Median Calprotectin Levels Research Articles

Consecutive Monitoring of Fecal Calprotectin and Lactoferrin for the Early Diagnosis and Prediction of Pouchitis after Restorative Proctocolectomy for Ulcerative Colitis.

This prospective study was conducted to evaluate the significance of consecutive monitoring of fecal calprotectin and lactoferrin for the early diagnosis and prediction of pouchitis after restorative proctocolectomy for ulcerative colitis (UC). Sixty patients who had ileostomy closure following total proctocolectomy and ileal pouch-anal anastomosis for UC were included. Stool samples were collected for the measurement of calprotectin and lactoferrin every 2 months up to 12 months after the ileostomy closure. When patients had symptoms suggestive of pouchitis, endoscopic examination was immediately undertaken. All asymptomatic patients underwent endoscopy at 12 months. Pouchitis was defined as a pouchitis disease activity index score of ≥7. During the 12 months, 10 patients (17%) developed pouchitis. In patients with pouchitis, fecal calprotectin and lactoferrin levels were elevated already 2 months before the diagnosis of pouchitis. In contrast, these fecal biomarkers remained at low levels, and they did not change significantly in patients without pouchitis. A cutoff value of 56 μg/g for calprotectin had a sensitivity of 100% and a specificity of 84% to predict pouchitis, whereas a cutoff value of 50 μg/g for lactoferrin had a sensitivity of 90% and a specificity of 86%. At the time of endoscopy, the median calprotectin and lactoferrin levels were significantly higher in patients with pouchitis than those without pouchitis. Elevated fecal calprotectin and lactoferrin levels appeared to be significant predictors of pouchitis after restorative proctocolectomy for UC. Consecutive monitoring of these fecal biomarkers is useful for the early diagnosis of pouchitis.

High faecal calprotectin levels in intestinal tuberculosis are associated with granulomas in intestinal biopsies

Background: The diagnosis of intestinal tuberculosis (ITB) is sometimes difficult to establish and requires endoscopic investigation with biopsies for histopathological examination. This study aimed to evaluate calprotectin as a marker of inflammation in ITB. Methods: Patients with ITB were prospectively recruited in Southern India from October 2009 until July 2012. Demographic, clinical, endoscopic and histological features were examined along with faecal calprotectin (FC), serum calprotectin (SC) and C-reactive protein (CRP). Results: Thirty patients (median age 34.5 years, 19 men) were included. Clinical features were abdominal pain (97%), weight loss (83%), cachexia (75%), fatigue (63%), watery diarrhoea (62%), nausea (55%) and fever (53%). Endoscopy showed transverse ulcers (61%), nodularity of mucosa (55%), aphthous ulcers (39%), strictures (10%) and fissures (10%). The terminal ileum and right colon harboured 81% of the lesions. Histology revealed granulomas in biopsies from 10 of the patients. FC and CRP levels showed a strong positive correlation (rs = 0.70, p < 0.01). FC, SC and CRP levels were higher in the granulomatous than the non-granulomatous patients, respectively (median FC 988 μg/g, interquartile range (IQR) 940 vs 87 μg/g, IQR 704, p < 0.01; median SC 8.2 μg/ml, IQR 7.3 vs 3.8 μg/ml, IQR 8.9, p = 0.23; median CRP 38.8 mg/L, IQR 42.9 vs 2.3 mg/L, IQR 13.5, p < 0.01). Higher median calprotectin and CRP levels were detected in patients with extensive than localized disease, but the differences did not reach statistical significance. Conclusion: ITB patients with granulomas on histology have high levels of faecal calprotectin and CRP.

Fecal calprotectin testing can identify ineffective colorectal cancer surveillance procedures in patients with longstanding colitis.

