Marker Of Gastrointestinal Inflammation Research Articles

Identification and validation of a blood- based diagnostic lipidomic signature of pediatric inflammatory bowel disease

Improved biomarkers are needed for pediatric inflammatory bowel disease. Here we identify a diagnostic lipidomic signature for pediatric inflammatory bowel disease by analyzing blood samples from a discovery cohort of incident treatment-naïve pediatric patients and validating findings in an independent inception cohort. The lipidomic signature comprising of only lactosyl ceramide (d18:1/16:0) and phosphatidylcholine (18:0p/22:6) improves the diagnostic prediction compared with high-sensitivity C-reactive protein. Adding high-sensitivity C-reactive protein to the signature does not improve its performance. In patients providing a stool sample, the diagnostic performance of the lipidomic signature and fecal calprotectin, a marker of gastrointestinal inflammation, does not substantially differ. Upon investigation in a third pediatric cohort, the findings of increased lactosyl ceramide (d18:1/16:0) and decreased phosphatidylcholine (18:0p/22:6) absolute concentrations are confirmed. Translation of the lipidomic signature into a scalable diagnostic blood test for pediatric inflammatory bowel disease has the potential to support clinical decision making.

Lower Diet Quality Associated with Subclinical Gastrointestinal Inflammation in Healthy United States Adults

BackgroundHigher diet quality has been associated with lower risk of developing inflammatory bowel disease, but associations between diet and gastrointestinal (GI) inflammation in healthy adults prior to disease onset are understudied. ObjectivesThe purpose of this project was to examine associations between reported dietary intake and markers of GI inflammation in a healthy adult human cohort. MethodsIn a cross-sectional observational trial of 358 healthy adults, participants completed ≤3 unannounced 24-h dietary recalls using the Automated Self-Administered Dietary Assessment Tool and a Block 2014 Food Frequency Questionnaire to assess recent and habitual intake, respectively. Those who provided a stool sample were included in this analysis. Inflammation markers from stool, including calprotectin, neopterin, and myeloperoxidase, were measured by ELISA along with LPS-binding protein from plasma. ResultsRecent and habitual fiber intake was negatively correlated with fecal calprotectin concentrations (n = 295, P = 0.011, 0.009). Habitual soluble fiber intake was also negatively correlated with calprotectin (P = 0.01). Recent and habitual legume and vegetable intake was negatively correlated with calprotectin (P = 0.013, 0.026, 0.01, 0.009). We observed an inverse correlation between recent Healthy Eating Index (HEI) scores and calprotectin concentrations (n = 295, P = 0.026). Dietary Inflammatory Index scores were calculated and positively correlated with neopterin for recent intake (n = 289, P = 0.015). When participants with clinically elevated calprotectin were excluded, recent and habitual fiber, legume, vegetable, and fruit intake were negatively correlated with calprotectin (n = 253, P = 0.00001, 0.0002, 0.045, 0.001, 0.009, 0.001, 0.004, 0.014). Recent total HEI score was inversely correlated with subclinical calprotectin (P = 0.003). ConclusionsHigher diet quality may be protective against GI inflammation even in healthy adults.This trial was registered at clinicaltrials.gov as NCT02367287.

No Associations between Dairy Intake and Markers of Gastrointestinal Inflammation in Healthy Adult Cohort.

Dairy products are a good source of essential nutrients and past reviews have shown associations of dairy consumption with decreased systemic inflammation. Links between dairy intake and gastrointestinal (GI) inflammation are under-investigated. Therefore, we examined associations between reported dairy intake and markers of GI inflammation in healthy adults in a cross-sectional observational study, hypothesizing a negative association with yogurt intake, suggesting a protective effect, and no associations with total dairy, fluid milk, and cheese intake. Participants completed 24-h dietary recalls and a food frequency questionnaire (FFQ) to assess recent and habitual intake, respectively. Those who also provided a stool sample (n = 295), and plasma sample (n = 348) were included in analysis. Inflammation markers from stool, including calprotectin, neopterin, and myeloperoxidase, were measured along with LPS-binding protein (LBP) from plasma. Regression models tested associations between dairy intake variables and inflammation markers with covariates: age, sex, and body mass index (BMI). As yogurt is episodically consumed, we examined differences in inflammation levels between consumers (>0 cup equivalents/day reported in recalls) and non-consumers. We found no significant associations between dairy intake and markers of GI inflammation. In this cohort of healthy adults, dairy intake was not associated with GI inflammation.

