scholarly journals Reduced Transferrin Levels in Active Inflammatory Bowel Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Malgorzata Matusiewicz ◽  
Katarzyna Neubauer ◽  
Paulina Lewandowska ◽  
Andrzej Gamian ◽  
Malgorzata Krzystek-Korpacka

Inflammatory bowel disease (IBD) is an inflammatory disease of unclear etiopathogenesis and challenging diagnosis, frequently complicated by anemia and malnutrition. C-reactive protein (CRP) remains the only biochemical marker of clinical relevance. The aim of this study was to test hypothesis that transferrin, coinfluenced by inflammation, malnutrition, anemia, and oxidative stress, may better reflect global IBD patient’s condition than any other more specific index. Transferrin and other indices of inflammation, anemia, malnutrition, and oxidative stress were measured in 137 IBD patients (Crohn’s disease (CD): n=63 and ulcerative colitis (UC): n=74) and 97 controls. Transferrin is reduced in active CD and UC and negatively correlates with the disease activity scores (CD: ρ=-0.49; UC: ρ=-0.52). In UC, transferrin correlates negatively with CRP, erythrocyte sedimentation rate (ESR), leukocytes, platelets, interleukin-6, interleukin-10, and TNF-α and positively with albumins, cholesterol, hemoglobin, hematocrit, erythrocytes, iron, and paraoxonase-1. In CD, transferrin correlates negatively with CRP, leukocytes, platelets, interleukin-1, and interleukin-6 and positively with albumins, iron, catalase, glutathione peroxidase-1, superoxide dismutase-1, and paraoxonase-1. The associations with inflammation and anemia/malnutrition were more pronounced in UC and with oxidative stress in CD. As UC activity marker, transferrin outperforms ESR and hemoglobin, indices used in calculating the disease clinical severity score.

2011 ◽  
Vol 57 (2) ◽  
pp. 458-464 ◽  
Author(s):  
Tulay Akman ◽  
Mesut Akarsu ◽  
Hale Akpinar ◽  
Halil Resmi ◽  
Ebru Sezer

1992 ◽  
Vol 37 (6) ◽  
pp. 818-826 ◽  
Author(s):  
Chris Stevens ◽  
Gerd Walz ◽  
Chander Singaram ◽  
Mark L. Lipman ◽  
Bernd Zanker ◽  
...  

2011 ◽  
Vol 57 (3) ◽  
pp. 824-824
Author(s):  
Tulay Akman ◽  
Mesut Akarsu ◽  
Hale Akpinar ◽  
Halil Resmi ◽  
Ebru Taylan

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A38-A38
Author(s):  
Shilpa Ravindran ◽  
Heba Sidahmed ◽  
Harshitha Manjunath ◽  
Rebecca Mathew ◽  
Tanwir Habib ◽  
...  

BackgroundPatients with inflammatory bowel disease (IBD) have increased risk of developing colorectal cancer (CRC), depending on the duration and severity of the disease. The evolutionary process in IBD is driven by chronic inflammation leading to epithelial-to-mesenchymal transition (EMT) events in colonic fibrotic areas. EMT plays a determinant role in tumor formation and progression, through the acquisition of ‘stemness’ properties and the generation of neoplastic cells. The aim of this study is to monitor EMT/cancer initiating tracts in IBD in association with the deep characterization of inflammation in order to assess the mechanisms of IBD severity and progression towards malignancy.Methods10 pediatric and 20 adult IBD patients, admitted at Sidra Medicine (SM) and Hamad Medical Corporation (HMC) respectively, have been enrolled in this study, from whom gut tissue biopsies (from both left and right side) were collected. Retrospectively collected tissues (N=10) from patients with malignancy and history of IBD were included in the study. DNA and RNA were extracted from fresh small size (2–4 mm in diameter) gut tissues using the BioMasher II (Kimble) and All Prep DNA/RNA kits (Qiagen). MicroRNA (miRNA; N=700) and gene expression (N=800) profiling have been performed (cCounter platform; Nanostring) as well as the methylation profiling microarray (Infinium Methylation Epic Bead Chip kit, Illumina) to interrogate up to 850,000 methylation sites across the genome.ResultsDifferential miRNA profile (N=27 miRNA; p<0.05) was found by the comparison of tissues from pediatric and adult patients. These miRNAs regulate: i. oxidative stress damage (e.g., miR 99b), ii. hypoxia induced autophagy; iii. genes associated with the susceptibility to IBD (ATG16L1, NOD2, IRGM), iv. immune responses, such as TH17 T cell subset (miR 29). N=6 miRNAs (miR135b, 10a196b, 125b, let7c, 375) linked with the regulation of Wnt/b-catenin, EM-transaction, autophagy, oxidative stress and play role also in cell proliferation and mobilization and colorectal cancer development were differentially expressed (p<0.05) in tissues from left and right sides of gut. Gene expression signature, including genes associated with inflammation, stemness and fibrosis, has also been performed for the IBD tissues mentioned above. Methylation sites at single nucleotide resolution have been analyzed.ConclusionsAlthough the results warrant further investigation, differential genomic profiling suggestive of altered pathways involved in oxidative stress, EMT, and of the possible stemness signature was found. The integration of data from multiple platforms will provide insights of the overall molecular determinants in IBD patients along with the evolution of the disease.Ethics ApprovalThis study was approved by Sidra Medicine and Hamad Medical Corporation Ethics Boards; approval number 180402817 and MRC-02-18-096, respectively.


2017 ◽  
Vol 2017 ◽  
pp. 1-18 ◽  
Author(s):  
Tian Tian ◽  
Ziling Wang ◽  
Jinhua Zhang

Inflammatory bowel disease (IBD) is a chronic gastrointestinal disease whose incidence has risen worldwide in recent years. Accumulating evidence shows that oxidative stress plays an essential role in the pathogenesis and progression of IBD. This review highlights the generation of reactive oxygen species (ROS) and antioxidant defense mechanisms in the gastrointestinal (GI) tract, the involvement of oxidative stress signaling in the initiation and progression of IBD and its relationships with genetic susceptibility and the mucosal immune response. In addition, potential therapeutic strategies for IBD that target oxidative stress signaling are reviewed and discussed. Though substantial progress has been made in understanding the role of oxidative stress in IBD in humans and experimental animals, the underlying mechanisms are still not well defined. Thus, further studies are needed to validate how oxidative stress signaling is involved in and contributes to the development of IBD.


1994 ◽  
Vol 39 (9) ◽  
pp. 1893-1899 ◽  
Author(s):  
Jeffrey S. Hyams ◽  
John E. Fitzgerald ◽  
Nancy Wyzga ◽  
William R. Treem ◽  
Christopher J. Justinich ◽  
...  

2014 ◽  
Vol 41 (3) ◽  
pp. 1299-1310 ◽  
Author(s):  
Hongchao Lv ◽  
Yongshuai Jiang ◽  
Jin Li ◽  
Mingming Zhang ◽  
Zhenwei Shang ◽  
...  

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