Introduction

Inflammatory bowel disease (IBD) is chronic inflammatory disorder originating from the gastrointestinal tract but with extraintestinal manifestations and complications. Although previous studies have suggested a link between IBD and myocarditis, the association has not been well-established.

Aims & Methods

This study aimed to investigate the long-term risk of myocarditis in patients with IBD. This nationwide cohort involved all patients with biopsy-confirmed IBD in Sweden between 1969 and 2017 [n=83,264, Crohn’s disease (CD, n=24,738), ulcerative colitis (UC, n=46,409), and IBD-unclassified (IBD-U, n=12,117)], individually matched population references individuals (n=391,342), and IBD-free full siblings (n=96,148). Primary outcome was any incident myocarditis and secondary outcome was severe myocarditis (see below for definition). Flexible parametric model estimated adjusted hazard ratios (aHRs) and cumulative incidence of the outcomes, along with 95% confidence intervals (CIs).
Definition for severe myocarditis:
1. Readmission of any cause within 90 days of discharge for myocarditis; 2. Newly diagnosed heart failure within 90 days of hospitalization for new onset myocarditis; 3. Death from any cause within 90 days of hospitalization for new onset myocarditis.

Results

During a median follow-up of 14 years, there were 257 myocarditis cases in IBD patients (incidence rate (IR)=22.7 per 100,000 person-years) and 717 in population reference individuals (IR=13.1), with an aHR=1.54 (95%CI: 1.32 to 1.80). The increased risk persisted through 20 years after the diagnosis of IBD, corresponding to one extra case of myocarditis in 308 IBD patients followed for 20 years. This increase risk was also observed in patients with CD (IR: 21.9 vs. 12.5; aHR=1.49, 95%CI: 1.12 to 1.99) and UC (IR: 22.8 vs. 13.0; aHR=1.57, 95%CI: 1.29 to 1.92). An increased risk for severe myocarditis was also observed in IBD patients (IR=10.2 vs. 3.5; aHR=2.47, 95%CI: 1.92 to 3.19). The risk was irrespective of IBD subtypes [CD (IR: 9.4 vs. 3.3; aHR=2.49, 95%CI: 1.49-4.15), UC (IR: 10.1 vs. 3.4; aHR=2.82, 95%CI: 1.99-3.99), and IBD-U (IR: 13.1 vs. 22.8; aHR=4.6, 95%CI: 1.55-6.33)]. Similar results were found when IBD patients were compared with IBD-free full siblings.

Conclusion

Patients with IBD were at an increased risk of myocarditis for at least 20 years, especially of severe myocarditis, but their absolute risks were low.

Disclosure

JFL has coordinated a study on behalf of the Swedish IBD quality register (SWIBREG). That study received funding from Janssen corporation. JFL has also received financial support from MSD developing a paper reviewing national healthcare registers in China. The other authors report no disclosures relevant to the manuscript.

Introduction

There is evidence linking inflammatory bowel disease (IBD) and cardiovascular diseases. However, the roles of histologic and clinical activity of IBD in the development of arrhythmias remain unknown.

Aims & Methods

In this nationwide cohort study in Sweden, we included IBD patients with histologic data (n = 61,383; diagnosed 1969–2017; classified as histologic inflammation vs. remission based on the Swedish version of the Systematized Nomenclature of Medicine codes) and clinical activity data (n = 96,154; diagnosed 1969–2020; classified as clinically active vs. quiescent IBD based on IBD-related hospitalization, surgery, and treatment escalation) and followed them through December 31, 2021. The primary outcome was incident arrhythmias (including atrial fibrillation/flutter, bradyarrhythmias, other supraventricular arrhythmias, and ventricular arrhythmias/cardiac arrest) within 2 years after documented histologic inflammation (vs. remission) or clinically active IBD (vs. quiescent IBD). Poisson regression models estimated incidence rates (IRs) of arrhythmias, while Cox proportional hazards models estimated adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs). We adjusted for age at IBD diagnosis, sex, calendar year at index date, county of residence, educational attainment, country of birth, number of health care visits, and history of CVD-related comorbidities in the model.

Results

Histologic inflammation was associated with an increased risk of developing any arrhythmias compared to histologic remission (IR: 62.0 vs. 47.2 per 10,000 person-years; aHR = 1.35, 95%CI: 1.18–1.54), corresponding to one additional event of arrhythmia per 338 IBD patients over 2 years after histologic inflammation. We found an excess risk for atrial fibrillation/flutter (aHR = 1.38, 95%CI: 1.18–1.62) and ventricular arrhythmias/cardiac arrest (aHR = 1.73, 95%CI: 1.22–2.44), but not for bradyarrhythmias or other supraventricular arrhythmias. Compared to clinically quiescent IBD, active IBD was also related to a higher risk of arrhythmias (IR: 67.4 vs. 108.4; aHR = 1.77, 95%CI: 1.66–1.88), affecting all subtypes except bradyarrhythmias. In patients with clinically quiescent IBD, histologic inflammation was also associated with an increased risk of arrhythmias (aHR = 1.16, 95%CI: 1.00–1.36, P=0.054).

Conclusion

Histologic and clinical activity were associated with a slightly increased risk of arrhythmias in patients with IBD.