OR10-03-23 Associations Between Diet and Markers of Gastrointestinal Inflammation in Healthy Adult Cohort

OR10-03-23 Associations Between Diet and Markers of Gastrointestinal Inflammation in Healthy Adult Cohort

Effects of Canine-Obtained Lactic-Acid Bacteria on the Fecal Microbiota and Inflammatory Markers in Dogs Receiving Non-Steroidal Anti-Inflammatory Treatment.

Simple SummaryThe use of non-steroidal anti-inflammatory drugs (NSAIDs) has prolonged the longevity and well-being of dogs with osteoarthritis and other painful conditions. However, this treatment is also associated with diarrhea in dogs, but the pathogenetic mechanisms and possible prevention strategies remain unknown. This study aimed to determine whether canine-obtained lactic acid bacteria affect the frequency of diarrhea, fecal microbiota (dysbiosis index), and gastrointestinal inflammation (assessed by calprotectin and S100A12/Calgranulin C) in dogs receiving NSAIDs. Diarrhea occurred in 4/12 dogs (33%) receiving placebo and 1/10 dogs (10%) receiving canine-obtained lactic acid bacteria (LAB), but this difference was not significant. The fecal dysbiosis index, calprotectin, and S100A12 were not significantly different between dogs receiving NSAIDs and LAB and dogs receiving NSAIDs and placebo. This study suggests that LAB is safe to use in NSAID-treated dogs, but further studies are needed to determine its potential to ameliorate diarrhea and gastrointestinal inflammation in dogs receiving NSAIDs.Non-steroidal anti-inflammatory drugs (NSAIDs) may cause enteropathy in dogs and probiotics may be one option to prevent this. The objective of this study was to determine whether the administration of canine-obtained lactic acid bacteria (LAB) has an effect on the frequency of diarrhea, the composition of the fecal microbiota, and/or markers of gastrointestinal inflammation in dogs receiving NSAIDs when compared to dogs given NSAIDs and a placebo. A total of 22 dogs treated with NSAIDs for various clinical indications were enrolled in a seven-day randomized, double-blinded placebo-controlled interventional study. Dogs were randomized to receive either placebo or LAB, a product containing Limosilactobacillus fermentum, Lacticaseibacillus rhamnosus, and Lactiplantibacillus plantarum. Fecal samples were collected on days one and seven. The fecal microbiota was evaluated using the fecal dysbiosis index (DI) and individual bacterial taxa. Fecal calprotectin (CP) and S100A12/Calgranulin C concentrations were used as markers of gastrointestinal inflammation. There was a difference in frequency of diarrhea between groups, with it affecting 4/12 dogs (33%) in the placebo group and 1/10 dogs (10%) in the LAB group, but this difference did not reach statistical significance (p = 0.32). There was a correlation between S100A12 and CP (p < 0.001), and Clostridium perfringens correlated with S100A12 (p < 0.015). Neither treatment significantly affected S100A12 (p = 0.37), CP (p = 0.12), or fecal DI (p = 0.65). This study suggests that LAB is a safe supplement to use for short-term treatment in NSAID-treated dogs, but further studies are needed to determine its potential to prevent NSAID-induced enteropathy in dogs.

Fecal Lactoferrin levels as a Marker of Gastrointestinal Inflammation in Toddlers and Adults

Fecal Lactoferrin levels as a Marker of Gastrointestinal Inflammation in Toddlers and Adults

High fecal calprotectin levels are associated with SARS-CoV-2 intestinal shedding in COVID-19 patients: A proof-of-concept study.

