Systematic Reviews and Meta-analyses
Progression of Elderly Onset Inflammatory Bowel Diseases: A Systematic Review and Meta-Analysis of Population-Based Cohort Studies

https://doi.org/10.1016/j.cgh.2020.02.048Get rights and content

Background & Aims

The incidence of inflammatory bowel diseases (IBDs) in older adults is increasing. We performed a systematic review and meta-analysis to evaluate progression of elderly onset (EO) IBD in population-based cohorts and compared it with adult onset (AO) IBD.

Methods

In a systematic review through June 1, 2019, we identified population-based cohort studies of EO IBD reporting the cumulative risk of hospitalization, surgery, mortality, treatment patterns, escalation, and/or malignancy. Data were synthesized using random-effects meta-analysis as cumulative risk of events at 1 year, 5 years, and 10 years, and compared with data from patients with AO IBD in the same cohorts.

Results

We identified 9 studies, comprising 14,765 patients with EO IBD. In patients with EO Crohn’s disease (CD), the cumulative 5-year risk of surgery was 22.6% (95% CI, 18.7–27.2) and was similar to that of patients with AO CD (relative risk [RR], 1.04; 95% CI, 0.80–1.34). Overall exposure to corticosteroids was comparable between patients with EO CD vs AO CD (5-year risk: 55.4%; 95% CI, 53.4–57.4; RR, 0.88; 95% CI, 0.78–1.00), but exposure to immunomodulators (31.5%; 95% CI, 29.7–33.4; RR, 0.62; 95% CI, 0.51–0.77) or biologic agents (6.5%; 95% CI, 5.6–7.6; RR, 0.36; 95% CI, 0.25–0.52) was significantly lower for patients with EO CD than for patients with AO CD. Similarly, in patients with EO ulcerative colitis (UC), the cumulative 5-year risk of surgery was 7.8% (95% CI, 5.0–12.0), similar to the risk for patients with AO UC (RR, 1.29; 95% CI, 0.79–2.11). Overall exposure to corticosteroids was comparable between patients with EO UC vs AO UC (5-year risk: 57.2%; 95% CI, 55.6–58.7; RR, 0.98; 95% CI, 0.91–1.06), but exposure to immunomodulators (16.1%; 95% CI, 15.0–17.2; RR, 0.58; 95% CI, 0.54–0.62) or biologic agents (2.0%; 95% CI, 1.6–2.5; RR, 0.36; 95% CI, 0.24–0.52) was significantly lower for patients with EO UC than for patients with AO UC. Patients with EO IBD appeared to have increased mortality, but not malignancy, compared with the general population. There were few data on comorbidities or adverse effects of medications.

Conclusions

In a systematic review and meta-analysis, we found that patients with EO IBD have a similar risk of surgery as patients with AO IBD. However, patients with EO IBD are less likely to receive treatment with immunomodulators or biologic agents.

Section snippets

Methods

This systematic review followed the Preferred Reporting Items for Systematic reviews and Meta-Analysis standards and followed an a priori protocol.

Results

We identified 5204 unique studies using our search strategy, and after screening titles and abstracts, 51 full texts were reviewed. From this, 9 studies representing 7 unique population-based cohort studies were included in our synthesis.12, 13, 14, 15, 16, 17, 18, 19, 20 The study selection flowchart is shown in Figure 1.

Study characteristics are summarized in Table 1. Of the 7 cohorts, 6 were based in Europe and 1 in Canada. Each study compared a cohort of EO IBD patients vs 1 or more cohorts

Discussion

In this systematic review of population-based observational studies on EO IBD, we made several key observations regarding EO IBD vs AO IBD. First, we observed that risk of surgery, hospitalization, and disease progression is similar between EO IBD and AO IBD at a population level. Surgery carries a high risk in older patients; approximately 10% experience serious complications within the first 30 days, and 4% of patients die. Second, although the cumulative use of corticosteroids is high (and

CRediT Authorship Contributions

Jacob J. Rozich (Conceptualization: Supporting; Data curation: Lead; Formal analysis: Supporting; Writing – original draft: Supporting); Parambir S. Dulai (Conceptualization: Supporting; Formal analysis: Supporting; Writing – review & editing: Equal); Mathurin Fumery (Conceptualization: Supporting; Formal analysis: Supporting; Writing – review & editing: Supporting); William J. Sandborn (Conceptualization: Supporting; Writing – review & editing: Supporting); Siddharth Singh, MD

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    Conflicts of interest These authors disclose the following: Parambir S. Dulai has received research support from Takeda, Pfizer, AbbVie, Janssen, Polymedco, ALPCO, Buhlmann, and Prometheus, and consulting fees from Takeda, Pfizer, AbbVie, and Janssen; Mathurin Fumery has received honoraria from AbbVie, MSD, Takeda, Janssen, Pfizer, Ferring, Celgene, Gilead, and Boehringer; William J. Sandborn has received research grants from Atlantic Healthcare Limited, Amgen, Genentech, Gilead Sciences, AbbVie, Janssen, Takeda, Lilly, Celgene/Receptos, consulting fees from AbbVie, Allergan, Amgen, Arena Pharmaceuticals, Avexegen Therapeutics, BeiGene, Boehringer Ingelheim, Celgene, Celltrion, Conatus, Cosmo, Escalier Biosciences, Ferring, Forbion, Genentech, Gilead Sciences, Gossamer Bio, Incyte, Janssen, Kyowa Kirin Pharmaceutical Research, Landos Biopharma, Lilly, Oppilan Pharma, Otsuka, Prizer, Precision IBD, Progenity, Prometheus Laboratories, Reistone, Ritter Pharmaceuticals, Robarts Clinical Trials (owned by Health Academic Research Trust), Series Therapeutics, Shire, Sienna Biopharmaceuticals, Sigmoid Biotechnologies, Sterna Biologicals, Sublimity Therapeutics, Takeda, Theravance Biopharma, Tigenix, Tillotts Pharma, UCB Pharma, Ventyx Biosciences, Vimalan Biosciences, Vivelix Pharmaceuticals, and stock or stock options from BeiGene, Escalier Biosciences, Gossamer Bio, Oppilan Pharma, Precision IBD, Progenity, Ritter Pharmaceuticals, Ventyx Biosciences, Vimalan Biosciences; and Siddharth Singh has received research grant support from AbbVie, has served as a consultant for AbbVie, Takeda, and AMAG Pharmaceuticals, and has received honorarium from Pfizer for ad hoc grant review. The remaining author discloses no conflicts.

    Funding Research reported in this publication was supported by the National Institute of Diabetes and Digestive and Kidney Diseases grant K23DK117058 (S.S.) and P30 DK120515 (W.J.S.), by an American Gastroenterological Association Research Scholar Award (P.S.D.), by the American College of Gastroenterology Junior Faculty Development Award the Crohn’s and the Colitis Foundation Career Development Award 404614 and the IOIBD Operating Grant (S.S.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

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