Disclosure

All authors have completed the ICMJE uniform disclosure form and declare:
OO has been PI on projects at Karolinska Institutet financed by grants from Janssen, Pfizer, AbbVie, Takeda, Galapagos/Alfasigma, Ferring, and Bristol Myer Squibb. JH served as speaker or advisory board member for AbbVie, BMS, Celltrion, Eli Lilly, Ferring, Galapagos, Gilead, Index Pharma, Janssen, Medtronic, Merck, MSD, Novartis, Pfizer, Sandoz, Shire, Takeda, Thermo Fisher Scientific, Tillotts Pharma, and Vifor Pharma and received grant support from Takeda, Janssen, and MSD. FE has served as an advisory board member for Boehringer Ingelheim. JFL has coordinated a study for the Swedish IBD Quality Register (SWIBREG), which received funding from Janssen Corporation. JFL has also received financial support from MSD to develop a paper reviewing national healthcare registers in China. JFL has a research collaboration on celiac disease with Takeda and has a research collaboration on fibrosis in IBD with MSD. The other authors report no disclosures relevant to the manuscript.

Introduction

Microscopic colitis (MC) is an inflammatory condition of the large intestine. Primarily diagnosed in middle-aged and older adults, the age-specific incidence of the disease peaks in patients 75-79 years of age. While MC is associated with a reduced quality of life, large-scale studies on the association with future psychiatric disorders are lacking.

Aims & Methods

Due to the burden of symptoms as well as inflammatory similarities between MC and certain psychiatric disorders, we hypothesized that patients with MC were at an increased risk of psychiatric disease. Using the nationwide histopathology cohort ESPRESSO, we identified 5,816 patients in Sweden with MC. These patients were matched, according to birth year, sex, and county, with reference individuals (n=21,509) from the general population. All individuals with previously recorded psychiatric disorders or dispensation of medication indicative of psychiatric morbidity were excluded. Our main outcome measure was a pre-devised collection of ICD-codes, all indicating psychiatric disease. Moreover, to control for the impact of intrafamilial confounding, full siblings to patients with MC were identified, and in a sensitivity analysis, used as reference population. Adjusted hazard ratios were computed using Cox proportional hazards modelling. Our main analysis included adjustments for the matching factors (birth year, county, sex) as well as educational attainment (as a proxy for socioeconomic status) and inflammatory bowel disease, celiac disease, and type 1 diabetes.

Results

From 2006-2021, 519 patients with MC and 1,313 reference individuals were diagnosed with psychiatric disorders (9.9 vs. 6.5 events per 1,000 person-years), corresponding to one extra case of psychiatric disorder in 29 patients with MC over 10 years. After adjustments, this represented a hazard ratio (HR) of 1.57 (95% confidence interval [CI]=1.42-1.74). We found significantly elevated estimates up to 10 years after MC diagnosis and similar HRs in lymphocytic and collagenous colitis. More specifically, we observed increased risks for unipolar depression, anxiety disorders, stress-related disorders, substance abuse, and suicide attempts in patients with MC.
Our result was robust across several sensitivity analyses
(Table 1).

Conclusion

Patients with MC are at increased risk of incident psychiatric disorders compared to the general population. Specifically, this increased risk applies to unipolar depression, anxiety disorders, stress-related disorders, substance abuse, and suicide attempts. The increased risk was most pronounced among older patients with MC.

References

NA

Disclosure

Dr Ludvigsson has coordinated a study for the Swedish IBD quality register (SWIBREG). That study received funding from the Janssen Corporation. Dr Ludvigsson has also received financial support from MSD to develop a paper reviewing national healthcare registers in China. Dr Ebrahimi has served as an advisory board member for Boehringer Ingelheim. Dr Pardi has consulted for Immunic Therapeutics, Takeda, AbbVie, Boehringer Ingelheim, and Lilly.

Introduction

Long-term health outcomes of children of mother with inflammatory bowel disease (IBD) are poorly understood. Therefore, this study aimed to evaluate the long-term impact of maternal IBD on disease in children, including IBD.

Aims & Methods

This nationwide retrospective study included women who delivered a singleton baby after 37 weeks between 2003 and 2004 in South Korea. Women gave birth to low birth weight babies were excluded from the study. We compared risk of diseases in offspring according to maternal IBD. Multivariate analysis was performed to estimate the hazard ratios (HRs) for the future disease risk.

Results

Among a total 542,780 woman who gave birth during study periods, 1,096 women with IBD and 541,684 non-IBD control were identified. In multivariate analysis, the offspring of IBD women frequently had lower respiratory infections (HR 1.124[1.018-1.242]), asthma (HR 1.209[1.065-1.372]), atopic dermatitis (HR 1.217[1.112-1.332]), allergic urticaria (HR 1.276[1.129-1.443])HRHR, and allergic rhinitis (HR 1.151[1.084-1.222]) than those of women without IBD. And the offspring of IBD mother had a higher risk of developing ulcerative colitis (UC) (HR 6.334[4.391-9.136]) and Crohn’s disease (CD) (HR 2.325[1.463-3.694]) than others. Offspring of CD women were significantly associated with asthma (HR 1.244[1.048-1.476]), allergic rhinitis (HR 1.132[1.043-1.229]), and CD (HR 3.44[2.035-5.813]). The offspring of UC women had higher rates of pneumonia (HR 1.332[1.052-1.687]), gastroenteritis (HR 1.469[1.151-1.873]), juvenile arthritis (HR 2.872[1.194-6.909]), atopic dermatitis (HR 1.33[1.174-1.507]), allergic urticaria (HR 1.39[1.174-1.647]), allergic rhinitis (HR 1.158[1.063-1.261]), and UC (HR 11.776[8-17.336]).

Conclusion

Our results show that the offspring of IBD women have higher risk of developing allergic and autoimmune disorders including UC and CD.