O-015 YI The Impact of Clinic Visits and Disease Activity on Adherence Rates in Children With Inflammatory Bowel Diseases

2014 ◽  
Vol 20 ◽  
pp. S9
Author(s):  
Kluthe Cheryl ◽  
Huynh Hien ◽  
Carroll Matthew ◽  
Spady Donald ◽  
Wine Eytan ◽  
...  
2020 ◽  
Vol 27 (1) ◽  
pp. 10-11
Author(s):  
Yejoo Jeon ◽  
Berkeley N Limketkai

The Mediterranean diet was recently shown to benefit hepatic steatosis and disease activity in inflammatory bowel diseases. These findings advance our knowledge on dietary approaches for IBD and motivate inquiry on the role of obesity in IBD pathogenesis.


Author(s):  
Yonghong Yang ◽  
Cui Zhang ◽  
Dehuai Jing ◽  
Heng He ◽  
Xiaoyu Li ◽  
...  

Abstract Background Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn’s disease (CD), are chronic inflammatory disorders. As is well known, interferon regulatory factor (IRF) 5 is closely associated with the pathogenesis of various inflammatory diseases. But the exact role of IRF5 in IBD remains unclear. Methods In this study, we detected IRF5 expression in peripheral blood mononuclear cells (PBMCs) and inflamed mucosa from IBD patients by immunohistochemistry, western blot, and quantitative real-time polymerase chain reaction. Peripheral blood CD4+ T cells were stimulated with inflammatory cytokines and transfected by lentivirus. Results In active IBD patients, the expression of IRF5 in PBMCs and inflamed colonic tissues was obviously increased and significantly associated with disease activity. Ectopic overexpression of IRF5 could promote the differentiation of IBD CD4+ T cells into Th1 and Th17 cells by regulating T-bet and RAR related orphan receptor C, whereas knockdown of IRF5 had the opposite effects. Tumor necrosis factor (TNF)-α upregulated expression of IRF5 in CD4+ T cells, but anti-TNF treatment with infliximab could markedly reduce IRF5 expression in CD4+ T cells and intestinal mucosa of CD patients. Conclusion Our study reveals a novel mechanism that IRF5 levels are correlated with disease activity in IBD and might function as a possible marker for the management of IBD via regulating Th1 and Th17 immune responses and cytokine production.


2019 ◽  
Vol 13 (Supplement_1) ◽  
pp. S436-S437
Author(s):  
L Godskesen ◽  
M Lindholm ◽  
J Høg Mortensen ◽  
A Krag ◽  
T Manon-Jensen ◽  
...  

2016 ◽  
Vol 31 (6) ◽  
pp. 1120-1125 ◽  
Author(s):  
Mustafa Kaplan ◽  
Mahmut Yuksel ◽  
Ihsan Ates ◽  
Zeki Mesut Yalın Kilic ◽  
Hasan Kilic ◽  
...  

2019 ◽  
Vol 17 (1) ◽  
pp. 203-204
Author(s):  
Ashwin N. Ananthakrishnan ◽  
Christopher Martin ◽  
Sunanda Kane ◽  
Robert S. Sandler ◽  
Millie D. Long

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2253
Author(s):  
Miguel Gonzalez Acera ◽  
Marvin Bubeck ◽  
Fabrizio Mascia ◽  
Leonard Diemand ◽  
Gregor Sturm ◽  
...  

Inflammatory bowel diseases (IBD) are characterized by chronic dysregulation of immune homeostasis, epithelial demise, immune cell activation, and microbial translocation. Each of these processes leads to proinflammatory changes via the release of cytokines, damage-associated molecular patterns (DAMPs), and pathogen-associated molecular patterns (PAMPs), respectively. The impact of these noxious agents on the survival and function of the enteric nervous system (ENS) is poorly understood. Here, we show that in contrast to an expected decrease, experimental as well as clinical colitis causes an increase in the transcript levels of enteric neuronal and glial genes. Immunostaining revealed an elevated neuronal innervation of the inflamed regions of the gut mucosa. The increase was seen in models with overt damage to epithelial cells and models of T cell-induced colitis. Transcriptomic data from treatment naïve pediatric IBD patients also confirmed the increase in the neuroglial genes and were replicated on an independent adult IBD dataset. This induction in the neuroglial genes was transient as levels returned to normal upon the induction of remission in both mouse models as well as colitis patients. Our data highlight the dynamic and robust nature of the enteric nervous system in colitis and open novel questions on its regulation.


2021 ◽  
Vol 14 ◽  
pp. 175628482110531
Author(s):  
Henit Yanai ◽  
Hadar Amir Barak ◽  
Jacob E Ollech ◽  
Irit Avni Biron ◽  
Idan Goren ◽  
...  

Background and Aims: Skin eruptions are prevalent among patients with inflammatory bowel diseases (IBD), often associated with therapies and frequently leading to dermatological consults and treatment interruptions. We aimed to assess the impact of joint shared decision-making in a multidisciplinary (MDT) IBD-DERMA clinic. Methods: This retrospective cohort study assessed a consecutive group of patients with IBD who were referred for consultation in an MDT clinic at a tertiary referral center in Israel. Results: Over 1 year, 118 patients were evaluated in the MDT-IBD-DERMA clinic: 68 (57.6%) males; age – 35.2 ± 13.5 years, disease duration – 7.1 (interquartile range: 3.7–13.9) years; Crohn’s disease – 94/118 (79.6%). Skin eruption induced by an anti–tumor necrosis factor (TNF) were the most common diagnoses [46/118 (39%)], including psoriasiform dermatitis (PD) – 31/46 (67.4%) and inflammatory alopecia (IA) – 15/46 (32.6%). Of these, 18 patients (39.1%) continued the anti-TNF agent concomitantly with a topical or systemic anti-inflammatory agent to control the eruption. The remaining 28 patients (60.9%) discontinued the anti-TNF, of whom 16/28 (57.1%) switched to ustekinumab. These strategies effectively treated the majority [38/46 (82.6%)] of patients. Continuation of the anti-TNF was possible in a significantly higher proportion of patients with PD: 12/31 (38.7%) than only one in the IA group, p = 0.035. There was a higher switch to ustekinumab among the IA 7/15 (46.6%) compared with the PD 7/31 (22.6%) group, P = .09. Following IBD-DERMA advised intervention, IBD deteriorated in 9/4 6(19.5%) patients, 5/9 on ustekinumab (PD versus IA, P = NS). Conclusion: Shared decision-making in an integrated IBD-DERMA clinic allowed successful control of skin eruptions while preserving control of the underlying IBD in more than 80% of cases. Patients with IA profited from a switch to ustekinumab.


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