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Start Over Author "Rieder, Florian" Journal gastroenterology (00165085)
98 results on '"Rieder, Florian"'

2. The Future of Precision Medicine to Predict Outcomes and Control Tissue Remodeling in Inflammatory Bowel Disease.

Author

Lamb, Christopher A., Saifuddin, Aamir, Powell, Nick, and Rieder, Florian

Abstract

Inflammatory bowel disease is characterized by significant interindividual heterogeneity. With a wider selection of pharmacologic and nonpharmacologic interventions available and in advanced developmental stages, a priority for the coming decade is to determine accurate methods of predicting treatment response and disease course. Precision medicine strategies will allow tailoring of preventative and therapeutic decisions to individual patient needs. In this review, we consider the future of precision medicine in inflammatory bowel disease. We discuss the critical need to extend from research focused on short-term symptomatic response to integrative multi-omic systems biology strategies to identify and validate biomarkers that underpin precision approaches. Crucially, the international community has collective responsibility to provide well-phenotyped and -curated longitudinal datasets for scientific discovery and validation. Research must also study broader aspects of the immune response, including components of the extracellular matrix, to better understand biological pathways initiating and perpetuating tissue fibrosis and longer-term disease complications. [ABSTRACT FROM AUTHOR]

Published
2022
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9. 1142 INTEGRIN INHIBITION REDUCES PROFIBROTIC RESPONSES IN CROHN'S DISEASE (CD) HUMAN INTESTINAL MYOFIBROBLASTS IN VITRO AND AMELIORATES EXPERIMENTAL INTESTINAL FIBROSIS IN VIVO - A POTENTIAL NOVEL APPROACH TO CD STRICTURE THERAPY.

Author

Mukherjee, Pranab K., Czarnecki, Doug, Chandra, Jyotsna, Hu, Shaomin, Nguyen, Quang Tam, Liu, Weiwei, Massey, William J., Wang, Yan, Wong, Jamie, Liu, Min, West, Gail A., Banerjee, Suhanti, Goren, Idan, and Rieder, Florian

Published
2024
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15. An International Consensus to Standardize Integration of Histopathology in Ulcerative Colitis Clinical Trials.

Author

Ma, Christopher, Sedano, Rocio, Almradi, Ahmed, Casteele, Niels Vande, Parker, Claire E., Guizzetti, Leonardo, Schaeffer, David F., Riddell, Robert H., Pai, Reetesh K., Battat, Robert, Sands, Bruce E., Rosty, Christophe, Dubinsky, Marla C., Rieder, Florian, Harpaz, Noam, Abreu, Maria T., Bryant, Robert V., Lauwers, Gregory Y., Kirsch, Richard, and Valasek, Mark A.

Abstract

Histopathology is an emerging treatment target in ulcerative colitis (UC) clinical trials. Our aim was to provide guidance on standardizing biopsy collection protocols, identifying optimal evaluative indices, and defining thresholds for histologic response and remission after treatment. An international, interdisciplinary expert panel of 19 gastroenterologists and gastrointestinal pathologists was assembled. A modified RAND/University of California, Los Angeles appropriateness methodology was used to address relevant issues. A total of 138 statements were derived from a systematic review of the literature and expert opinion. Each statement was anonymously rated as appropriate, uncertain, or inappropriate using a 9-point scale. Survey results were reviewed and discussed before a second round of voting. Histologic measurements collected using a uniform biopsy strategy are important for assessing disease activity and determining therapeutic efficacy in UC clinical trials. Multiple biopsy strategies were deemed acceptable, including segmental biopsies collected according to the endoscopic appearance. Biopsies should be scored for architectural change, lamina propria chronic inflammation, basal plasmacytosis, lamina propria and epithelial neutrophils, epithelial damage, and erosions/ulcerations. The Geboes score, Robarts Histopathology Index, and Nancy Index were considered appropriate for assessing histologic activity; use of the modified Riley score and Harpaz Index were uncertain. Histologic activity at baseline should be required for enrollment, recognizing this carries operational implications. Achievement of histologic improvement or remission was considered an appropriate and realistic therapeutic target. Current histologic indices require validation for pediatric populations. These recommendations provide a framework for standardized implementation of histopathology in UC trials. Additional work is required to address operational considerations and areas of uncertainty. [ABSTRACT FROM AUTHOR]

Published
2021
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21. Tu1246 CROHN'S DISEASE STRICTURE MATRISOME ANALYSIS REVEALS THE ANTI-FIBROTIC ACTIVITY OF MILK-FAT GLOBULE-EPIDERMAL GROWTH FACTOR 8 (MFGE8).