Active colitis impairs neoplasia detection during colonoscopic surveillance for colorectal cancer in patients with inflammatory bowel disease. We investigated whether fecal calprotectin testing before surveillance colonoscopy might identify ineffective surveillance procedures. All consecutive patients with Crohn's disease or ulcerative colitis scheduled for surveillance colonoscopy were asked to collect a stool sample before the start of bowel cleansing. Ineffective surveillance was defined as at least 1 colonic segment with moderate or severe inflammation. Calprotectin was analyzed using an enzyme-linked immunosorbent assay (Ridascreen; R-Biopharm). Receiver operator characteristics statistics were used to determine the optimal cutoff for calprotectin. A total of 176 surveillance colonoscopies were performed in 164 patients, of which 83 had Crohn's disease and 81 had ulcerative colitis or inflammatory bowel disease-unclassified. Complete endoscopic remission or mild inflammation categorized as effective surveillance was observed in 151 colonoscopies (86%), whereas moderate or severe inflammation categorized as ineffective surveillance was observed in 25 colonoscopies (14%). Median calprotectin levels for the effective and ineffective surveillance group were 84 mg/kg (range, 20-4609) and 1605 mg/kg (range, 66-26,336), respectively (P < 0.01). A cutoff of 539 mg/kg identified patients with ineffective surveillance with 84% sensitivity, 89% specificity, 55% positive predictive value, 97% negative predictive value, and an area under the curve of 0.89. Low fecal calprotectin accurately identifies inflammatory bowel disease patients without colonic inflammation in whom colorectal cancer surveillance is most effective.

Diagnostic yield of endoscopy in patients with abdominal complaints: incremental value of faecal calprotectin on guidelines of appropriateness

BackgroundEuropean Panel on the Appropriateness of Gastrointestinal Endoscopy (EPAGE) criteria have been developed to increase diagnostic yield, but their predictive value is limited. We investigated the incremental diagnostic value of faecal calprotectin to EPAGE criteria.MethodsIn a post-hoc analysis of a prospective study, EPAGE criteria were applied to 298 of 575 (51.8%) patients who had undergone esophagogastroduodenoscopy (EGD), colonoscopy or both for abdominal complaints at the Division of Gastroenterology & Hepatology at the University Hospital Basel in Switzerland. Faecal calprotectin was measured in stool samples collected within 24 hours before the investigation using an enzyme-linked immunosorbent assay. Final endoscopic diagnoses were blinded to calprotectin values.ResultsOf 149 EGDs and 224 colonoscopies, 17.6% and 14.7% respectively were judged inappropriate by EPAGE criteria. Appropriate or uncertain indications revealed more endoscopic findings in both EGD (46.3% vs. 23.1%, P = 0.049) and colonoscopy (23.6% vs. 6.1%, P = 0.041) than inappropriate indications. Median calprotectin levels were higher (81.5 μg/g, interquartile range 26-175, vs. 10 μg/g, IQR 10–22, P < 0.001) and testing was more often positive (>50 μg/g) in patients with endoscopic findings, both in EGD (58.2% vs. 33.0%, P = 0.005) and in colonoscopy (57.3% vs. 7.4%, P < 0.001). The use of faecal calprotectin in addition to EPAGE criteria improved the risk reclassification of patients by endoscopic findings. The calculated net reclassification index was 37.8% (P = 0.002) for EGD and 110.9% (P <0.001) for colonoscopy, thus improving diagnostic yield to 56.8% and 70.2%, respectively.ConclusionsThe use of faecal calprotectin in addition to EPAGE criteria improved diagnostic yield in patients with abdominal complaints.

Novel Serum and Urine Markers for Pediatric Appendicitis

The objective was to describe the association between two novel biomarkers, calprotectin and leucine-rich alpha glycoprotein-1 (LRG), and appendicitis in children. This was a prospective, cross-sectional study of children 3 to 18 years old presenting to a pediatric emergency department (ED) with possible appendicitis. Blood and urine samples were assayed for calprotectin and LRG via enzyme-linked immunosorbent assay (ELISA). Final diagnosis was determined by histopathology or telephone follow-up. Biomarker levels were compared for subjects with and without appendicitis. Recursive partitioning was used to identify thresholds that predicted appendicitis. Of 176 subjects, mean (±SD) age was 11.6 (±4.0) years and 52% were male. Fifty-eight patients (34%) were diagnosed with appendicitis. Median plasma calprotectin, serum LRG, and urine LRG levels were higher in appendicitis versus nonappendicitis (p < 0.008). When stratified by perforation status, median plasma calprotectin and serum LRG levels were higher in nonperforated appendicitis versus nonappendicitis (p < 0.01). Median serum LRG, urine LRG, and plasma calprotectin levels were higher in perforated appendicitis compared to nonperforated appendicitis (p < 0.05). Urine calprotectin did not differ among groups. A serum LRG < 40,150 ng/mL, a urine LRG < 42 ng/mL, and a plasma calprotectin < 159 ng/mL, each provided a sensitivity and negative predictive value of 100% to identify children at low risk for appendicitis, but with specificities ranging from 23% to 35%. The standard white blood cell (WBC) count achieved 100% sensitivity at a higher specificity than both novel biomarkers. Plasma calprotectin and serum/urine LRG are elevated in pediatric appendicitis. No individual marker performed as well as the WBC count.

