Role of faecal calprotectin as non-invasive marker of intestinal inflammation

BACKGROUND/AIM: Faecal calprotectin, a neutrophil granulocyte cytosol protein, is considered a promising marker of intestinal inflammation. We assessed and compared the faecal calprotectin concentration in patients with organic and functional chronic intestinal disorders. PATIENTS AND METHODS: The study was carried out, using a commercially available ELISA test, measuring calprotectin in stool samples collected from 131 patients with inflammatory bowel diseases, 26 with intestinal neoplasms, 48 with irritable bowel syndrome and 34 healthy subjects. RESULTS: Median faecal calprotectin was significantly increased in Crohn's disease (231 microg/g, 95% confidence interval (CI) 110-353 microg/g), ulcerative colitis (167 microg/g, 95% CI 59-276 microg/g), and neoplasms (105 microg/g, 95% CI 0-272 microg/g), whereas normal values were found in patients with irritable bowel syndrome (22 microg/g, 95% CI 9-35 microg/g) and in healthy subjects (11 microg/g, 95% CI 3-18 microg/g). A positive correlation was observed with clinical activity scores in Crohn's disease and ulcerative colitis. In both groups, patients with clinically active disease showed higher calprotectin levels than those observed in patients with quiescent disease (405 microg/g, 95% CI 200-610 microg/g vs. 213 microg/g, 95% CI 85-341 microg/g in CD patients, p<0.05, and 327 microg/g, 95% CI 104-550 microg/g vs. 123 microg/g, 95% CI 40-206 microg/g in UC patients, p<0.001). CONCLUSIONS: Faecal calprotectin appears to be a promising and non-invasive biomarker of intestinal inflammation. If these findings are confirmed, it may provide a useful test for the diagnosis and follow up of inflammatory bowel diseases.     

Fecal calprotectin is an effective diagnostic tool that differentiates inflammatory from functional intestinal disorders

Abstract

Background. The clinical pictures of functional gastrointestinal disorders and inflammatory diseases can be quite similar leading to inappropriate and expensive investigations. Objective. To investigate fecal calprotectin (FC) diagnostic performance in different gastrointestinal conditions. Material and methods. Stool specimens of 66 outpatients referred for colonoscopy were collected for further FC determination. Diagnostic accuracy was assessed by the area under the curve (AUC). Sensitivity (Se), specificity (Sp), positive (PPV), and negative predictive values (NPV) were calculated according to the presence of inflammation and the main final diagnosis. Results. Histological inflammation was found in 45 (68%) patients: 24 had a diagnosis of inflammatory bowel disease (IBD) while 21 reported miscellaneous conditions (5 microscopic colitis, 2 eosinophilic colitis, and 14 nonspecific chronic colitis). The diagnosis in the 21 (32%) patients without inflammation was irritable bowel syndrome (IBS). Median FC values were 268 µg/g (95% CI, 151–343) and 49 µg/g (95% CI, 23–101) in patients with and without inflammation, respectively (p = 0.0001). AUC value of FC was 0.811 (Se = 68.9%, Sp = 71.4%, PPV = 83.8%, and NPV = 56.3% with a cutoff value of 100 µg/g) for discriminating between patients with and without inflammation and 0.931 (Se = 87.5%, Sp = 90.5%, PPV = 91.3%, and NPV = 86.4% with a cutoff value of 150 µg/g) for discriminating between patients with IBS and IBD. Using the cutoff value recommended by the manufacturer (50 µg/g), we found Se =100%, Sp =52.4%, PPV =70.6%, and NPV =100% for the diagnosis of IBD. Conclusions. FC appears to be a reliable noninvasive biomarker of intestinal inflammation useful to improve the appropriateness of colonoscopy requests.     