BACKGROUNDOne third of coronavirus disease 2019 (COVID-19) patients have gastrointestinal symptoms. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA has been detected in stool samples of approximately 50% of COVID-19 individuals. Fecal calprotectin is a marker of gastrointestinal inflammation in the general population.AIMTo investigate if fecal calprotectin correlates with SARS-CoV-2 intestinal shedding in COVID-19 patients with pneumonia.METHODSPatients with SARS-CoV-2 pneumonia admitted to the Infectious Disease Unit (University Hospital of Trieste, Italy) from September to November 2020 were consecutively enrolled in the study. Fecal samples were collected and analyzed for quantification of fecal calprotectin (normal value < 50 mg/kg) and SARS-CoV-2 RNA presence by polymerase chain reaction (PCR). Inter-group differences were determined between patients with and without diarrhea and patients with and without detection of fecal SARS-CoV-2.RESULTSWe enrolled 51 adults (40 males) with SARS-CoV-2 pneumonia. Ten patients (20%) presented with diarrhea. Real-time-PCR of SARS-CoV-2 in stools was positive in 39 patients (76%), in all patients with diarrhea (100%) and in more than two thirds (29/41, 71%) of patients without diarrhea. Obesity was one of the most common comorbidities (13 patients, 25%); all obese patients (100%) (P = 0.021) tested positive for fecal SARS-CoV-2. Median fecal calprotectin levels were 60 mg/kg [interquartile range (IQR) 21; 108]; higher fecal calprotectin levels were found in the group with SARS-CoV-2 in stools (74 mg/kg, IQR 29; 132.5) compared to the group without SARS-CoV-2 (39 mg/kg, IQR 14; 71) (P < 0.001).CONCLUSIONHigh fecal calprotectin levels among COVID-19 patients correlate with SARS-CoV-2 detection in stools supporting the hypothesis that this virus can lead to bowel inflammation and potentially to the ‘leaky gut’ syndrome.

No Associations Between Dairy Intake and Markers of Gastrointestinal Inflammation in Healthy Adult Cohort

ObjectivesWe examined associations between reported dairy intake and markers of gastrointestinal (GI) inflammation in a healthy human adult population. We hypothesized there would be a negative association of yogurt intake with GI inflammation, suggesting a protective effect, and no associations of total dairy, fluid milk, and cheese intake with GI inflammation. MethodsParticipants completed up to 3 unannounced 24-hour dietary recalls using ASA24 and a Block 2014 Food Frequency Questionnaire (FFQ) to assess recent and habitual intake, respectively. Those who also provided a stool sample were included in this analysis (n = 342). Stool samples were stored on ice immediately after collection and homogenized within 24 hours. Inflammatory markers from stool, including calprotectin, neopterin, and myeloperoxidase were measured by ELISA along with LPS-binding protein (LBP) from plasma. Regression models tested associations between dairy intake variables and inflammatory markers with and without covariates: sex, age, and body mass index (BMI). As yogurt is episodically consumed, t-tests were used to examine differences in inflammatory marker levels between consumers (>1 cup per month reported in FFQ) and non-consumers. Each dairy variable was also expressed as a percentage of mean energy intake from 24-hour recalls and regressed with inflammatory markers. ResultsWithout covariates, we found no associations between total dairy, fluid milk, and yogurt from both dietary assessments with any inflammatory markers. Cheese intake reported in the FFQ was positively associated with plasma LBP (P = 0.02). However, this association was not significant after covariate adjustment. There were no significant differences in GI inflammatory marker levels between yogurt consumers and non-consumers (P > 0.05). When expressed as a percentage of mean energy intake, cheese from ASA24 was associated with increased LBP (P = 0.03), but this was not significant after adjustment for covariates. There were no other associations of dairy variables as a percentage of energy intake with GI inflammatory markers. ConclusionsWe found no clinically relevant associations between dairy intake and markers of GI inflammation in a healthy human adult cohort. Funding SourcesCalifornia Dairy Research Foundation, USDA ARS 2032–51,530-026–00D.

Evaluation of fecal calprotectin as a marker of gastrointestinal inflammation in rosacea: A case-control study.

