Faecal calprotectin in the assessment of Crohn's disease activity

Background: Clinical and laboratory assessment of activity in Crohn's disease (CD) correlate poorly with endoscopic findings. Calprotectin is a calcium-binding protein abundant in neutrophil cytosol, and extremely stable in faeces. Faecal calprotectin (FC) is an excellent surrogate marker of neutrophil influx into the bowel lumen. Aim: To assess whether FC concentration from a spot stool sample reliably detects active inflammation in patients with CD. Design: Cross-sectional comparative study. Methods: Subjects had a previously confirmed diagnosis of CD and were suspected on clinical grounds to be in the midst of a relapse. Thirty-five entered the study; they underwent radiolabelled white cell scanning (WCS) and had a stool sample collected for calprotectin measurement on the same day. A Crohn's disease activity index (CDAI) was also calculated for each. The WCS scans were scored at six standard sites to give a mean total, ‘extent‘, ‘severity’ and ‘combined extent and severity’ scores. Results: FC was significantly and positively correlated with mean total (r = 0.73, p<0.001), ‘extent’ (r = 0.71, p<0.001), ‘severity’ (r = 0.64, p<0.001) and combined ‘extent and severity’ WCS scores (r = 0.71, p<0.001). A cut-off of faecal calprotectin >100 µg/g gave a sensitivity of 80%, specificity of 67%, positive predictive value of 87% and a negative predictive value of 64% in identifying those with and without any inflammation on WCS. There was, however, no significant correlation between CDAI and mean total WCS score (r = 0.21, p = 0.24), nor between CDAI and FC (r = 0.33, p = 0.06). Discussion: While the CDAI does not accurately reflect inflammatory activity in CD, a one-off FC reliably detects the presence or absence of intestinal inflammation in adult patients with CD, compared to WCS

Wilson's disease: acute and presymptomatic laboratory diagnosis and monitoring

Wilson's disease, the most common inherited disorder of copper metabolism, is a recessive genetic condition. The clinical presentation of Wilson's disease is very variable. It is characterised by low serum copper and caeruloplasmin concentrations coupled with the pathological accumulation of copper in the tissues. However, there are diagnostic difficulties and these are discussed. The current value of DNA diagnosis, both in gene tracking in families or as applied to de novo cases, is examined. Wilson's disease can be treated successfully but treatment must be life long. Patients are best treated by specialist centres with experience and expertise in the condition. Key Words: Wilson's disease • copper • diagnosi