Fecal calprotectin as a biomarker to distinguish between organic and functional gastrointestinal disease]

INTRODUCTION: There is growing evidence showing the importance of the fecal calprotectin assay in differentiating organic from functional gastrointestinal disease. It is a simple, non-invasive biomarker that is especially useful in children, who may require general anesthesia for colonoscopy. The aim of this study was to assess the use and sensitivity of fecal calprotectin (FCP) in pediatric patients with signs and symptoms of IBD to avoid unnecessary invasive techniques and to distinguish between organic and functional gastrointestinal pathology. MATERIAL AND METHODS: A single stool sample was collected from 47 children (mean age: 10.1 years) referred for non-specific gastrointestinal symptoms suggestive of organicity. On the basis of clinical criteria 13 children had functional bowel disorders and 34 had organic gastrointestinal disease, 15 with IBD and 19 with other organic (non-IBD) gastrointestinal conditions. Thirty healthy children were included as controls. Calprotectin concentrations were measured by enzyme immunoassay. RESULTS: Children with IBD had FCP levels [median (interquartile range); 1,219 microg/g (322-2,967 microg/g)] higher than children with functional gastrointestinal disease [20 microg/g (16-25 microg/g); p < 0.0001], those with organic non-IBD disease [113 microg/g (36-193 microg/g); p = 0.002], and healthy children [25 microg/g (19.2-32.5 microg/g); p < 0.0001]. Fecal calprotectin concentration also was significantly higher in children with organic (non-IBD) disease as compared to controls (p = 0.004) and children with functional pathology (p = 0.002). FCP levels were similar in controls and children with functional gastrointestinal disease (p = 0.264). DISCUSSION: CPF is a sensitive, but not disease-specific, marker to identify patients with IBD who should undergo diagnostic colonoscopy, and to avoid unnecessary invasive procedures in patients with functional gastrointestinal disorders.     

Potential roles of neutrophils in regulating intestinal mucosal inflammation of inflammatory bowel disease

Inflammatory bowel diseases (IBD), comprising of ulcerative colitis and Crohn's disease, are inflammatory disorders of the gastrointestinal tract characterized by chronically relapsing mucosal inflammation. Neutrophils, as the effector cells of acute inflammation, have long been reported to play a role in the maintenance of intestinal homeostasis and pathogenesis of IBD. At the early stage of mucosal inflammation in patients with IBD, neutrophils flood into intestinal mucosa, phagocytose pathogenic microbes, and promote mucosal healing and resolution of inflammation. However, large numbers of neutrophils infiltrating in the inflamed mucosa and accumulating in the epithelia cause damage of mucosal architecture, compromised epithelial barrier and production of inflammatory mediators. In this review we discuss the critical roles of neutrophils in modulating innate and adaptive immune responses in intestinal mucosa, and, importantly, clarify the potential roles of neutrophils related to their production of inflammatory mediators, transenthothelial and transepithelial migration into intestinal mucosa, and the underlying mechanisms in regulating mucosal inflammation of IBD. Moreover, we also describe a new subset of neutrophils (i.e., CD177⁺ neutrophils) and illustrate its protective role in modulating intestinal mucosal immune responses in IBD.     

感染后肠易激综合征肠道局部免疫-神经-内分泌网络功能的变化

肠易激综合征(IBS)是临床上最常见的功能性胃肠病之一。近年来肠道炎症,特别是急性肠道感染后遗留的肠道黏膜低度炎症在IBS中的作用越来越受到重视,此文就肠道黏膜低度炎症和肠道局部免疫变化、肠道神经-内分泌网络变化在IBS发病中的作用作一综述。     

Diagnostic utility of faecal biomarkers in patients with irritable bowel syndrome

