General population
306,769
2,301
Reference
2.85
Psoriasis
306,769
4,265
1.37 (1.31–1.45)a
4.08
Group
General population
59,741
484
Reference
2.45
Psoriatic arthritis
59,741
943
1.52 (1.36–1.70)a
5.16
The general population was identified by ICD-10-CM = Z02 (encounter for administrative examination), excluding ICD-10-CM = M45, M46, and L40.
CI, confidence interval.
Considered statistically significant.
Discussion
In this large-scale, propensity score-matched cohort study using longitudinal real-world data, we provide a comprehensive, direct comparison of IBD risk between patients with AS and those with psoriatic disease (PSO/PsA), integrating both definitive (CD and UC) and possible (IC and MC) subtypes. Our analysis reveals a clear and consistent risk gradient: AS conferred the highest independent risk for definite IBD compared to the general population (HR = 4.22), followed by PsA (HR = 1.52), with PSO alone showing a more modest elevation (HR = 1.37). Critically, the risk of definite IBD in AS was nearly threefold higher than in PSO (HR = 2.96) and 2.6-fold higher than in PsA (HR = 2.60). We further identified a novel, specific association between AS and an increased incidence of IC, whereas the risk of MC was comparable between AS and PSO.
Our findings provide independent validation and quantitative refinement to the risk hierarchy suggested in prior literature. Consistent with a large Swedish national register study, which reported incidence rate ratios of 6.2 for IBD in AS versus 2.3 in PsA (22), we observed a markedly higher risk burden in AS compared to PsA (HR = 4.22 vs. 1.52). The direct, adjusted comparison between AS and PSO in our study (HR = 2.96) provides crucial missing data that refines this gradient. Prior studies within the psoriatic disease spectrum have detailed increased IBD risk in PSO (13, 14), further amplified by concomitant PsA (21), but often lacked a methodologically parallel AS cohort for direct comparison. Our study addresses this gap by analyzing all three cohorts within the same framework, employing rigorous propensity score matching to balance key demographic, comorbidity, and treatment confounders.
Our analysis also included an evaluation of possible IBD subtypes. To our knowledge, direct comparisons of IC and MC risks between AS and PSO in large cohorts have been limited. In our cohort, AS was associated with a significantly higher risk of IC compared to PSO (HR = 2.45), a difference that has not been well characterized in prior large-scale studies. IC is a recognized diagnostic category reserved for chronic colitis that cannot be definitively classified as either CD or UC based on endoscopic, histological, and radiographic features (36). It often represents a transitional or overlapping inflammatory state within the IBD spectrum (28). Our data, linking AS specifically to a higher incidence of IC, suggest that the gut inflammation in AS may present in an atypical or evolving pattern that defies early conventional classification. In contrast, the risk of MC was found to be comparable between AS and PSO patients. MC is a distinct, immune-mediated colonic disorder characterized by chronic watery diarrhea and specific histopathological findings (lymphocytic or collagenous colitis) (37–39). Its pathogenesis involves mucosal dysregulation of T-cell responses (40) and is known to share genetic susceptibility loci (41) and immunological pathways with other autoimmune conditions, notably psoriasis (31). Our observation of comparable MC risk between AS and PSO is supported by large-scale epidemiological evidence. A nationwide case–control study confirmed that MC is significantly associated with a wide range of autoimmune diseases, demonstrating an increased odds ratio for both AS and psoriasis (32). However, the precise mechanisms underlying MC, and its specific associations with AS and PSO, remain to be fully elucidated.
Some factors are significant influencers in the development of IBD (42–44). Uria Shani et al. carried out a population-based study with the aim of exploring the predictors associated with the development of IBD among patients with PSO. They determined that advanced age, male gender, and Jewish ethnicity were risk factors for IBD (14). Therefore, in order to investigate whether the risk factors for IBD had an impact on the incident rate of IBD between AS and PSO, we performed a subgroup analysis based on several cofounding variables. We discovered that the relatively higher risk of IBD in patients with AS compared to those with PSO was consistently observed in different subgroups categorized by age, sex, BMI, and race. Our results, at least to some extent, indicated the robust and enhanced effect of AS on the risk of IBD in comparison to PSO.
The marked risk gradient identified necessitates a re-evaluation of clinical surveillance. For patients with AS, the substantially elevated risks for CD, UC, and specifically IC warrant a high index of suspicion. Proactive inquiry about gastrointestinal symptoms should be integrated into rheumatological follow-up, with prompt gastroenterological referral for symptomatic patients. The specific increase in IC risk suggests that gut inflammation in AS may often be atypical, making comprehensive ileocolonoscopy with serial biopsies crucial for accurate classification.