Fecal Pancreatitis-Associated Protein: A Novel Biomarker in IBD?

Background & Aim: IBD is characterized by recurrent episodes of inflammation. Adequate detection and monitoring of disease activity is required for optimal management. Ileocolonoscopy remains the gold standard, but is an invasive procedure with potential risk of complications. Activity indices have been well validated in clinical trials, but employ subjective parameters and do not always (correctly) reflect disease activity in daily practice. Serological markers such as Creactive protein (CRP) and Erythrocyte sedimentation rate (ESR) are widely used. Previous studies have pointed to varying sensitivity and specificity in the prediction of disease activity. The role of the fecal marker calprotectin is promising, but needs further validation. Our aim was to study the correlation between clinical activity indices and the biochemical markers CRP, ESR and calprotectin in a large prospective cohort of IBD patients in daily practice. Materials & methods: 322 consecutive IBD patients were recruited at the outpatient department and participated in a large ongoing prospective followup study. At study entry and at regular visits thereafter, clinical activity indices (Harvey Bradshaw (HB) for Crohn's disease and Simplified Clinical Colitis Activity Index (SCCAI) for ulcerative colitis), serum CRP, ESR and fecal calprotectin were assessed and correlations were calculated using Spearman's correlation. Results: 189 CD (mean age 43 years; 64% female) and 133 UC (mean age 49 years; 49% female) patients were included. Data are given from first visit (cross sectional). Median HBscore and SCCAI-score were 3 (range 0-17) and 1 (0-11), respectively. Active disease was present in 32% of CD and 28% of UC. Median CRP was 3.2 mg/l (range 0.9112) in CD and 2.4 (0.998) in UC patients. Median ESR was 12 mm/ 1h (range 2-52) in CD and 10 (2-56)in UC. Median calprotectin levels in UC were 89 μg/g (range 14-3366) and in CD patients 99 μg/g (range 14-1531). We found a weak but significant correlation of the HBscore with ESR (r= 0.19; p= 0.04), but not with CRP (r= 0.08; p= 0.28) nor with calprotectin (r= 0.09; p= 0.24). However in UC, the SCCAIscore correlated significantly with CRP (r= 0.26; p= 0.01), ESR (r= 0.28; p= 0.01) and calprotectin (r= 0.42; p= <0.01). Furthermore, ESR correlated significantly with calprotectin (r= 0.36; p= <0.01) in UC but not in CD patients. In addition, CRP and calprotectin correlated well in both CD (r= 0.36; p= <0.01) and UC patients (r= 0.43; p= <0.01). Disease location (ileum versus colon involvement) did not affect correlations in CD patients. Conclusion: In this cross sectional evaluation of a large prospective follow up cohort of IBD patients, the biochemical markers CRP, ESR and calprotectin correlate poorly with disease activity in CD but not in UC. Identification of new and sensitive non-invasive markers in CD is needed.

