The diagnosis of Crohn’s disease (CD) does not rely on a single gold standard but requires the integration of clinical data with endoscopic, histologic, radiological and biochemical investigat
The diagnosis of Crohn’s disease (CD) does not rely on a single gold standard but requires the integration of clinical data with endoscopic, histologic, radiological and biochemical investigations.1
Biomarkers have become essential to discriminate CD from ulcerative colitis (UC), to grade the severity of inflammation since symptoms based scores are subjective, to measure the response to pharmacological options, to predict the risk of relapse and to monitor for postoperative recurrence.2
While erythrocyte sedimentation rate should be abandoned because of its low specificity, being also affected by haematocrit and physiological states such as pregnancy and age, C-reactive protein and faecal calprotectin (FC) are now widely used.
CRP is produced by hepatocytes in response to proinflammatory cytokines, chiefly interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-alpha) and IL-1beta, and has a short half-life of about 19 hours, making it a more responsive indicator of acute inflammation. Meta-analyses have shown its role in the differential diagnosis between IBD and IBS and the correlation with endoscopic findings; however, specificity is low and about 25% of patients with active CD on endoscopy do not express levels of CRP above the normal threshold because of genetic variants.
FC is a neutrophil-derived protein excreted in the faeces and is a more reliable surrogate marker of inflammation with a significant correlation with endoscopy. FC predicts mucosal healing and response to anti-TNF therapy, and has a prognostic role for disease course, even in the postoperative setting.3 There are, however, potential barriers in implementing its use in clinical practice as compared with CRP: patients’ disinclination to collect stools, lack of specificity as opposed to other infectious or inflammatory processes of the gut, different accuracy according to disease type (CD vs UC) and location (colitis vs enteritis), need for standardisation due to variability among different assays and different cutoff thresholds depending upon the clinical scenario.