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  • Title: Metabolic and inflammatory faecal markers in collagenous colitis.
    Author: Wildt S, Nordgaard-Lassen I, Bendtsen F, Rumessen JJ.
    Journal: Eur J Gastroenterol Hepatol; 2007 Jul; 19(7):567-74. PubMed ID: 17556903.
    Abstract:
    OBJECTIVES: To evaluate the excretion of the inflammatory and metabolic faecal markers calprotectin, lactoferrin, and short-chain fatty acids in symptomatic and quiescent collagenous colitis. METHODS: Faecal samples from 21 patients with active collagenous colitis, 12 patients retested in remission, and 13 controls were analysed. Calprotectin was determined using an enzyme-linked immunosorbent assay. Lactoferrin was estimated by a latex agglutination test. Short-chain fatty acids were determined by steam distillation followed by gas-liquid chromatography. RESULTS: Calprotectin was increased in patients with active collagenous colitis [80 microg/g (6.25-1899)] (median and range) compared with patients with quiescent collagenous colitis [26 microg/g (6.25-340)], P=0.025 and controls [6.25 microg/g (6.25-99)], P=0.002. Eight patients (38%) with active collagenous colitis had normal levels of calprotectin. Lactoferrin was detected in one patient only. Concentrations of total short-chain fatty acids did not differ in patients with active collagenous colitis compared with quiescent collagenous colitis or controls (P=0.75), whereas concentrations of the branched-chain fatty acids were decreased in patients with active collagenous colitis versus controls (P<0.005). In-vitro incubations demonstrated increased ratios of acetate in patients with active and quiescent collagenous colitis compared with controls (P<0.05), with a corresponding decrease in branched-chain fatty acids ratios (P<0.05). CONCLUSION: Faecal calprotectin was increased in collagenous colitis; however, increased excretion was not a universal finding limiting the use of calprotectin as an inflammatory marker in collagenous colitis. Faecal lactoferrin was almost undetectable. Luminal fermentative conditions are altered in collagenous colitis. Fermentative alterations could be secondary to changes in substrate availability and intestinal transit time.
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