title: Increased Cell Adhesion Molecules, PECAM-1, ICAM-3, or VCAM-1, Predict Increased Risk for Flare in Patients With Quiescent Inflammatory Bowel Disease.
abstract: OBJECTIVE
  Predicting the risk of flare-ups for patients with inflammatory bowel disease (IBD) is difficult. Alterations in gut endothelial regulation of mucosal immune homeostasis might be early events leading to flares in IBD. Cell adhesion molecules (CAMs), in particular, are important in maintaining endothelial integrity and regulating the migration of leukocytes into the gut.
  
  
  METHODS
  We evaluated the mRNA expression of various tight junction proteins, with an emphasis on CAMs, in 40 patients with IBD in clinical remission. Patients were retrospectively assessed at 6, 12, and 24 months after baseline colonoscopy, and at the end of all available follow-up (maximum 65 mo), for flare events to determine whether baseline mRNA expression was associated with subsequent flares.
  
  
  RESULTS
  At all follow-up points, the baseline expression of platelet endothelial cell adhesion molecule-1 (PECAM-1), ICAM-3, and VCAM-1 was significantly higher in patients who flared than in those who did not (2.4-fold elevation, P=0.012 for PECAM-1; 1.9-fold increased, P=0.03 for ICAM-3; and 1.4-fold increased, P=0.02 for VCAM-1). PECAM-1 and ICAM-3 expression was significantly increased in patients who flared as early as 6 months after baseline colonoscopy. In contrast, there were no significant differences between patients with and without flares in baseline expression of other CAMs (ESAM, ICAM-1, ICAM-2, E-selectin, P-selectin, and MadCAM1).
  
  
  CONCLUSIONS
  Increased expression of PECAM-1, ICAM-3, and VCAM-1 in colonic biopsies from patients with IBD in clinical remission is associated with subsequent flares. This suggests that increases in the expression of these proteins may be early events that lead to flares in patients with IBD.
authors.affiliation: *Divisions of Gastroenterology and Hepatology, Dallas VA Medical Center, VA North Texas Healthcare System †The University of Texas Southwestern Medical Center §Baylor Research Institute, Baylor University Medical Center, Dallas, TX ‡Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA.
authors.forename: Phillip
authors.initials: P
authors.lastname: Gu
authors.forename: Arianne
authors.initials: A
authors.lastname: Theiss
authors.forename: Jie
authors.initials: J
authors.lastname: Han
authors.forename: Linda A
authors.initials: LA
authors.lastname: Feagins
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001706:Biopsy; D003113:Colonoscopy; D005260:Female; D005500:Follow-Up Studies; D005786:Gene Expression Regulation; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000235:genetics / Q000503:physiopathology*; D000074001:Intercellular Adhesion Molecule-3 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000235:genetics*; D012333:RNA, Messenger / Q000378:metabolism; D012189:Retrospective Studies; D013997:Time Factors; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics*
chemical_list: D000074001:Intercellular Adhesion Molecule-3; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D012333:RNA, Messenger; D019010:Vascular Cell Adhesion Molecule-1