Laboratory markers in IBD: useful, magic, or unnecessary toys?

• Published in: Gut 2006-03, Vol.55 (3), p.426-431
• Main Authors: Vermeire, S, Van Assche, G, Rutgeerts, P
• Format: Article
• Language: English
• Subjects: Acute-Phase Reaction; Biomarkers - blood; Blood Sedimentation; C reactive protein; C-Reactive Protein - metabolism; calprotectin; Clinical trials; Crohn’s disease; Diagnosis, Differential; erythrocyte sedimentation rate; Feces - chemistry; Gangrene; Humans; Inflammation; Inflammatory bowel disease; Inflammatory Bowel Diseases - diagnosis; Laboratories; laboratory markers; Laboratory Markers in IBD; Leukocyte L1 Antigen Complex - analysis; Mortality; Proteins; Response rates; Tumor necrosis factor-TNF; ulcerative colitis
• ISSN: 0017-5749; 1468-3288
• DOI: 10.1136/gut.2005.069476

Laboratory markers have been investigated in inflammatory bowel disease (IBD) for diagnostic and differential diagnostic purposes, for assessment of disease activity and risk of complications, for prediction of relapse, and for monitoring the effect of therapy. The introduction of biological therapies in IBD has renewed interest in inflammatory markers (especially C reactive protein (CRP)), given their potential to select responders to these treatments. Of all the laboratory markers, CRP is the most studied and has been shown to have the best overall performance. CRP is an objective marker of inflammation and correlates well with disease activity in Crohn's disease (CD). Increased CRP levels are associated with better response rates and normal CRP levels predict high placebo response rates in clinical trials with biologicals. However, despite the advantages of CRP over other markers, it is still far from ideal. Furthermore, CRP correlates less well with disease activity in patients with ulcerative colitis (UC) as compared with CD. Other laboratory markers, including erythrocyte sedimentation rate (ESR), leucocyte and platelet count, albumin, and 1 acid glycoprotein (orosomucoid), have been studied either less extensively in IBD or have proven to be less useful than CRP. Faecal markers seem promising and may be more specific in detecting gut inflammation in patients with established IBD. Promising results have been reported with the use of faecal calprotectin in CD as well as in UC. Recent data however suggest that the performance of the faecal calprotectin test is superior for UC than for CD. Taken together, laboratory markers are useful and should be part of the global management of our IBD patients. They are however not magic and until more data become available, the use of CRP and other laboratory markers should be seen as an additive tool to clinical observation and physical examination rather than a replacement.