Irritable bowel syndrome(IBS)is a common functional gastrointestinal(GI)disorder characterized by unspecific symptoms.In clinical practice it is crucial to distinguish between non-inflammatory functional problems and inflammatory,malignant or infectious diseases of the GI tract.Differentiation between these involves the use of clinical,radiological,endoscopic,histological and serological techniques,which are invasive,expensive,time-consuming and/or hindered by inaccuracies arising from subjective components.A range of faecal markers now appears to have the potential to greatly assist in the differentiation of inflammatory bowel disease(IBD)and IBS.Faecal markers of neutrophil influx into the mucosa are reliable indicators of intestinal inflammation and their role has been mainly studied in discriminating IBD from non-IBD conditions(including IBS)rather than organic from non-organic diseases.Phagocytespecific proteins of the S100 family(S100A12,calprotectin)are amongst the most promising faecal biomarkers of inflammation.Faecal leukocyte degranulation markers(lactoferrin,polymorphonuclear elastase and myeloperoxidase)have also been suggested as diagnostic tools for the differentiation of IBD and IBS.More recently,additional proteins,including granins,defensins and matrix-metalloproteases,have been discussed as differential diagnostic markers in IBD and IBS.In this review,some of the most promising faecal markers,which have the potential to differentiate IBD and IBS and to advance diagnostic practices,will be discussed.     

NF-κB信号通路与炎症性肠病

炎症是多种细胞及细胞因子参与的机体防御性反应,但严重或长期的炎症则会造成机体损伤.炎症性肠病(inflammatory bowel disease,IBD)是一组以慢性、周期性炎症为特征的胃肠道疾病,长期、反复的胃肠道炎症不仅影响患者生活质量,而且增加了肠道纤维化及癌变的风险,而核因子Kappa B(nuclear f...     

Epithelial restitution and wound healing in inflammatory bowel disease

Inflammatory bowel disease is characterized by a chronic inflammation of the intestinal mucosa. The mucosal epithelium of the alimentary tract constitutes a key element of the mucosal barrier to a broad spectrum of deleterious substances present within the intestinal lumen including bacterial microorganisms, various dietary factors, gastrointestinal secretory products and drugs. In addition, this mucosal barrier can be disturbed in the course of various intestinal disorders including inflammatory bowel diseases. Fortunately, the integrity of the gastrointestinal surface epithelium is rapidly reestablished even after extensive destruction. Rapid resealing of the epithelial barrier following injuries is accomplished by a process termed epithelial restitution, followed by more delayed mechanisms of epithelial wound healing including increased epithelial cell proliferation and epithelial cell differentiation. Restitution of the intestinal surface epithelium is modulated by a range of highly divergent factors among them a broad spectrum of structurally distinct regulatory peptides, variously described as growth factors or cytokines. Several regulatory peptide factors act from the basolateral site of the epithelial surface and enhance epithelial cell restitution through TGF-13-dependent pathways. In contrast, members of the trefoil factor family （TFF peptides） appear to stimulate epithelial restitution in conjunction with mucin glycoproteins through a TGF-13-independent mechanism from the apical site of the intestinal epithelium. In addition, a number of other peptide molecules like extracellular matrix factors and blood clotting factors and also non- peptide molecules including phospholipids~ short-chain fatty acids （SCFA）, adenine nucleotides, trace elements and pharmacological agents modulate intestinal epithelial repair mechanisms. Repeated damage and injury of the intestinal surface are key features of various intestinal disorders including inflammatory bowel diseases and require constant repair of the epi     

Clinicians’ guide to the use of fecal calprotectin to identify and monitor disease activity in inflammatory bowel disease

BACKGROUND:

Objective monitoring of the severity of inflammation in patients with inflammatory bowel disease (IBD) is an essential part of disease management. However, repeat endoscopy to define extent and severity of inflammation is not practical. Fecal calprotectin (FC) is a biomarker that can be used as a surrogate test to distinguish inflammatory from noninflammatory gastrointestinal disease.

METHODS:

A targeted search of the literature regarding FC, focusing primarily on the past three years, was conducted to develop practical clinical guidance on the current utility of FC in the routine management of IBD patients.

