P-027 YI Are Patients With Inflammatory Bowel Disease on Chronic Immunosuppressive Therapy at Increased Risk of Cervical High-Grade Dysplasia/Cancer? A Meta-Analysis

2014 ◽  
Vol 20 ◽  
pp. S34-S36
Author(s):  
Allegretti Jessica ◽  
Barnes Edward ◽  
Cameron Anna
2020 ◽  
Vol 91 (6) ◽  
pp. 1334-1342.e1 ◽  
Author(s):  
Michiel E. de Jong ◽  
Heleen Kanne ◽  
Loes H.C. Nissen ◽  
Joost P.H. Drenth ◽  
Lauranne A.A. P. Derikx ◽  
...  

Author(s):  
Daniele Piovani ◽  
Claudia Pansieri ◽  
Soumya R R Kotha ◽  
Amanda C Piazza ◽  
Celia-Louise Comberg ◽  
...  

Abstract Background and aims The association between smoking and inflammatory bowel disease (IBD) relies on old meta-analyses including exclusively non-Jewish White populations. Uncertainty persists regarding the role of smoking in other ethnicities. Methods We systematically searched Medline/PubMed, Embase and Scopus for studies examining tobacco smoking and the risk of developing IBD, i.e., Crohn’s disease (CD) or ulcerative colitis (UC). Two authors independently extracted study data and assessed each study’s risk-of-bias. We examined heterogeneity and small-study effect, and calculated summary estimates using random-effects models. Stratified analyses and meta-regression were employed to study the association between study-level characteristics and effect estimates. The strength of epidemiological evidence was assessed through prespecified criteria. Results We synthesized 57 studies examining the smoking-related risk of developing CD and UC. Non-Jewish White smokers were at increased risk of CD (29 studies; RR: 1.95, 95% CI: 1.69‒2.24; moderate evidence). No association was observed in Asian, Jewish and Latin-American populations (11 studies; RR: 0.97; 95% CI: 0.83–1.13), with no evidence of heterogeneity across these ethnicities. Smokers were at reduced risk of UC (51 studies; RR: 0.55, 95% CI: 0.48–0.64; weak evidence) irrespectively of ethnicity; however, cohort studies, large studies and those recently published showed attenuated associations. Conclusions This meta-analysis did not identify any increased risk of CD in smokers in ethnicities other than non-Jewish Whites, and confirmed the protective effect of smoking on UC occurrence. Future research should characterize the genetic background of CD patients across different ethnicities to improve our understanding on the role of smoking in CD pathogenesis.


2021 ◽  
Vol 8 (1) ◽  
pp. e000774
Author(s):  
Fatema Alrashed ◽  
Robert Battat ◽  
Israa Abdullah ◽  
Aline Charabaty ◽  
Mohammad Shehab

BackgroundDuring COVID-19 pandemic, the safety of medical therapies for inflammatory bowel disease (IBD) in relation to COVID-19 has emerged as an area of concern. This study aimed to evaluate the association between IBD therapies and severe COVID-19 outcomes.MethodWe performed a systematic review and meta-analysis of all published studies from December 2019 to August 2021 to identify studies that reported severe COVID-19 outcomes in patients on current IBD therapies including 5-aminosalicylic acid (5-ASA), immunomodulators, corticosteroids, biologics, combination therapy, or tofacitinib.ResultsTwenty-two studies were identified. Corticosteroids (risk ratio (RR) 1.91 (95% CI 1.25 to 2.91, p=0.003)) and 5-ASA (RR 1.50 (95% CI 1.17 to 1.93, p=0.001)) were associated with increased risk of severe COVID-19 outcomes in patients with IBD patients. However, possible confounders for 5-ASA use were not controlled for. Sub-analysis showed that corticosteroids increased the risk of intensive care unit (ICU) admission but not mortality. Immunomodulators alone (RR 1.18 (95% CI 0.87 to 1.59, p=0.28)) or in combination with anti-TNFs ((RR 0.96 (95% CI 0.80 to 1.15, p=0.63)), tofacitinib (RR 0.81 (95% CI 0.49 to 1.33, p=0.40)) and vedolizumab ((RR 1.02 (95% CI 0.79 to 1.31, p=0.89)) were not associated with severe disease. Anti-TNFs (RR 0.47 (95% CI 0.40 to 0.54, p<0.00001)) and ustekinumab (RR 0.55 (95% CI 0.43 to 0.72, p<0.00001)) were associated with decreased risk of severe COVID-19.ConclusionIn patients with IBD, the risk of severe COVID-19 is higher among patients receiving corticosteroids. Corticosteroid use was associated with ICU admission but not mortality. The risk is also higher among patients receiving 5-ASAs. However, patient-level data were lacking and insufficient data existed for meta-regression analyses to adjust for confounding. Vedolizumab, tofacitinib, and immunomodulators alone or in combination with anti-TNF were not associated with severe disease. Anti-TNFs, and ustekinumab were associated with favourable outcomes.


2013 ◽  
Vol 144 (5) ◽  
pp. S-618-S-619
Author(s):  
Siddharth Singh ◽  
Sajan Jiv Singh Nagpal ◽  
Mohammad H. Murad ◽  
Siddhant Yadav ◽  
Sunanda V. Kane ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-17 ◽  
Author(s):  
Ran Ao ◽  
Ying Wang ◽  
Dao-Rong Zhnag ◽  
Ya-Qi Du

Objective. The present meta-analysis investigated the contribution ofTLR4rs4986790A>G and rs4986791C>T genetic polymorphisms in increasing the risk of inflammatory bowel disease (IBD).Methods. Databases were searched using a combination of keywords related toTLR4and IBD. Relevant studies were selected based on strict inclusion and exclusion criteria. Meta-analysis of the data extracted from the selected studies was performed using CMA 2.0 statistical analysis software.Results. Out of the 70 studies retrieved by database search, only 13 studies were eligible for inclusion in this meta-analysis and these 13 studies contained a total number of 4409 IBD patients and 5693 healthy controls. The meta-analysis results demonstrated thatTLR4rs4986790A>G polymorphism is associated with an increased risk of IBD (allele model: OR = 1.268, 95% CI = 1.124~1.431, andP<0.001; dominant model: OR = 1.240, 95% CI = 1.090~1.409, andP=0.001). Similarly, TLR4 rs4986791C>T polymorphism also conferred an increased risk of IBD (allele model: OR = 1.259, 95% CI = 1.092~1.453, andP=0.002; dominant model: OR = 1.246, 95% CI = 1.072~1.447, andP=0.004).Conclusion. Our meta-analysis results demonstrate thatTLR4rs4986790A>G and rs4986791C>T genetic polymorphisms are associated with the etiopathogenesis of IBD.


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