Author

Lin, Sinan, Wang, Jie, Mukherjee, Pranab, Mao, Ren, West, Gail A., Czarnecki, Doug, Zhao, Shuai, Nguyen, Quang Tam, Chandra, Jyotsna, Le, Thi Hong Nga, Dejanovic, Dina, Chen, Minhu, Holubar, Stefan D., Olman, Mitch, Southern, Brian D., Hu, Shaomin, Gordon, Ilyssa O., Atabai, Kamran, Fiocchi, Claudio, and Rieder, Florian

Published
2023
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23. Mo1726 INTESTINAL ULTRASOUND OF FIBROSTENOTIC CROHN'S DISEASE CORRELATES WITH HISTOLOGY OF SURGICALLY RESECTED STRICTURES.

Author

St-Pierre, Joelle, Rosentreter, Ryan E., Cooper, Jared, Danois, Karen, Szostakiwskyj, Jessie Hart, Novak, Kerri L., Panaccione, Remo, Kaplan, Gilaad, Devlin, Shane M., Seow, Cynthia H., Ingram, Richard J., Ma, Christopher, Wilson, Stephanie R., Medellin, Alexandra, Gui, Sean X., Koro, Konstantin, Rieder, Florian, and Lu, Cathy

Published
2023
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33. Gastroesophageal Reflux Disease–Associated Esophagitis Induces Endogenous Cytokine Production Leading to Motor Abnormalities.

Author

Rieder, Florian, Cheng, Ling, Harnett, Karen M., Chak, Amitabh, Cooper, Gregory S., Isenberg, Gerard, Ray, Monica, Katz, Jeffry A., Catanzaro, Andrew, O’Shea, Robert, Post, Anthony B., Wong, Richard, Sivak, Michael V., McCormick, Thomas, Phillips, Manijeh, West, Gail A., Willis, Joseph E., Biancani, Piero, and Fiocchi, Claudio

Subjects
GASTROESOPHAGEAL reflux, INTERLEUKIN-1, CYTOKINES, MUSCLE cells
Abstract

Background & Aims: Gastroesophageal reflux disease is a condition frequently associated with esophagitis and motor abnormalities. Recent evidence suggests that proinflammatory cytokines, such as interleukin (IL)-1β and IL-6, may be implicated because they reduce esophageal muscle contractility, but these results derive from in vitro or animal models of esophagitis. This study used human esophageal cells and tissues to identify the cellular source of cytokines in human esophagitis investigate whether cytokines can be induced by gastric refluxate, and examine whether esophageal tissue– or cell-derived mediators affect muscle contractility. Methods: Endoscopic mucosal biopsy specimens were obtained from patients with and without esophagitis, organ-cultured, and undernatants were assessed for cytokine content. The cytokine profile of esophageal epithelial, fibroblast, and muscle cells was analyzed, and esophageal mucosa and cell products were tested in an esophageal circular muscle contraction assay. Results: The mucosa of esophagitis patients produced significantly greater amounts of IL-1β and IL-6 compared with those of control patients. Cultured esophageal epithelial cells produced IL-6, as did fibroblasts and muscle cells. Epithelial cells exposed to buffered, but not denatured, gastric juice produced IL-6. Undernatants of mucosal biopsy cultures from esophagitis patients reduced esophageal muscle contraction, as did supernatants from esophageal epithelial cell cultures. Conclusions: The human esophagus produces cytokines capable of reducing contractility of esophageal muscle cells. Exposure to gastric juice is sufficient to stimulate esophageal epithelial cells to produce IL-6, a cytokine able to alter esophageal contractility. These results indicate that classic cytokines are important mediators of the motor disturbances associated with human esophageal inflammation. [Copyright &y& Elsevier]

Published
2007
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34. Development and Validation of a Novel Computed-Tomography Enterography Radiomic Approach for Characterization of Intestinal Fibrosis in Crohn's Disease.