RESULTS:

It is recommended that samples for FC testing be obtained from the first bowel excretion of the day. FC testing should be used as standard of care to accurately confirm inflammation and ‘real-time’ disease activity when a clinician suspects an IBD flare. Although FC is a reliable marker of inflammation, its role in routine monitoring in improving long-term outcomes has not yet been fully assessed. Based on available evidence, the authors suggest the following cut-off values and management strategies: when FC levels are <50 μg/g to 100 μg/g, quiescent disease is likely and therapy should be continued; when FC levels are >100 μg/g to 250 μg/g, inflammation is possible and further testing (eg, colonoscopy) is required to confirm inflammation; and when FC levels are >250 μg/g, active inflammation is likely and strategies to control inflammation should be initiated (eg, optimizing current therapies or switching to an alternative therapy).

DISCUSSION:

FC is a useful biomarker to accurately assess the degree of inflammation and should be incorporated into the management of patients with IBD.     

Calprotectina fecal,marcador eficaz en la diferenciación de enfermedades inflamatorias intestinales y trastornos funcionales gastrointestinales

Introduction

Diagnostic discrimination between inflammatory bowel disease (IBD) and functional gastrointestinal disorders is complex, as they cause similar signs and symptoms. Faecal calprotectin (FC) is a useful marker in this context, and can be used to select patients who will most benefit from colonoscopy. The aim of this study was to evaluate the utility of FC in discriminating between organic disease and functional disorders.

Fecal calprotectin use in inflammatory bowel disease and beyond: A mini-review

Given the number of inflammatory disorders affecting the gastrointestinal tract directly and indirectly, coupled with the considerable overlap with functional disorders, it is evident that more useful noninvasive diagnostic tests are required to aid with diagnosis. If these tests can also have some utility for individual patient follow-up in terms of disease activity and response to treatment, as well as providing forewarning of disease relapse, it would be extremely useful information for the clinician. One recently described test that may fulfill several of these attributes is based on leakage of a mononuclear cell cytoplasmic protein, calprotectin, along the intestinal tract, which can then be quantified in feces. This has been used to distinguish patients exhibiting symptoms of irritable bowel syndrome from patients with inflammatory bowel disease, with a measure of success greater than with currently used techniques. The present article summarizes the experience with this test used in inflammatory bowel disease, as well as a variety of gastrointestinal disorders.     

Chemokines in inflammatory bowel disease

Ulcerative colitis (UC) and Crohn’s disease (CD), collectively termed inflammatory bowel diseases (IBD), represent chronic relapsing and remitting inflammatory disorders of the gastrointestinal tract that are charcterized by leukocytic infiltration of the intestinal mucosa and submucosa. In CD, the inflammation is transmural and frequently associated with granuloma formation. Chemokines have emerged as the most important regulators of leukocyte trafficking during infection or inflammation and, therefore, have been implicated in the pathogenesis of IBD. In this review, recent advances on the role of chemokines and their receptors in mucosal immunity and inflammation are discussed, and the potential use of chemokine/chemokine-receptor antagonists as novel therapeutic targets for the treatment of human IBD is highlighted.     

Gut-lung crosstalk in pulmonary involvement with inflammatory bowel diseases

Pulmonary abnormalities,dysfunction or hyper-reactivity occurs in association with inflammatory bowel disease(IBD) more frequently than previously recognized.Emerging evidence suggests that subtle inflammation exists in the airways among IBD patients even in the absence of any bronchopulmonary symptoms,and with normal pulmonary functions. The pulmonary impairment is more pronounced in IBD patients with active disease than in those in remission. A growing number of case reports show that the IBD patients develop rapidly progressive respiratory symptoms after colectomy,with failure to isolate bacterial pathogens on repeated sputum culture,and often request oral corticosteroid therapy. All the above evidence indicates that the inflammatory changes in both the intestine and lung during IBD. Clinical or subclinical pulmonary inflammation accompanies the main inflammation of the bowel.Although there are clinical and epidemiological reports of chronic inflammation of the pulmonary and intestinal mucosa in IBD,the detailed mechanisms of pulmonaryintestinal crosstalk remain unknown. The lung has no anatomical connection with the main inflammatory site of the bowel. Why does the inflammatory process shift from the gastrointestinal tract to the airways? The clinical and subclinical pulmonary abnormalities,dysfunction,or hyper-reactivity among IBD patients need further evaluation. Here,we give an overview of the concordance between chronic inflammatory reactions in the airways and the gastrointestinal tract. A better understanding of the possible mechanism of the crosstalk among the distant organs will be beneficial in identifying therapeutic strategies for mucosal inflammatory diseases such as IBD and allergy.     

