title: [Role of biological markers in inflammatory bowel disease].
abstract: The role played by the distinct biological markers in chronic inflammatory bowel disease (IBD) remains insufficiently characterized. C-reactive protein (CRP) has a short half-life and consequently it is elevated early after the onset of the inflammatory process and rapidly decreases after its resolution, making it an attractive marker of disease activity. Moreover, this test is inexpensive and easy to perform and is unaffected by medication. While Crohn's disease is associated with a marked CRP response, there is little or no elevation in the synthesis of this protein in ulcerative colitis. Erythrocyte sedimentation rate provides some advantages such as its ease of determination, availability, and reduced cost. Nevertheless, it also has several disadvantages, notably the fact that its concentration depends on age, the presence of anemia, smoking, and the use of certain drugs. Moreover, its utility is limited by its long half life and consequent prolonged latency period after changes in chronic IBD activity. In theory, fecal markers have the advantages of showing greater specificity in the diagnosis of chronic IBD. Several gastrointestinal diseases, including chronic IBD, show greater leukocyte elimination in feces and a close correlation has been described between fecal calprotectin concentration and leukocyte excretion quantified by 111indium. Advantages of this fecal marker are that it can be detected through a simple and inexpensive technique and also shows excellent stability in feces for prolonged periods. Like calprotectin, fecal lactoferrin is also quantified by a simple and inexpensive ELISA method, although there is considerably less experience with this latter marker.
authors: Servicio de Aparato Digestivo, Hospital Universitario de La Princesa, Madrid, España. gisbert@meditex.es
authors: Javier P
authors: JP
authors: Gisbert
authors: Yago
authors: Y
authors: González-Lama
authors: José
authors: J
authors: Maté
mesh_terms: D000068879:Adalimumab; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D015415:Biomarkers; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000032:analysis; D002986:Clinical Trials as Topic; D003093:Colitis, Ulcerative / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy; D003424:Crohn Disease / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy; D003937:Diagnosis, Differential; D005243:Feces / Q000737:chemistry; D005765:Gastrointestinal Agents / Q000627:therapeutic use; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000097:blood / Q000175:diagnosis* / Q000188:drug therapy; D000069285:Infliximab; D007781:Lactoferrin / Q000032:analysis; D039841:Leukocyte L1 Antigen Complex / Q000032:analysis; D011237:Predictive Value of Tests; D012307:Risk Factors; D012680:Sensitivity and Specificity; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D015415:Biomarkers; D005765:Gastrointestinal Agents; D039841:Leukocyte L1 Antigen Complex; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000069285:Infliximab; D007781:Lactoferrin; D000068879:Adalimumab