Some limitations within the study warrant acknowledgment. First, despite the independent analyses for patients with AS, PsA, and PSO, a certain degree of overlap among the diagnoses remain unavoidable. Second, patients with a milder disease who were managed in primary healthcare might be overlooked, thereby potentially limiting the generalizability of the current findings. Third, the observational design precludes confirmation of causality, and residual confounding from unmeasured factors (e.g., smoking intensity, disease duration, and time-varying treatment exposure) cannot be excluded. Fourth, our AS cohort, defined by ICD-10 codes, primarily captures patients with axSpA. Therefore, our findings should be interpreted in the context of established AS and may not be generalizable to the broader spectrum of non-radiographic axSpA without further validation.
In conclusion, this study delineates a clear gradient of IBD risk across AS, PsA, and PSO, with AS representing the highest-risk phenotype. The specifically elevated risk of IC in AS underscores the importance of heightened clinical suspicion and tailored diagnostic evaluation in this population. These findings together support the recognition of AS as a distinct high-risk IBD phenotype, suggesting that surveillance and management strategies should be differentiated from those for PSO and PsA.
Data availability statement
The original contributions presented in the study are included in the article/Supplementary Material. Further inquiries can be directed to the corresponding authors.
Ethics statement
The studies involving humans were approved by Institutional Review Board of Chung Shan Medical University Hospital (No: CS2-21176). The studies were conducted in accordance with the local legislation and institutional requirements. The participants provided their written informed consent to participate in this study.
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Supplementary material
The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fimmu.2026.1762379/full#supplementary-material
ReferencesSieperJRudwaleitMBaraliakosXBrandtJBraunJBurgos-VargasR.
The Assessment of SpondyloArthritis international Society (ASAS) handbook: a guide to assess spondyloarthritis. Ann Rheum Dis. (2009) 68 Suppl 2:ii1–44. doi: 10.1136/ard.2008.104018, PMID: 19433414KuhnKAYomogidaKKnoopKWuHJZaissMM.
More than a leaky gut: how gut priming shapes arthritis. Nat Rev Rheumatol. (2025) 21:513–25. doi: 10.1038/s41584-025-01282-1, PMID: 40745056MeasePvan den BoschF.
IL-23 and axial disease: do they come together? Rheumatol (Oxford). (2021) 60:iv28–33. doi: 10.1093/rheumatology/keab617, PMID: 34668015MacleodTBridgewoodCMcGonagleD.
Role of neutrophil interleukin-23 in spondyloarthropathy spectrum disorders. Lancet Rheumatol. (2023) 5:e47–57. doi: 10.1016/S2665-9913(22)00334-4, PMID: 38251507OharaDTakeuchiYHirotaK.
Type 17 immunity: novel insights into intestinal homeostasis and autoimmune pathogenesis driven by gut-primed T cells. Cell Mol Immunol. (2024) 21:1183–200. doi: 10.1038/s41423-024-01218-x, PMID: 39379604GirolomoniGStrohalRPuigLBachelezHBarkerJBoehnckeWH.
The role of IL-23 and the IL-23/T(H) 17 immune axis in the pathogenesis and treatment of psoriasis. J Eur Acad Dermatol Venereol. (2017) 31:1616–26. doi: 10.1111/jdv.14433, PMID: 28653490BittarMDeodharA.
Axial spondyloarthritis: A review. JAMA. (2025) 333:408–20. doi: 10.1001/jama.2024.20917, PMID: 39630439LewisJDParlettLEJonsson FunkMLBrensingerCPateVWuQ.
Incidence, prevalence, and racial and ethnic distribution of inflammatory bowel disease in the United States. Gastroenterology. (2023) 165:1197–1205 e1192. doi: 10.1053/j.gastro.2023.07.003, PMID: 37481117HracsLWindsorJWGorospeJCummingsMCowardSBuieMJ.
Global evolution of inflammatory bowel disease across epidemiologic stages. Nature. (2025) 642:458–66. doi: 10.1038/s41586-025-08940-0, PMID: 40307548KaplanGG.
The global burden of inflammatory bowel disease: from 2025 to 2045. Nat Rev Gastroenterol Hepatol. (2025) 22:708–20. doi: 10.1038/s41575-025-01097-1, PMID: 40681759MahadevanUSilverbergMS.
Inflammatory bowel disease-gastroenterology diamond jubilee review. Gastroenterology. (2018) 154:1555–8. doi: 10.1053/j.gastro.2017.12.025, PMID: 29550591AlinaghiFTekinHGBurischJWuJJThyssenJPEgebergA.
Global prevalence and bidirectional association between psoriasis and inflammatory bowel disease-A systematic review and meta-analysis. J Crohns Colitis. (2020) 14:351–60. doi: 10.1093/ecco-jcc/jjz152, PMID: 31504363CharltonRGreenAShaddickGSnowballJNightingaleATillettW.
