OBJECTIVE: To assess the potential of measuring the calcium-binding protein calprotectin in faeces as a method of screening for alimentary inflammation and neoplasia. SETTING: Hospital day services unit for endoscopy and faecal analysis in the clinical biochemistry department. PARTICIPANTS: Consented patients attending for routine endoscopy were requested to provide faeces. Seventeen of the initial 30 patients provided faeces before and 1 week after endoscopy. After this, 116 patients for planned endoscopy provided faeces before endoscopy. The group comprised 43 patients with upper-gastrointestinal lesions, seven patients with inflammatory bowel disease, seven patients with irritable bowel syndrome, 31 patients with colonic disorders, and 28 normal people. A final 18 patients with known inflammatory bowel disease (seven patients), gastric carcinoma (one patient), colorectal cancer (eight patients) and colorectal adenoma (two patients) had faeces analysed. METHOD: Faeces were analysed by the Nycotest PhiCal enzyme-linked immunosorbent assay (ELISA) (Nycomed, Oslo, Norway), and the final 18 patients were analysed by the newer version marketed as Calprest. RESULTS: No definite differences between pre- and post-endoscopy calprotectin were found, but it was considered preferable in the subsequent patients to analyse pre-endoscopy faeces. Upper-gastrointestinal disorders showed little difference in calprotectin levels, Barrett's oesophagus (median 6.8 mg/l), gastric ulcer (median 6.5 mg/l) or gastritis/duodenitis (median 5.2 mg/l), but these levels were all higher than the median calprotectin level of normal subjects (4.5 mg/l). The oesophageal and gastric carcinoma median was elevated significantly at 30 mg/l. Inflammatory bowel disease was also associated with marked elevation (Crohn's disease, 31.2 mg/l; ulcerative colitis, 116.2 mg/l). Colorectal polyps (median 3.7 mg/l) and adenoma (median 3.8 mg/l) showed no elevated levels in contrast to colorectal carcinoma (median 53.4 mg/l). The elevated calprotectin in inflammatory bowel disease and colorectal carcinoma combined gave a sensitivity of 81.8% and a specificity of 73.2%. CONCLUSIONS: Calprotectin levels are elevated in inflammation and cancer but are not helpful in differentiating between these disorders. In our series, calprotectin was not elevated in colonic polyps or adenomata. Calprotectin could be helpful as a screening method in a general gastroenterology population for inflammatory bowel disease and those with carcinoma, as well as assessing and monitoring disease activity in inflammatory bowel disease.
OBJECTIVE: To assess the potential of measuring the calcium-binding protein calprotectin in faeces as a method of screening for alimentary inflammation and neoplasia. SETTING: Hospital day services unit for endoscopy and faecal analysis in the clinical biochemistry department. PARTICIPANTS: Consented patients attending for routine endoscopy were requested to provide faeces. Seventeen of the initial 30 patients provided faeces before and 1 week after endoscopy. After this, 116 patients for planned endoscopy provided faeces before endoscopy. The group comprised 43 patients with upper-gastrointestinal lesions, seven patients with inflammatory bowel disease, seven patients with irritable bowel syndrome, 31 patients with colonic disorders, and 28 normal people. A final 18 patients with known inflammatory bowel disease (seven patients), gastric carcinoma (one patient), colorectal cancer (eight patients) and colorectal adenoma (two patients) had faeces analysed. METHOD: Faeces were analysed by the Nycotest PhiCal enzyme-linked immunosorbent assay (ELISA) (Nycomed, Oslo, Norway), and the final 18 patients were analysed by the newer version marketed as Calprest. RESULTS: No definite differences between pre- and post-endoscopy calprotectin were found, but it was considered preferable in the subsequent patients to analyse pre-endoscopy faeces. Upper-gastrointestinal disorders showed little difference in calprotectin levels, Barrett's oesophagus (median 6.8 mg/l), gastric ulcer (median 6.5 mg/l) or gastritis/duodenitis (median 5.2 mg/l), but these levels were all higher than the median calprotectin level of normal subjects (4.5 mg/l). The oesophageal and gastric carcinoma median was elevated significantly at 30 mg/l. Inflammatory bowel disease was also associated with marked elevation (Crohn's disease, 31.2 mg/l; ulcerative colitis, 116.2 mg/l). Colorectal polyps (median 3.7 mg/l) and adenoma (median 3.8 mg/l) showed no elevated levels in contrast to colorectal carcinoma (median 53.4 mg/l). The elevated calprotectin in inflammatory bowel disease and colorectal carcinoma combined gave a sensitivity of 81.8% and a specificity of 73.2%. CONCLUSIONS: Calprotectin levels are elevated in inflammation and cancer but are not helpful in differentiating between these disorders. In our series, calprotectin was not elevated in colonic polyps or adenomata. Calprotectin could be helpful as a screening method in a general gastroenterology population for inflammatory bowel disease and those with carcinoma, as well as assessing and monitoring disease activity in inflammatory bowel disease.
Authors: Michael Wagner; Christer G B Peterson; Peter Ridefelt; Per Sangfelt; Marie Carlson Journal: World J Gastroenterol Date: 2008-09-28 Impact factor: 5.742
Authors: Andrea Vieira; Chia Bin Fang; Ernani Geraldo Rolim; Wilmar Artur Klug; Flávio Steinwurz; Lucio Giovanni Battista Rossini; Paulo Azevedo Candelária Journal: BMC Res Notes Date: 2009-10-29