A higher incidence of gastrointestinal diseases has been well established in patients with rosacea. However, no screening tool has been introduced for gastrointestinal disease development in rosacea. Fecal calprotectin (FC) is a calcium-binding protein, mainly derived from polymorpho-nuclear cells, such as neutrophils. It has been established as a marker of gastrointestinal inflammation. The aim of the present study was to evaluate FC levels in patients with rosacea without any gastrointestinal diseases. A prospective, case-control study was planned to investigate the relationship between rosacea and gastrointestinal involvement by evaluating FC levels and the Gastrointestinal Symptom Rating Scale (GSRS). A total of 47 patients with rosacea and 39 healthy control subjects were included in the study. The FC levels were statistically significantly higher in rosacea group than in the control group (65.96 ± 58.86 ng/mL vs 31.99 ± 20.12 ng/mL, P = .026, respectively). A statistically significant difference was also observed in GSRS values between the patient and the control groups (30.26 ± 12.48 vs 22.62 ± 7.64, P = .001, respectively). A positive correlation was noted between FC levels and the values of GSRS in the study group (r: 0.354; P = .001) and in the rosacea group (r = 0.392, P = .006). The measurement of FC may be useful in the early detection of gastrointestinal system diseases that may accompany rosacea and may provide a pathway to develop treatment strategies targeting both skin and intestinal mucosa.

Association of clinical characteristics and lifestyle factors with fecal S100/calgranulin concentrations in healthy dogs.

BackgroundFecal S100/calgranulin (S100A12 and calprotectin) concentrations are useful markers of gastrointestinal inflammation in dogs. In people, fecal S100/calgranulin concentrations are affected by age, obesity, diet and other lifestyle factors. Knowledge about the effects of such factors on fecal S100/calgranulin concentrations in dogs is currently scarce.ObjectiveTo evaluate the association between several factors and fecal S100/calgranulin concentrations in a large cohort of healthy adult dogs.MethodsSingle‐spot fecal samples from 181 healthy pet dogs and data derived from a standard questionnaire served to evaluate the effect of age, sex, reproductive status, body weight and body condition, breed type and size, vaccination, endoparasite treatment, diet, environment and travel history on fecal S100/calgranulin concentrations and the fecal calgranulin ratio (fCalR).ResultsUnivariate analysis showed a significant association of reproductive status (in female dogs) and breed size with fecal S100A12, fecal calprotectin and fCalR. Breed type was linked to fecal S100A12 concentrations and fCalR; recent vaccination (particularly with a vaccine against canine parvovirus) to fCalR. In multivariate models, breed size was linked to fecal S100A12 and calprotectin concentrations, and recent vaccination affected S100A12 concentrations.ConclusionsBreed size, recent vaccination and reproductive status in female dogs can affect fecal S100/calgranulin concentrations, and these biomarkers should be interpreted in light of those confounding factors. The utility of reference intervals for fecal canine S100/calgranulin concentrations might be improved through stratification by sex/reproductive status and breed size. Fecal canine S100/calgranulin concentrations are not confounded by age, body condition, deworming, diet, environment or travel history.

DYSREGULATION OF GASTROINTESTINAL RAGE (RECEPTOR FOR ADVANCED GLYCATION END PRODUCTS) EXPRESSION IN A SPONTANEOUS ANIMAL MODEL OF INFLAMMATORY BOWEL DISEASE

