37 Sixty-one children presenting with intestinal symptoms were enrolled prospectively, with fecal S100A12 and calprotectin measured.

Thirty one of these children were shown to have IBD on subsequent tests. In these children, both fecal S100A12 (median: 55.2 mg/kg) and calprotectin (median: 1265 mg/kg) were elevated compared to those children without IBD (n = 30, S100A12 median: 1.1 mg/kg, P < 0.0001; calprotectin median: 30.5 mg/kg, P < 0.0001). Upon further analysis, using a cut-off of 10 mg/kg, S100A12 gave a sensitivity and specificity of 97%, respectively, for the detection of IBD. However, a 50 mg/kg cut-off for calprotectin yielded a sensitivity of 100% and specificity of 67%, lower than the specificities reported by other studies.50 Both fecal markers were superior compared to the sensitivities and specificities of any standard inflammatory test in this population.37 Several

studies have also demonstrated CT99021 in vivo a role for S100A12 in the adult setting. Foell et al.35 demonstrated correlations between serum S100A12 and disease activity, and showed that serum levels fell after intervention with infliximab. Subsequent studies have also shown elevated serum S100A12 in IBD, however, with only modest sensitivities and specificities in distinguishing IBD and non-IBD patients.21,51 Following earlier work examining serum levels of S100A12 in the context of IBD, Kaiser et al.49 illustrated that fecal S100A12 levels could distinguish IBD from IBS, MCE公司 with 86% sensitivity and 96% specificity, and to also differentiate IBD from normal

controls, with 86% sensitivity and 100% specificity. Their study also Temozolomide ic50 demonstrated that S100A12 was superior to calprotectin or other biomarkers in correlation, with an inflammatory score incorporating endoscopic and histological findings.49 The role of S100A12 as a marker of future relapse has not yet been considered in pediatric or adult settings. Prospective studies are required to elucidate this potential role. Lactoferrin is an iron-binding glycoprotein identified in the secretions overlying most mucosal surfaces that interact directly with external pathogens, including saliva, tears, vaginal secretions, feces, synovial fluid, and mammalian breast milk.52–54 Lactoferrin is a major component of the secondary granules of polymorphonuclear neutrophils and is shown to be a primary factor in the acute inflammatory response.54,55 In the intestinal lumen, fecal lactoferrin levels quickly increase with the influx of neutrophils during inflammation.12 Lactoferrin has antibacterial activity and is resistant to proteolysis in the feces;56 it is unaffected by multiple freeze/thaw cycles54 and might remain stable in stool for as long as 5 days, compared to 7 days for calprotectin.24,57 Following storage at room temperature for 48 h, fecal concentrations of lactoferrin were 90% of initial levels, contrasting with fecal concentrations of calprotectin being 82%.