Monitoring Disease Activity in IBD: Correlation Between Clinical Activity Indices and Biomarkers

Background & Aim: IBD is characterized by recurrent episodes of inflammation. Adequate detection and monitoring of disease activity is required for optimal management. Ileocolonoscopy remains the gold standard, but is an invasive procedure with potential risk of complications. Activity indices have been well validated in clinical trials, but employ subjective parameters and do not always (correctly) reflect disease activity in daily practice. Serological markers such as Creactive protein (CRP) and Erythrocyte sedimentation rate (ESR) are widely used. Previous studies have pointed to varying sensitivity and specificity in the prediction of disease activity. The role of the fecal marker calprotectin is promising, but needs further validation. Our aim was to study the correlation between clinical activity indices and the biochemical markers CRP, ESR and calprotectin in a large prospective cohort of IBD patients in daily practice. Materials & methods: 322 consecutive IBD patients were recruited at the outpatient department and participated in a large ongoing prospective followup study. At study entry and at regular visits thereafter, clinical activity indices (Harvey Bradshaw (HB) for Crohn's disease and Simplified Clinical Colitis Activity Index (SCCAI) for ulcerative colitis), serum CRP, ESR and fecal calprotectin were assessed and correlations were calculated using Spearman's correlation. Results: 189 CD (mean age 43 years; 64% female) and 133 UC (mean age 49 years; 49% female) patients were included. Data are given from first visit (cross sectional). Median HBscore and SCCAI-score were 3 (range 0-17) and 1 (0-11), respectively. Active disease was present in 32% of CD and 28% of UC. Median CRP was 3.2 mg/l (range 0.9112) in CD and 2.4 (0.998) in UC patients. Median ESR was 12 mm/ 1h (range 2-52) in CD and 10 (2-56)in UC. Median calprotectin levels in UC were 89 μg/g (range 14-3366) and in CD patients 99 μg/g (range 14-1531). We found a weak but significant correlation of the HBscore with ESR (r= 0.19; p= 0.04), but not with CRP (r= 0.08; p= 0.28) nor with calprotectin (r= 0.09; p= 0.24). However in UC, the SCCAIscore correlated significantly with CRP (r= 0.26; p= 0.01), ESR (r= 0.28; p= 0.01) and calprotectin (r= 0.42; p= <0.01). Furthermore, ESR correlated significantly with calprotectin (r= 0.36; p= <0.01) in UC but not in CD patients. In addition, CRP and calprotectin correlated well in both CD (r= 0.36; p= <0.01) and UC patients (r= 0.43; p= <0.01). Disease location (ileum versus colon involvement) did not affect correlations in CD patients. Conclusion: In this cross sectional evaluation of a large prospective follow up cohort of IBD patients, the biochemical markers CRP, ESR and calprotectin correlate poorly with disease activity in CD but not in UC. Identification of new and sensitive non-invasive markers in CD is needed.

Calprotectin as a Biomarker for Remission in UC Patients Under IFX Therapy

Background: Faecal calprotectin correlates with endoscopic and histological disease activity in patients with ulcerative colitis (UC). Recently, it has been shown that infliximab therapy is effective for the induction and the maintenance of UC disease remission. Aims: To evaluate the evolution of calprotectin levels under infliximab therapy. Patients and Methods: 53 patients with active UC from 17 centers were treated with infliximab therapy (5 mg/kg) at baseline, week 2, and week 6. Patients were evaluated at each infusion and week 10 by clinical Mayo score and lab testing. Faecal calprotectin was measured every week. Sigmoidoscopies were performed at baseline, week 6 and week 10 and graded from 0-3. Endoscopic remission was further defined by a score of 1 or less. Remission per protocol was defined as endoscopic remission and a decrease of calprotectin with 80 % or < 50 mg/kg. Results: After 10 weeks, 2 patients stopped therapy due to inefficacy. Three patients stopped due to safety reasons: 2 allergic reactions, 1 patient had a vertebral fracture. Additionally, 12 patients had missing data, mostly attributable to refusal of the week 10 colonoscopy. Those patients were excluded from complete case analysis, further depicted with an asterisk (*). Remission per protocol was obtained in 58%* of patients (or 54% by ITT analysis with multiple imputation). Endoscopic remission in 63%* of patients (or 59% by ITT analysis). Median calprotectin levels decreased from 1767 (IQR 3140)* at baseline to 72.5 (IQR 444)* at week 10 (p<0.001). Moreover, patients who went in endoscopic remission at week 10 showed a significant steep decrease of calpro scores between baseline and week 2 (p< 0.001) compared to patients who did not show a remission. From week 3 on, this course was more flattened (Figure). Clinical Mayo score and faecal calprotectin measurements showed an excellent correlation with endoscopic remission, reflected by an AUC of ROC analyses of 0.94 (0.87-1) for Mayo score and 0.91 (0.81-1) for calpro measurements at week 10*: all patients (63%*) with a Calpro score of <50, and all patients (63%*) with a normal clinical Mayo score (=0) were in colonoscopic remission. Similar results were obtained with ITT repeated measures analysis: AUC of 0.97 (0.94-1) for the Clinical Mayo score and 0.85 (0.77-0.92) for the calpro measurements. A calprotecin level of 50 mg/kg or a decrease of at least 80% at week predicted an endoscopic remission at week 10 with a specificity of 67%* and sensitivity of 54%*. Conclusions: Infliximab induces a remission in 58% of UC patients with active disease associated with a fast and significant decrease of faecal calprotectin levels. Calprotectin levels are as reliable as the Clinical Mayo score to evaluate the effect of infliximab therapy and correlate with endoscopic scores.