Abstract The receptor for advanced glycation end products (RAGE), a pattern recognition receptor, plays a role in chronic inflammation. Abrogation of proinflammatory RAGE signaling by ligand binding (e.g., S100/calgranulins) to soluble RAGE decoy (sRAGE) is a promising novel therapeutic avenue for chronic inflammatory diseases, such as inflammatory bowel disease (IBD). However, the opportunities for studying S100/calgranulin-RAGE pathways in conventional animal models are limited due to species differences in the expression and function of S100/calgranulins (e.g., lack of the S100A12 protein in rodents). The pathogenesis of IBD in dogs involves dysregulated innate immune responses, and serum sRAGE levels are decreased in canine IBD and normalize only with clinical remission. Thus, canine IBD may serve as a spontaneous model of IBD for such studies. This study evaluated gastrointestinal mucosal RAGE expression in dogs with IBD and the binding of RAGE to canine S100/calgranulin ligands. Epithelial RAGE expression was quantified in endoscopic gastrointestinal (i.e., gastric, duodenal, ileal, and colonic) biopsies from 12 dogs with IBD and 9 healthy control dogs by laser scanning microscopy. RAGE expression was compared between both groups of dogs and was tested for an association with patient characteristics, clinical variables, histologic lesion severity, and biomarkers of extra-gastrointestinal disease, systemic or gastrointestinal inflammation, function, or protein loss. Statistical significance (non-parametric tests) was set at p&amp;lt;0.05. RAGE:S100/calgranulin binding was investigated by immunoassay and electrophoretic techniques. RAGE expression was detected in all biopsies evaluated. Epithelial RAGE expression in the duodenum and colon was significantly higher in dogs with IBD than in healthy controls (p&amp;lt;0.04), with a trend for overexpression in the ileum, underexpression in the stomach, and a general shift towards more basal than apical epithelial RAGE expression. Serum sRAGE was correlated with duodenal RAGE expression. Several histologic (structural and inflammatory) lesion criteria and markers of gastrointestinal inflammation or protein loss were related to segmental RAGE expression (all p&amp;lt;0.04). In vitro, canine RAGE:S100A12 binding appeared more pronounced than RAGE:S100A8/A9 binding. Alterations in the epithelial expression of RAGE along the gastrointestinal tract provide evidence for a dysregulated sRAGE/RAGE axis as a characteristic of canine IBD. S100/calgranulin (S100A8/A9 and S100A12) proteins are ligands for RAGE in dogs. The role of RAGE signaling in IBD pathogenesis and its potential for developing novel targeted therapeutics warrants further exploration. Furthermore, canine IBD is a suitable spontaneous model for human IBD that may benefit further research into pathway-specific IBD treatment options that target the sRAGE/RAGE axis.

Study design, rationale and methods of the Revitalising Informal Settlements and their Environments (RISE) study: a cluster randomised controlled trial to evaluate environmental and human health impacts of a water-sensitive intervention in informal settlements in Indonesia and Fiji

IntroductionIncreasing urban populations have led to the growth of informal settlements, with contaminated environments linked to poor human health through a range of interlinked pathways. Here, we describe the design...

Fecal markers of inflammation, protein loss, and microbial changes in dogs with the acute hemorrhagic diarrhea syndrome (AHDS).

Idiopathic acute hemorrhagic diarrhea syndrome (AHDS) is characterized by acute onset of bloody diarrhea, severe dehydration, and increased vascular and intestinal mucosal permeability. Markers of gastrointestinal inflammation, protein loss, and changes in the intestinal microbiota have not been studied extensively in dogs with AHDS. For 3 consecutive days, feces were collected from dogs with AHDS, and assayed for calprotectin and S100A12 (both markers of inflammation), α1 -proteinase inhibitor (a marker of gastrointestinal protein loss), and the presence of selected species of bacteria. Concentrations of all assayed markers were significantly greater than the institutional reference intervals at the time of presentation, and all decreased significantly by Day 3 of treatment. Abundances of selected bacterial groups (Ruminococcaceae, Faecalibacterium spp., Bifidobacterium spp., and Proteobacteria) at the time of diagnosis were consistent with an intestinal bacterial dysbiosis. No differences in the abundance of bacterial groups over time was seen, except for a mild but significant decrease in Ruminococcaceae at Day 3. These results suggest that canine AHDS is associated with a significant but transient gastrointestinal loss of protein and intestinal inflammation. The intestinal bacterial dysbiosis appears to outlast the protein loss and inflammation.

Abnormal lipopolysaccharide binding protein as marker of gastrointestinal inflammation in Parkinson disease.