Author

Li, Xuehua, Liang, Dong, Meng, Jixin, Zhou, Jie, Chen, Zhao, Huang, Siyun, Lu, Baolan, Qiu, Yun, Baker, Mark E., Ye, Ziyin, Cao, Qinghua, Wang, Mingyu, Yuan, Chenglang, Chen, Zhihui, Feng, Shengyu, Zhang, Yuxuan, Iacucci, Marietta, Ghosh, Subrata, Rieder, Florian, and Sun, Canhui

Abstract

No reliable method for evaluating intestinal fibrosis in Crohn's disease (CD) exists; therefore, we developed a computed-tomography enterography (CTE)–based radiomic model (RM) for characterizing intestinal fibrosis in CD. This retrospective multicenter study included 167 CD patients with 212 bowel lesions (training, 98 lesions; test, 114 lesions) who underwent preoperative CTE and bowel resection at 1 of the 3 tertiary referral centers from January 2014 through June 2020. Bowel fibrosis was histologically classified as none–mild or moderate–severe. In the training cohort, 1454 radiomic features were extracted from venous-phase CTE and a machine learning–based RM was developed based on the reproducible features using logistic regression. The RM was validated in an independent external test cohort recruited from 3 centers. The diagnostic performance of RM was compared with 2 radiologists' visual interpretation of CTE using receiver operating characteristic (ROC) curve analysis. In the training cohort, the area under the ROC curve (AUC) of RM for distinguishing moderate–severe from none–mild intestinal fibrosis was 0.888 (95% confidence interval [CI], 0.818–0.957). In the test cohort, the RM showed robust performance across 3 centers with an AUC of 0.816 (95% CI, 0.706–0.926), 0.724 (95% CI, 0.526–0.923), and 0.750 (95% CI, 0.560–0.940), respectively. Moreover, the RM was more accurate than visual interpretations by either radiologist (radiologist 1, AUC = 0.554; radiologist 2, AUC = 0.598; both, P <. 001) in the test cohort. Decision curve analysis showed that the RM provided a better net benefit to predicting intestinal fibrosis than the radiologists. A CTE-based RM allows for accurate characterization of intestinal fibrosis in CD. [Display omitted] [ABSTRACT FROM AUTHOR]

Published
2021
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50. Collagenous Colitis Is Associated With HLA Signature and Shares Genetic Risks With Other Immune-Mediated Diseases.

Author

Stahl, Eli, Roda, Giulia, Dobbyn, Amanda, Hu, Jianzhong, Zhang, Zhongyang, Westerlind, Helga, Bonfiglio, Ferdinando, Raj, Towfique, Torres, Joana, Chen, Anli, Petras, Robert, Pardi, Darrell S., Iuga, Alina C., Levi, Gabriel S., Cao, Wenqing, Jain, Prantesh, Rieder, Florian, Gordon, Ilyssa O., Cho, Judy H., and D'Amato, Mauro

Abstract

Collagenous colitis (CC) is an inflammatory bowel disorder with unknown etiopathogenesis involving HLA-related immune-mediated responses and environmental and genetic risk factors. We carried out an array-based genetic association study in a cohort of patients with CC and investigated the common genetic basis between CC and Crohn's disease (CD), ulcerative colitis (UC), and celiac disease. DNA from 804 CC formalin-fixed, paraffin-embedded tissue samples was genotyped with Illumina Immunochip. Matching genotype data on control samples and CD, UC, and celiac disease cases were provided by the respective consortia. A discovery association study followed by meta-analysis with an independent cohort, polygenic risk score calculation, and cross-phenotype analyses were performed. Enrichment of regulatory expression quantitative trait loci among the CC variants was assessed in hemopoietic and intestinal cells. Three HLA alleles (HLA-B∗08:01, HLA-DRB1∗03:01, and HLA-DQB1∗02:01), related to the ancestral haplotype 8.1, were significantly associated with increased CC risk. We also identified an independent protective effect of HLA-DRB1∗04:01 on CC risk. Polygenic risk score quantifying the risk across multiple susceptibility loci was strongly associated with CC risk. An enrichment of expression quantitative trait loci was detected among the CC-susceptibility variants in various cell types. The cross-phenotype analysis identified a complex pattern of polygenic pleiotropy between CC and other immune-mediated diseases. In this largest genetic study of CC to date with histologically confirmed diagnosis, we strongly implicated the HLA locus and proposed potential non-HLA mechanisms in disease pathogenesis. We also detected a shared genetic risk between CC, celiac disease, CD, and UC, which supports clinical observations of comorbidity. [ABSTRACT FROM AUTHOR]

Published
2020
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