Exploring & exploiting our ‘other self’ – Does the microbiota hold the key to the future therapy in Crohn's?

Inflammatory bowel diseases (IBD) with its two major forms Crohn's disease (CD) and ulcerative colitis (UC) are chronic relapsing disorders leading to inflammation of the gastrointestinal tract. Although the precise aetiology of IBD remains unclear, several factors are believed to contribute to disease pathogenesis. Among these, the role of the intestinal microbiota has become more and more appreciated. Evidence from experimental and clinical studies strongly suggests that chronic intestinal inflammation results from a dysregulated immune response towards components of the microbiota in genetically susceptible hosts. The growing perception of the microbiota as a major driver of disease pathogenesis raises the question, if the intestinal microbiota can be used as a therapeutic target in CD. Based on what we know about host microbiota interactions in health and disease, the objective of this review is to address the question if the microbiota holds the key to the future therapy in CD.     

Sobreposición entre los trastornos funcionales de dolor abdominal y enfermedades orgánicas en niños

Functional abdominal pain disorders are highly prevalent in children. These disorders can be present in isolation or combined with organic diseases, such as celiac disease and inflammatory bowel diseases. Intestinal inflammation (infectious and non-infectious) predisposes children to the development of visceral hypersensitivity that can manifest as functional abdominal pain disorders, including irritable bowel syndrome. The new onset of irritable bowel syndrome symptoms in a patient with an underlying organic disease, such as inflammatory bowel disease, is clinically challenging, given that the same symptomatology may represent a flare-up of the inflammatory bowel disease or an overlapping functional abdominal pain disorder. Similarly, irritable bowel syndrome symptoms in a child previously diagnosed with celiac disease may occur due to poorly controlled celiac disease or the overlap with a functional abdominal pain disorder. There is little research on the overlap of functional abdominal disorders with organic diseases in children. Studies suggest that the overlap between functional abdominal pain disorders and inflammatory bowel disease is more common in adults than in children. The causes for these differences in prevalence are unknown. Only a handful of studies have been published on the overlap between celiac disease and functional abdominal pain disorders in children. The present article provides a review of the literature on the overlap between celiac disease, inflammatory bowel disease, and functional abdominal pain disorders in children and establish comparisons with studies conducted on adults.     

Diagnostic precision of fecal calprotectin for inflammatory bowel disease and colorectal malignancy

OBJECTIVES: Fecal calprotectin (FC) is a relatively new marker of intraluminal intestinal inflammation. Using meta-analytical techniques, the study aimed to evaluate the diagnostic precision of FC for inflammatory bowel disease (IBD) and colorectal cancer (CRC) in adults and children. METHODS: Quantitative meta-analysis was performed on prospective studies, comparing FC levels against the histological diagnosis. Sensitivity, specificity, and diagnostic odds ratio (DOR) were calculated for each study. Summary receiver-operating characteristic (sROC) curves and subgroup analysis were undertaken. Study quality and heterogeneity were evaluated. RESULTS: Thirty studies of 5,983 patients were included. FC levels in patients with IBD were higher by 219.2 micrograms per gram (microg/g) compared with normal patients (P < 0.001). sROC curve analysis showed a sensitivity of 0.95 (95% CI 0.93-0.97), specificity of 0.91 (95% CI 0.86-0.91), and an area under the curve (AUC) of 0.95 for the diagnosis of IBD. Patients with colorectal neoplasia had nonsignificantly higher FC levels by 132.2 microg/g compared with noncancer controls (P= 0.18). Sensitivity and specificity of FC for the diagnosis of CRC were 0.36 and 0.71, respectively, with an AUC of 0.66. The diagnostic precision of FC for IBD was higher in children than adults with better accuracy at a cutoff level of 100 microg/g versus 50 microg/g. Sensitivity analysis and metaregression analysis did not significantly alter the results. CONCLUSIONS: FC cannot be recommended as a screening test for CRC in the general population. FC appeared to offer a good diagnostic precision in distinguishing IBD from non-IBD diagnoses, with higher precision at a cutoff of 100 microg/g.     