Objective: An inflammation-driven model of PD has been proposed based on the endotoxin lipopolysaccaride (LPS), a potential source of inflammation in the gastrointestinal system linked to neurotoxicity. Systemic exposure to bacterial endotoxin (LPS) can be determined by measuring plasma LPS binding protein (LBP). We aimed to evaluate whether lipopolysaccharide binding protein (LBP) can be used to distinguish PD subjects from control subjects and to assess whether LBP levels correlate with PD disease severity.Methods: We measured plasma LBP (ng/ml) using an ELISA kit in 94 PD subjects of various stages and 97 control subjects. Disease severity was assessed using the UPDRS and Hoehn and Yahr staging. The LBP level between the PD and control groups was compared using analysis of covariance. Spearman correlation was used to explore the relationship between LBP level and disease severity.Results: The mean LBP level in PD subjects (n = 94) was significantly different from control subjects (n = 95, p = 0.018). In PD subjects, we did not find a correlation between mean LBP level and disease severity.Conclusions: Our data suggests that LBP is one GI biomarker related to LPS induced neurotoxicity. However, there was significant variability in LBP levels within the PD and control groups, limiting its utility as a stand-alone biomarker. This study supports the role of LPS induced neurotoxicity in PD and further exploration of this pathway may be useful in developing sensitive and specific biomarkers for PD.

Complement C1q formation of immune complexes with milk caseins and wheat glutens in schizophrenia

Immune system factors including complement pathway activation are increasingly linked to the etiology and pathophysiology of schizophrenia. Complement protein, C1q, binds to and helps to clear immune complexes composed of immunoglobulins coupled to antigens. The antigenic stimuli for C1q activation in schizophrenia are not known. Food sensitivities characterized by elevated IgG antibodies to bovine milk caseins and wheat glutens have been reported in individuals with schizophrenia. Here, we examined the extent to which these food products might comprise the antigen component of complement C1q immune complexes in individuals with recent onset schizophrenia (n=38), non-recent onset schizophrenia (n=61) and non-psychiatric controls (n=63). C1q seropositivity was significantly associated with both schizophrenia groups (recent onset, odds ratio (OR)=8.02, p≤0.008; non-recent onset, OR=3.15, p≤0.03) compared to controls (logistic regression models corrected for age, sex, race and smoking status). Casein- and/or gluten-IgG binding to C1q was significantly elevated in the non-recent onset group compared to controls (OR=4.36, p≤0.01). Significant amounts of C1q-casein/gluten-related immune complexes and C1q correlations with a marker for gastrointestinal inflammation in non-recent onset schizophrenia suggests a heightened rate of food antigens in the systemic circulation, perhaps via a disease-associated altered intestinal permeability. In individuals who are in the early stages of disease onset, C1q activation may reflect the formation of immune complexes with non-casein- or non-gluten-related antigens, the presence of C1q autoantibodies, and/or a dissociated state of immune complex components. In conclusion, complement activation may be a useful biomarker to diagnose schizophrenia early during the course of the disease. Future prospective studies should evaluate the impacts of casein- and gluten-free diets on C1q activation in schizophrenia.

Fecal dimeric M2-pyruvate kinase (tumor M2-PK) in the differential diagnosis of functional and organic bowel disorders

Fecal inflammatory markers have been shown to be useful as noninvasive screening tools to differentiate patients with functional from organic bowel pathology. Of these markers calprotectin has been the most intensively studied. More recently, the dimeric isoform of M2-pyruvate kinase (tumor M2-PK) has been suggested as a marker of gastrointestinal inflammation. The aim of this study was to investigate fecal tumor M2-PK in the differentiation of functional from organic bowel disease. Fecal calprotectin and tumor M2-PK were measured in 94 controls and 105 gastroenterology outpatients with a possible diagnosis of organic bowel disease. The diagnosis was made by clinical, endoscopic, and radiological criteria. Organic bowel disease was diagnosed in 14 patients (13%). Median calprotectin and tumor M2-PK concentrations were 24.5 microg/g and 1 U/mL in controls, 23 microg/g and 1 U/mL in functional, and 227.5 microg/g and 12.6 U/mL in organic bowel disease. Sensitivity, specificity, and positive and negative likelihood ratios for diagnosis of organic bowel disease were 93%, 92%, 11.6, and 0.07 for calprotectin and 67%, 88% 5.6, and 0.18 for tumor M2-PK, respectively. Calprotectin in combination with tumor M2-PK gave a sensitivity of 64%, specificity of 98%, and likelihood ratios of 32 and 0.03. Elevated calprotectin or tumor M2-PK decreased specificity to 87%, but increased sensitivity to 100%. Tumor M2-PK is able to differentiate organic from functional bowel disease but has a lower sensitivity, specificity, and predictive value than calprotectin. Further studies are required, alone or in combination with other markers, before its usefulness in this setting can be recommended.

