scholarly journals Erratum to: Timely Monitoring of Inflammation by Fecal Lactoferrin Rapidly Predicts Therapeutic Response in Inflammatory Bowel Disease

2021 ◽  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Therapeutic Response ◽  
Fecal Lactoferrin ◽  
Inflammatory Bowel

scholarly journals Evaluation of anti-TNF therapeutic response in patients with inflammatory bowel disease: Current and novel biomarkers

EBioMedicine ◽  
2021 ◽  
Vol 66 ◽  
pp. 103329
Author(s):  
Guanglin Cui ◽  
Qingbo Fan ◽  
Zhenfeng Li ◽  
Rasmus Goll ◽  
Jon Florholmen
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Therapeutic Response ◽  
Novel Biomarkers ◽  
Inflammatory Bowel

Su1184 - Evaluation of Fecal Lactoferrin and Calprotectin Levels in Healthy Pregnant Women as a Reference for Detecting Inflammatory Bowel Disease

2018 ◽  
Vol 154 (6) ◽  
pp. S-497 ◽  
Author(s):  
James M. Gray ◽  
Allison Durica ◽  
Kristin Knight ◽  
Megan Lord ◽  
Lauren Irby ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Pregnant Women ◽  
Bowel Disease ◽  
Fecal Lactoferrin ◽  
Inflammatory Bowel

Systematic review: predictive biomarkers of therapeutic response in inflammatory bowel disease-personalised medicine in its infancy

2018 ◽  
Vol 48 (11-12) ◽  
pp. 1213-1231 ◽  
Author(s):  
Toer W. Stevens ◽  
Mijntje Matheeuwsen ◽  
Maria H. Lönnkvist ◽  
Claire E. Parker ◽  
Manon E. Wildenberg ◽  
...  
Keyword(s):  
Systematic Review ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Therapeutic Response ◽  
Personalised Medicine ◽  
Predictive Biomarkers ◽  
Inflammatory Bowel

scholarly journals Biomarkers of Therapeutic Response in the IL-23 Pathway in Inflammatory Bowel Disease

2012 ◽  
Vol 3 (2) ◽  
pp. e10 ◽  
Author(s):  
Corinne Cayatte ◽  
Barbara Joyce-Shaikh ◽  
Felix Vega ◽  
Katia Boniface ◽  
Jeffrey Grein ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Therapeutic Response ◽  
Inflammatory Bowel

scholarly journals Fecal lactoferrin accurately reflects mucosal inflammation in inflammatory bowel disease

2019 ◽  
Vol 10 (5) ◽  
pp. 54-63 ◽  
Author(s):  
Marrieth G Rubio ◽  
Kofi Amo-Mensah ◽  
James M Gray ◽  
Vu Q Nguyen ◽  
Sam Nakat ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Mucosal Inflammation ◽  
Fecal Lactoferrin ◽  
Inflammatory Bowel

FECAL LACTOFERRIN MEASUREMENTS ARE USEFUL IN THE INTERVAL ASSESSMENT OF PATIENTS WITH ACTIVE AND INACTIVE INFLAMMATORY BOWEL DISEASE

2003 ◽  
Vol 98 ◽  
pp. S246
Author(s):  
Thomas R. Walker ◽  
William J. Sandborn ◽  
James Boone ◽  
Daniel Sisco ◽  
David Lyerly ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Fecal Lactoferrin ◽  
Inflammatory Bowel

scholarly journals Metabolomics facilitate the personalized management in inflammatory bowel disease

2021 ◽  
Vol 14 ◽  
pp. 175628482110644
Author(s):  
Rirong Chen ◽  
Jieqi Zheng ◽  
Li Li ◽  
Chao Li ◽  
Kang Chao ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Disease Activity ◽  
Bowel Disease ◽  
Therapeutic Response ◽  
Gastrointestinal Disorder ◽  
Response Prediction ◽  
Personalized Management ◽  
Inflammatory Bowel ◽  
Histological Activity ◽  
Qualitative And Quantitative Study

Inflammatory bowel disease (IBD) is a gastrointestinal disorder characterized by chronic relapsing inflammation and mucosal lesions. Reliable biomarkers for monitoring disease activity, predicting therapeutic response, and disease relapse are needed in the personalized management of IBD. Given the alterations in metabolomic profiles observed in patients with IBD, metabolomics, a new and developing technique for the qualitative and quantitative study of small metabolite molecules, offers another possibility for identifying candidate markers and promising predictive models. With increasing research on metabolomics, it is gradually considered that metabolomics will play a significant role in the management of IBD. In this review, we summarize the role of metabolomics in the assessment of disease activity, including endoscopic activity and histological activity, prediction of therapeutic response, prediction of relapse, and other aspects concerning disease management in IBD. Furthermore, we describe the limitations of metabolomics and highlight some solutions.

scholarly journals m6A Modification Mediates Mucosal Immune Microenvironment and Therapeutic Response in Inflammatory Bowel Disease

2021 ◽  
Vol 9 ◽  
Author(s):  
Yongyu Chen ◽  
Jing Lei ◽  
Song He
Keyword(s):  
Inflammatory Bowel Disease ◽  
B Cells ◽  
Bowel Disease ◽  
Therapeutic Response ◽  
Plasma Cells ◽  
Immune Microenvironment ◽  
Hub Genes ◽  
Immune Infiltration ◽  
M1 Macrophage ◽  
Inflammatory Bowel

Accumulating evidence links m6A modification with immune infiltration. However, the correlation and mechanism by which m6A modification promotes intestinal immune infiltration in inflammatory bowel disease (IBD) is unknown. Here, genomic information from IBD tissues was integrated to evaluate disease-related m6A modification, and the correlation between the m6A modification pattern and the immune microenvironment in the intestinal mucosa was explored. Next, we identified hub genes from the key modules of the m6Acluster and analyzed the correlation among the hub genes, immune infiltration, and therapy. We found that IGF2BP1 and IGF2BP2 expression was decreased in Crohn’s disease (CD) tissues and that IGF2BP2 was decreased in ulcerative colitis (UC) tissues compared with normal tissues (P < 0.05). m6Acluster2, containing higher expressions of IL15, IL16, and IL18, was enriched in M0 macrophage, M1 macrophage, native B cells, memory B cells, and m6Acluster1 with high expression of IL8 and was enriched in resting dendritic and plasma cells (P < 0.05). Furthermore, we reveal that expression of m6A phenotype-related hub genes (i.e., NUP37, SNRPG, H2AFZ) was increased with a high abundance of M1 macrophages, M0 macrophages, and naive B cells in IBD (P < 0.01). Immune checkpoint expression in the genecluster1 with higher expression of hub genes was increased. The anti-TNF therapeutic response of patients in genecluster1 was more significant, and the therapeutic effect of CD was better than that of UC. These findings indicate that m6A modification may affect immune infiltration and therapeutic response in IBD. Assessing the expression of m6A phenotype-related hub genes might guide the choice of IBD drugs and improve the prediction of therapeutic response to anti-TNF therapy.

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