Dismicrobism in inflammatory bowel disease and colorectal cancer: Changes in response of colocytes

Patients with inflammatory bowel disease (IBD) have an increased risk of 10%-15% developing colorectal cancer (CRC) that is a common disease of high economic costs in developed countries. The CRC has been increasing in recent years and its mortality rates are very high. Multiple biological and biochemical factors are responsible for the onset and progression of this pathology. Moreover, it appears absolutely necessary to investigate the environmental factors favoring the onset of CRC and the promotion of colonic health. The gut microflora, or microbiota, has an extensive diversity both quantitatively and qualitatively. In utero, the intestine of the mammalian fetus is sterile. At birth, the intestinal microbiota is acquired by ingesting maternal anal or vaginal organisms, ultimately developing into a stable community, with marked variations in microbial composition between individuals. The development of IBD is often associated with qualitative and quantitative disorders of the intestinal microbial flora (dysbiosis). The healthy human gut harbours about 10 different bacterial species distributed in colony forming units which colonize the gastrointestinal tract. The intestinal microbiota plays a fundamental role in health and in the progression of diseases such as IBD and CRC. In healthy subjects, the main control of intestinal bacterial colonization occurs through gastric acidity but other factors such as endoluminal temperature, competition between different bacterial strains, peristalsis and drugs can influence the intestinal microenvironment. The microbiota exerts diverse physiological functions to include: growth inhibition of pathogenic microorganisms, synthesis of compounds useful for the trophism of colonic mucosa, regulation of intestinal lymphoid tissue and synthesis of amino acids. Furthermore, mucus seems to play an important role in protecting the intestinal mucosa and maintaining its integrity. Changes in the microbiota composition are mainly influenced by diet and age, as well as genetic factors. Increasing evidence indicates that dysbiosis favors the production of genotoxins and metabolites associated with carcinogenesis and induces dysregulation of the immune response which promotes and sustains inflammation in IBD leading to carcinogenesis. A disequilibrium in gut microflora composition leads to the specific activation of gut associated lymphoid tissue. The associated chronic inflammatory process associated increases the risk of developing CRC. Ulcerative colitis and Crohn’s disease are the two major IBDs characterized by an early onset and extraintestinal manifestations, such as rheumatoid arthritis. The pathogenesis of both diseases is complex and not yet fully known. However, it is widely accepted that an inappropriate immune response to microbial flora can play a pivotal role in IBD pathogenesis.     

Surgical strategies in paediatric inflammatory bowel disease

Inflammatory bowel disease (IBD) comprises two distinct but related chronic relapsing inflammatory conditions affecting different parts of the gastrointestinal tract. Crohn’s disease is characterised by a patchy transmural inflammation affecting both small and large bowel segments with several distinct phenotypic presentations. Ulcerative colitis classically presents as mucosal inflammation of the rectosigmoid (distal colitis), variably extending in a contiguous manner more proximally through the colon but not beyond the caecum (pancolitis). This article highlights aspects of the presentation, diagnosis, and management of IBD that have relevance for paediatric practice with particular emphasis on surgical considerations. Since 25% of IBD cases present in childhood or teenage years, the unique considerations and challenges of paediatric management should be widely appreciated. Conversely, we argue that the organizational separation of the paediatric and adult healthcare worlds has often resulted in late adoption of new approaches particularly in paediatric surgical practice.     