Fecal calprotectin levels in healthy children studied with an improved assay.

Calprotectin is a protein abundant in neutrophils. Fecal calprotectin can be used as a marker of gastrointestinal inflammation, and an improved assay has recently been developed. The aim of this study was to establish reference values for fecal calprotectin in healthy children aged between 4 and 17 years. Fecal samples were obtained from 117 healthy children classified into four age groups: 4 to 6 years, 7 to 10 years, 11 to 14 years, and 15 to 17 years. A health questionnaire was used to ensure that these children fulfilled the inclusion criterion and did not have intercurrent disease, nasal or menstrual bleeding, or nonsteroidal anti-inflammatory drug medication before the sampling period. Calprotectin was analyzed using a quantitative enzyme-linked immunosorbent assay (Calprest, Eurospital SpA, Trieste, Italy). Children with fecal calprotectin values >50 microg/g were asked to deliver an additional sample. The overall median fecal calprotectin concentration was 13.6 microg/g (95% confidence interval, 9.9-19.5 microg/g) in the 117 children. In the different age groups, 4 to 6 years, 7 to 10 years, 11 to 14 years, and 15 to 17 years, the median calprotectin concentrations were 28.2, 13.5, 9.9, and 14.6 microg/g, respectively. Of these children, 104 (89%) had a concentration <50 microg/g. The remaining 13 children with a calprotectin concentration >50 microg/g delivered one additional fecal sample. All showed a lower concentration in the second sample except for one teenager who later proved to have proctitis. The suggested cutoff level for adults (<50 microg/g) can be used for children aged from 4 to 17 years regardless of sex. A fecal calprotectin concentration >50 microg/g warrants follow-up.

Fecal Calprotectin Levels in Healthy Children Studied With an Improved Assay

ABSTRACTBackgroundCalprotectin is a protein abundant in neutrophils. Fecal calprotectin can be used as a marker of gastrointestinal inflammation, and an improved assay has recently been developed. The aim of this study was to establish reference values for fecal calprotectin in healthy children aged between 4 and 17 years.MethodsFecal samples were obtained from 117 healthy children classified into four age groups: 4 to 6 years, 7 to 10 years, 11 to 14 years, and 15 to 17 years. A health questionnaire was used to ensure that these children fulfilled the inclusion criterion and did not have intercurrent disease, nasal or menstrual bleeding, or nonsteroidal anti‐inflammatory drug medication before the sampling period. Calprotectin was analyzed using a quantitative enzyme‐linked immunosorbent assay (Calprest, Eurospital SpA, Trieste, Italy). Children with fecal calprotectin values &gt;50 μg/g were asked to deliver an additional sample.ResultsThe overall median fecal calprotectin concentration was 13.6 μg/g (95% confidence interval, 9.9–19.5 μg/g) in the 117 children. In the different age groups, 4 to 6 years, 7 to 10 years, 11 to 14 years, and 15 to 17 years, the median calprotectin concentrations were 28.2, 13.5, 9.9, and 14.6 μg/g, respectively. Of these children, 104 (89%) had a concentration &lt;50 μg/g. The remaining 13 children with a calprotectin concentration &gt;50 μg/g delivered one additional fecal sample. All showed a lower concentration in the second sample except for one teenager who later proved to have proctitis.ConclusionsThe suggested cutoff level for adults (&lt;50 μg/g) can be used for children aged from 4 to 17 years regardless of sex. A fecal calprotectin concentration &gt;50 μg/g warrants follow‐up.