Non-Invasive Markers for Early Diagnosis and Determination of the Severity of Necrotizing Enterocolitis

To improve diagnosis of necrotizing enterocolitis (NEC) by noninvasive markers representing gut wall integrity loss (I-FABP and claudin-3) and gut wall inflammation (calprotectin). Furthermore, the usefulness of I-FABP to predict NEC severity and to screen for NEC was evaluated. Urinary I-FABP and claudin-3 concentrations and fecal calprotectin concentrations were measured in 35 consecutive neonates suspected of NEC at the moment of NEC suspicion. To investigate I-FABP as screening tool for NEC, daily urinary levels were determined in 6 neonates who developed NEC out of 226 neonates included before clinical suspicion of NEC. Of 35 neonates suspected of NEC, 14 developed NEC. Median I-FABP, claudin-3, and calprotectin levels were significantly higher in neonates with NEC than in neonates with other diagnoses. Cutoff values for I-FABP (2.20 pg/nmol creatinine), claudin-3 (800.8 INT), and calprotectin (286.2 microg/g feces) showed clinically relevant positive likelihood ratios (LRs) of 9.30, 3.74, 12.29, and negative LRs of 0.08, 0.36, 0.15, respectively. At suspicion of NEC, median urinary I-FABP levels of neonates with intestinal necrosis necessitating surgery or causing death were significantly higher than urinary I-FABP levels in conservatively treated neonates. Of the 226 neonates included before clinical suspicion of NEC, 6 developed NEC. In 4 of these 6 neonates I-FABP levels were not above the cutoff level to diagnose NEC before clinical suspicion. Urinary I-FABP levels are not suitable as screening tool for NEC before clinical suspicion. However, urinary I-FABP and claudin-3 and fecal calprotectin are promising diagnostic markers for NEC. Furthermore, urinary I-FABP might also be used to predict disease severity.

P0663 THE EVALUATION OF FAECAL CALPROTECTIN AND LACTOFERRIN LEVELS IN THE DIAGNOSIS OF CHILDREN WITH INFLAMMATORY BOWEL DISEASE

Introduction: The management of Inflammatory Bowel Disease (IBD) is hampered by the lack of a reliable, non-invasive index of bowel inflammation. Faecal calprotectin and lactoferrin have been suggested as useful markers. The aim of our study was to assess the value of faecal calprotectin and lactoferrin as discriminators of active IBD. Methods: Stool samples were collected from 3 groups of children - A. active IBD (n = 46), B. children with other gastrointestinal diseases (n = 17) and C. controls with no gastrointestinal diseases (n = 19). Faecal calprotectin and lactoferrin was measured using an ELISA method. Results: Median calprotectin levels were: A. 247 microgram/gram (100–2251), B. 71 (3–1752) and C. 37 (4–304). Median lactoferrin levels in 15 patients were A. 33.1 (0.5–100.2), B. 2.8 (0.1–49.8) and C. 0.7 (0–15.9). Conclusion: Our results confirm that faecal calprotectin can be a useful non-invasive measure of active IBD but faecal lactoferrin may prove even more discriminating.