Risk of uveitis and inflammatory bowel disease in people with psoriatic arthritis: a population-based cohort study. Ann Rheum Dis. (2018) 77:277–80. doi: 10.1136/annrheumdis-2017-212328, PMID: 29092855ShaniUBen-ShabatNQassemRLahatAOmarMSavinE.
The association between psoriasis, psoriasis severity, and inflammatory bowel disease: a population-based analysis. Therap Adv Gastroenterol. (2024) 17:17562848241227037. doi: 10.1177/17562848241227037, PMID: 38282955StolwijkCEssersIvan TubergenABoonenABazelierMTDe BruinML.
The epidemiology of extra-articular manifestations in ankylosing spondylitis: a population-based matched cohort study. Ann Rheum Dis. (2015) 74:1373–8. doi: 10.1136/annrheumdis-2014-205253, PMID: 24658834StolwijkCvan TubergenACastillo-OrtizJDBoonenA.
Prevalence of extra-articular manifestations in patients with ankylosing spondylitis: a systematic review and meta-analysis. Ann Rheum Dis. (2015) 74:65–73. doi: 10.1136/annrheumdis-2013-203582, PMID: 23999006WangSTsouHKChiouJYWangYHZhangZWeiJC.
Increased risk of inflammatory bowel disease among patients with ankylosing spondylitis: A 13-year population-based cohort study. Front Immunol. (2020) 11:578732. doi: 10.3389/fimmu.2020.578732, PMID: 33123163KangHSHanKMKimJHYooDMChoiHGKimNY.
Psoriasis as a potential risk factor for inflammatory bowel disease: findings from a nationally representative korean population. Biomedicines. (2025) 13:2334. doi: 10.3390/biomedicines13102334, PMID: 41153620SchneeweissMCKirchgesnerJWyssRJinYYorkCMerolaJF.
Occurrence of inflammatory bowel disease in patients with chronic inflammatory skin diseases: a cohort study: Classification: Epidemiology. Br J Dermatol. (2022) 187:692–703. doi: 10.1111/bjd.21704, PMID: 35718888PittamBGuptaSHarrisonNLRobertsonSHughesDMZhaoSS.
Prevalence of extra-articular manifestations in psoriatic arthritis: a systematic review and meta-analysis. Rheumatol (Oxford). (2020) 59:2199–206. doi: 10.1093/rheumatology/keaa062, PMID: 32160297LiWQHanJLChanATQureshiAA.
Psoriasis, psoriatic arthritis and increased risk of incident Crohn’s disease in US women. Ann Rheum Dis. (2013) 72:1200–5. doi: 10.1136/annrheumdis-2012-202143, PMID: 22941766BengtssonKForsblad-d’EliaHDemingerAKlingbergEDehlinMExarchouS.
Incidence of extra-articular manifestations in ankylosing spondylitis, psoriatic arthritis and undifferentiated spondyloarthritis: results from a national register-based cohort study. Rheumatol (Oxford). (2021) 60:2725–34. doi: 10.1093/rheumatology/keaa692, PMID: 33216939EppingaHPoortingaSThioHBNijstenTECNuijVvan der WoudeCJ.
Prevalence and phenotype of concurrent psoriasis and inflammatory bowel disease. Inflammation Bowel Dis. (2017) 23:1783–9. doi: 10.1097/MIB.0000000000001169, PMID: 28617755WilliamsJCAlamUZhaoSS.
Incidence of uveitis and inflammatory bowel disease in psoriatic disease, and psoriatic disease in uveitis and inflammatory bowel disease. Rheumatol (Oxford). (2025) 64:3177–9. doi: 10.1093/rheumatology/keaf110, PMID: 39977376GeboesKColombelJFGreensteinAJewellDPSandbornWJVatnMH.
Indeterminate colitis: a review of the concept–what’s in a name? Inflammation Bowel Dis. (2008) 14:850–7. doi: 10.1002/ibd.20361, PMID: 18213696MeucciGBortoliARiccioliFAGirelliCMRadaelliFRivoltaR.
Frequency and clinical evolution of indeterminate colitis: a retrospective multi-centre study in northern Italy. GSMII (Gruppo di Studio per le Malattie Infiammatorie Intestinali). Eur J Gastroenterol Hepatol. (1999) 11:909–13. doi: 10.1097/00042737-199908000-00018, PMID: 10514127MartlandGTShepherdNA.
Indeterminate colitis: definition, diagnosis, implications and a plea for nosological sanity. Histopathology. (2007) 50:83–96. doi: 10.1111/j.1365-2559.2006.02545.x, PMID: 17204023VenkateswaranNWeismillerSClarkeK.