Fecal calprotectin is useful in predicting disease relapse in pediatric inflammatory bowel disease

BACKGROUND: Fecal calprotectin (FC) has been proposed as a noninvasive surrogate marker to determine the degree of intestinal inflammation and predicting relapse in patients with inflammatory bowel disease (IBD). The aim was to compare FC levels in IBD and healthy controls, to correlate FC levels with clinical disease activity, and to assess whether FC levels can be used to predict clinical relapse in children with IBD. METHODS: Enzyme-linked immunosorbent assay (ELISA) determined levels of FC were measured in more than 1 stool samples (n) from 32 IBD patients (n = 97) and from 34 healthy controls (n = 37). Disease activity was assessed by the Harvey-Bradshaw index in Crohn's disease (CD) and by Physician's Global Assessment (PGA) in both CD and ulcerative colitis (UC). Clinical events were recorded up to 9 months following stool collection in CD patients. Wilcoxon rank sum test and Fisher's exact tests were used to compare FC levels in IBD patients and in control. Kaplan-Meyer analysis was used to determine a risk of clinical relapse in relation to FC levels. RESULTS: The IBD group had higher FC levels (range 17-7500 g/g) compared with control (16-750 g/g, P < 0.0001). FC levels were higher during relapse (CD, 3214 +/- 2186; UC, 2819 +/- 1610) compared to remission (CD, 1373 +/- 1630; UC, 764 +/- 869; P < 0.0001). Among those with clinical relapse, 90% had FC levels more than 400 mug/g in CD. Eighty-nine percent of CD encounters with FC levels less than 400 mug/g remained in clinical remission. CONCLUSIONS: FC levels differentiate active IBD from controls. Among children with CD and in remission, FC levels may be useful in predicting impending clinical relapse.     

Relationship between fecal lactoferrin and inflammatory bowel disease

OBJECTIVE: Lactoferrin as a glucoprotein that can reflect the activity of neutrophil leukocytes is a specific and sensitive indicator in the evaluation of intestinal inflammation. The aim of this study was to evaluate the relationship between fecal lactoferrin and intestinal inflammation by quantitative analysis and the effect of fecal lactoferrin in measuring the activity of inflammatory bowel disease (IBD) including ulcerative colitis (UC) and Crohn's disease (CD). MATERIAL AND METHODS: A total of 177 fresh stool samples were collected from 42 active UC, 17 inactive UC, 13 active CD, 5 inactive CD, 41 infectious bowel disease, 25 irritable bowel syndrome (IBS) and 34 healthy volunteers. IBD-SCAN was used quantitatively to measure the level of fecal lactoferrin. A modified Harvey-Bradshaw Active Index was used to evaluate the activity of IBD. RESULTS: Fecal lactoferrin was 3.15+/-1.60 microg/g in healthy volunteers, 2.54+/-1.49 microg/g in IBS, 83.3+/-29.9 microg/g in infectious bowel disease, 1126.29+/-431.21 microg/g in active UC, 1035.25+/-456.59 microg/g in active CD, 96.58+/-82.46 microg/g in inactive UC and 133.52+/-88.89 microg/g in inactive CD. Fecal lactoferrin was significantly higher in active IBD than in inactive IBD, IBS and infectious bowel disease. The sensitivity and specificity of fecal lactoferrin were 92% and 88%, respectively, for UC, and 92% and 80%, respectively, for CD. CCONCLUSIONS: Fecal lactoferrin is a sensitive and specific marker in measuring the activity of IBD. It provides us with a valid method in discriminating between inflammatory and non-inflammatory bowel disease. In addition, an elevated fecal lactoferrin level can lead us to exclude IBS in clinical practice.