Faecal calprotectin: a marker of inflammation throughout the intestinal tract

To assess the potential of measuring the calcium-binding protein calprotectin in faeces as a method of screening for alimentary inflammation and neoplasia. Hospital day services unit for endoscopy and faecal analysis in the clinical biochemistry department. 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. 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. 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%. 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.

Surrogate markers of intestinal inflammation are predictive of relapse in patients with inflammatory bowel disease

Prediction of relapse of inflammatory bowel disease has important implications for therapeutic strategies. We assessed whether measurement of intestinal permeability and inflammation could predict relapse of inflammatory bowel disease (IBD). Forty-three patients with Crohn's disease (CD) and 37 with ulcerative colitis (UC) in clinical remission provided a stool sample to be assayed for calprotectin (a neutrophil-specific marker), and patients with CD additionally underwent a small intestinal permeability test. Relapse was defined using clinical disease activity indices. Twenty-five (58%) patients with CD and 19 (51%) with UC had a relapse over the 12-month period. Median calprotectin levels in the relapse groups (122 mg/L for CD, 123 mg/L for UC; normal <10 mg/L) differed significantly (P<0.0001) from those of the nonrelapse groups (41.5 mg/L for CD, 29.0 mg/L for UC). At 50 mg/L, the sensitivity and specificity of calprotectin for predicting relapse in all patients with IBD were 90% and 83%, respectively. Permeability in the CD patients who relapsed (median, 0.075; normal <0.04) differed significantly (P = 0. 004) from that in the nonrelapse group (median, 0.038). At the level of 0.05, the sensitivity and specificity of permeability in predicting relapse were 84% and 61%, respectively. Fecal calprotectin predicts clinical relapse of disease activity in patients with CD and UC, whereas small intestinal permeability is a useful predictor of relapse in patients with small intestinal CD.

Improved assay for fecal calprotectin

Fecal calprotectin is a marker of inflammatory and neoplastic disease in the lower gastrointestinal tract. A new fecal sample preparation procedure for the measurement of calprotectin has been developed, with higher calprotectin yield and lower contamination risk. Changes in the new method compared to the original [Røseth AG, Fagerhol MK, Aadland E, Schønsby H. Assessment of the neutrophil dominating protein calprotectin in feces. A methodologic study. Scand J Gastroenterol 1992;27(9):793–798] are smaller sample size, higher dilution of the sample, presence of dissociating agents in the extraction solution and procedure performed in closed disposable tubes. The extraction yield was 78% (41–100%) of total calprotectin, giving an overall five-fold increase compared to the original method. Samples with high calprotectin values were increased to a slightly higher degree, than low calprotectin samples, thus improving the separation between high and low calprotectin levels. Median calprotectin level in healthy subjects was 26 μg/g. Pathological samples with pancolitis showed levels up to 30 000 μg/g. The mean C.V. (coefficient of variation) in blended feces was lower than that of unblended, suggesting uneven distribution of calprotectin. However, no significant difference between spot measurements was found when five samples from each of 47 stools were measured. Thus measurements of calprotectin in fecal samples were accurate and reproducible. No interference with foods or relevant oral pharmaceuticals or nutraceuticals was found.

Assessment of disease activity in ulcerative colitis by faecal calprotectin, a novel granulocyte marker protein.

This study comprised 62 outpatients with ulcerative colitis who underwent 64 colonoscopies. The disease activity was evaluated according to endoscopic and histological criteria. The results revealed a significant correlation between both the endoscopic as well as the histological gradings of disease activity and faecal calprotectin. The median faecal calprotectin levels in the control group (6 mg/l) and in the patients with no or low disease activity (11.5 mg/l) were significantly different (p < 0.0001). The median calprotectin level among patients with active disease was 68 mg/l which was significantly different from the latter group (p < 0.0001). Furthermore, we suggest that the degree of inflammation rather than the extent of the disease determined the faecal calprotectin levels. In conclusion, assessment of faecal calprotectin seems to be a marker of disease activity in patients with ulcerative colitis.