Indeterminate colitis - update on treatment options. J Inflammation Res. (2021) 14:6383–95. doi: 10.2147/JIR.S268262, PMID: 34876831BergmanDKangXSunJEbrahimiFLudvigssonJF.
Autoimmune thyroid diseases and microscopic colitis: A nationwide matched case-control study in Sweden. J Clin Endocrinol Metab. (2025) 110:e3730–7. doi: 10.1210/clinem/dgaf140, PMID: 40038861BergmanDRoelstraeteBSunJEbrahimiFAsklingJLudvigssonJF.
Microscopic colitis and risk of incident rheumatoid arthritis: A nationwide population-based matched cohort study. Aliment Pharmacol Ther. (2023) 58:1028–40. doi: 10.1111/apt.17708, PMID: 37727878BergmanDRoelstraeteBSunJEbrahimiFLidstromRSvedbomA.
Microscopic colitis and risk of incident psoriasis: A nationwide population-based matched cohort study. Clin Epidemiol. (2024) 16:213–25. doi: 10.2147/CLEP.S454677, PMID: 38567370WildtSMunckLKWinther-JensenMJessTNyboe AndersenN.
Autoimmune diseases in microscopic colitis: A Danish nationwide case-control study. Aliment Pharmacol Ther. (2021) 54:1454–62. doi: 10.1111/apt.16614, PMID: 34653278LakatosPLVeghZLovaszBDDavidGPandurTErdelyiZ.
Is current smoking still an important environmental factor in inflammatory bowel diseases? Results from a population-based incident cohort. Inflammation Bowel Dis. (2013) 19:1010–7. doi: 10.1097/MIB.0b013e3182802b3e, PMID: 23399739BaumgartDCLe BerreC.
Newer biologic and small-molecule therapies for inflammatory bowel disease. N Engl J Med. (2021) 385:1302–15. doi: 10.1056/NEJMra1907607, PMID: 34587387PalchukMBLondonJWPerez-ReyDDrebertZJWiner-JonesJPThompsonCN.
A global federated real-world data and analytics platform for research. JAMIA Open. (2023) 6:ooad035. doi: 10.1093/jamiaopen/ooad035, PMID: 37193038TremaineWJ.
Review article: Indeterminate colitis–definition, diagnosis and management. Aliment Pharmacol Ther. (2007) 25:13–7. doi: 10.1111/j.1365-2036.2006.03159.x, PMID: 17229217BurkeKED’AmatoMNgSCPardiDSLudvigssonJFKhaliliH.
Microscopic colitis. Nat Rev Dis Primers. (2021) 7:39. doi: 10.1038/s41572-021-00273-2, PMID: 34112810ChettyRGovenderD.
Lymphocytic and collagenous colitis: an overview of so-called microscopic colitis. Nat Rev Gastroenterol Hepatol. (2012) 9:209–18. doi: 10.1038/nrgastro.2012.16, PMID: 22349169MunchALangnerC.
Microscopic colitis: clinical and pathologic perspectives. Clin Gastroenterol Hepatol. (2015) 13:228–36. doi: 10.1016/j.cgh.2013.12.026, PMID: 24407107KumawatAKStridHTyskCBohrJHornquistEH.
Microscopic colitis patients demonstrate a mixed Th17/Tc17 and Th1/Tc1 mucosal cytokine profile. Mol Immunol. (2013) 55:355–64. doi: 10.1016/j.molimm.2013.03.007, PMID: 23566938WesterlindHMellanderMRBressoFMunchABonfiglioFAssadiG.
Dense genotyping of immune-related loci identifies HLA variants associated with increased risk of collagenous colitis. Gut. (2017) 66:421–8. doi: 10.1136/gutjnl-2015-309934, PMID: 26525574YenEFPokhrelBDuHNweSBianchiLWittB.
Current and past cigarette smoking significantly increase risk for microscopic colitis. Inflammation Bowel Dis. (2012) 18:1835–41. doi: 10.1002/ibd.22838, PMID: 22147506YeYPangZChenWJuSZhouC.
The epidemiology and risk factors of inflammatory bowel disease. Int J Clin Exp Med. (2015) 8:22529–42.
LarsenMGROvergaardSHPetersenSRMøllegaardKMMunkHLNexøeAB.
Effects of smoking on clinical treatment outcomes amongst patients with chronic inflammatory diseases initiating biologics: secondary analyses of the prospective BELIEVE cohort study. Scand J Immunol. (2024) 100:e13395. doi: 10.1111/sji.13395, PMID: 38973149
Edited by: Raphael Sanches Peres, University of São Paulo, Brazil
Reviewed by: Levinus Albert Dieleman, University of Alberta, Canada