Elevated Fecal Calprotectin Levels Research Articles

RARE CASE OF ASCARIASIS DETECTED BY COLONOSCOPY ON THE BACKGROUND OF ELEVATED LEVELS OF FECAL CALPROTECTIN

Introduction: The causative agents of ascariasis in humans are two species: Ascaris lumbricoides and Ascaris suum. For diagnosis, a fecal sample is most often examined. In some cases, the parasite can be identified when coming out with the intestinal passage, and very rarely up on colonoscopy. Aim to present a rare case of ascariasis where the diagnosis was made by colonoscopy on the background of elevated levels of fecal calprotectin (f-CP). Case presentation: A colonoscopy was performed on a 52-year-old female patient due to elevated f-CP. The patient had no complaints. The colonoscopy did not detect pathological changes of the intestinal mucosa, but documented larval stages of Ascaris spp. freely moving in the lumen of the large intestine. The patient was treated with albendazole. Subsequent parasitological examinations of fecal samples were negative. Discussion: In developed countries, the transmission of Ascaris lumbricoides is greatly reduced. On the background of a very limited transmission of Ascaris lumbricoides, many authors consider that most of the sporadic cases of ascariasis are due to Ascaris suum. In the case described by us, the f-CP levels normalized after the treatment, and for this reason, we cannot categorically reject the relationship between Ascaris infection and elevated f-CP levels. Conclusion: The presented clinical case is of interest due to the unusual way of diagnosi ascariasis. In the absence of clinical symptoms, and pathological changes of blood and biochemical parameters, except for elevated fecal calprotectin, inflammatory colon disease was suspected and was colonoscopy performed on this occasion.

P913 Intestinal Ultrasound in paediatric Crohn’s disease reduces the need for subsequent ileocolonoscopy

Abstract Background Approximately 20% of patients with Crohn's disease (CD) are diagnosed during childhood (pCD). At diagnosis, the vast majority (87%) of patients with pCD demonstrate severe disease activity.(1) Severe disease activity necessitates intensive treatment followed by frequent blood tests, faecal calprotectin tests, and endoscopic procedures. Ileocolonoscopy is burdensome for the patient, as bowel preparation and general anaesthesia are needed, and furthermore, the procedure is costly. In recent European guidelines for pCD management, Intestinal Ultrasound (IUS) is recommended for clinical follow-up. Our objective was to investigate the extent to which patients with pCD underwent subsequent endoscopy after having IUS performed during their follow-up regimen. Methods We conducted a retrospective descriptive cohort study, encompassing all patients with pCD at a referral center (Department of Paediatric and Adolescence Medicine, Copenhagen University Hospital, Amager and Hvidovre) who had undergone a minimum of one ultrasound examination over a 2.5-year period (May 1, 2021, to November 1, 2023). Results A total of 29 patients with pCD were enrolled in the study. Demographic data can be found in Table 1. The median follow-up since time of diagnosis was 40 months (interquartile range (IQR) 30-57). Time to the first IUS examination after diagnosis was median 28 months (IQR 13-49). The indications for IUS were as follows: Clinical suspicion of disease activity and/or elevated faecal calprotectin levels (66% of cases), evaluation of disease activity after initiating biologic therapy (10%), assessment of disease activity status (14%), suspicion of treatment failure (7%) and other indications (3%). Following the IUS procedure, 10% of patients subsequently underwent ileocolonoscopy, which was performed within 11, 14, or 53 days after IUS. Among the remaining 90% of patients, 14% underwent ileocolonoscopy 8-16 months after the IUS procedure, while 76% never had a repeat ileocolonoscopy performed after a median follow-up of 342 days (IQR 247-441) after IUS. Conclusion In 90% of patients with pCD IUS can be used to evaluate disease activity without the necessity for an ileocolonscopy in the subsequent 12 moths of follow up.

Enteric health of children in coastal Bangladesh: A cross-sectional study

Objective: To investigate the environmental factors associated with enteric diseases among children in coastal Bangladesh. Methods: A cross-sectional descriptive study was conducted between July 2018 and November 2018, enrolling 59 preschool children from Nabipur village in Bhola district and Paikgacha village in Khulna district. Keraniganj in Dhaka district was selected as a control village for comparison. A self-administered semi-structured questionnaire was used to collect data, including health information (height, weight, food habits, and hygiene practices), age and history of medication. Food, water and stool samples were also collected from the participants. Results: Children in coastal zones experience an average of 6 episodes per year as compared to 3 diarrhea episodes in Dhaka. The salinity of drinking water varied significantly across the study sites (480±30 ppm in Bhola, 450±36 ppm Khulna, 180±17 ppm in Dhaka). The coastal children had higher fecal calprotectin levels (67±2.7 ng/mg and 77±12 ng/mg in Khulna and Bhola, respectively) compared to those living in Dhaka (25±1.5 ng/mg). The levels of fecal calprotectin and fecal s100A12 were both positively correlated with the salinity of drinking water in Bhola (r=0.66 for calprotectin; r=0.51 for s100A12) and Khulna (r=0.77 for calprotectin; r=0.54 for s100A12). Conclusions: The study revealed a positive correlation between the salinity levels in drinking water and the elevated levels of fecal calprotectin and fecal s100A12 in children living in coastal villages of Khulna and Bhola in Bangladesh, whereas no such association was found among children living in central Bangladeshi locality of Keraniganj, Dhaka.

Fecal calprotectin levels in acute anterior uveitis in patients with spondyloarthritis.

This study measured fecal calprotectin levels in a series of patients with anterior uveitis in order to determine whether anterior uveitis patients with associated spondyloarthritis have higher levels of fecal calprotectin than patients with anterior uveitis of other etiologies. A third group of patients with spondyloarthritis without uveitis was also evaluated to understand the role of acute anterior uveitis in increasing fecal calprotectin. In this cross-sectional study, 28 patients were divided into three groups: (a) Group 1, spondyloarthritis and uveitis (n=9); (b) Group 2, spondyloarthritis without uveitis (n=10); and (c) Group 3, uveitis without spondyloarthritis (n=9). The levels of fecal calprotectin were determined. Groups 1 and 2 showed higher median fecal calprotectin levels (101.0 and 93.0 µg/g, respectively) compared with Group 3 (9.0 µg/g) (p=0.02). However, no relationship between fecal calprotectin levels and the presence of uveitis with spondyloarthritis could be demonstrated. Patients with spondyloarthritis with or without acute anterior uveitis have significantly elevated levels of fecal calprotectin. This test may be useful for differentiating spondyloarthrit-associated uveitis from uveitis of other etiologies.

Possible Correlation between Giardia duodenalis Genotypes and Fecal Calprotectin in Children with Diarrhea.

Giardiasis is one of the leading causes of diarrhea, particularly among children under the age of five in developing countries. Fecal calprotectin (FC) is an important biomarker for diagnosis and monitoring of inflammtory bowel disease, but other diagnoses should be considered in light of its elevation. We aimed to evaluate FC level in patients diagnosed with giardiasis and elucidate a possible correlation between Giardia genotypes and FC levels. Overall, 120 fecal samples were collected from children aged 4-12 years and tested for giardiasis by light microscopy. Out of which, 50 samples were enrolled within two groups: group I "cases" and group II "controls" and then subjected to PCR amplification, sequencing of the beta-giardin (bg) gene of the parasite, and FC evaluation. Assemblage B was identified in 75%, and assemblage A in 25% of samples. FC levels were statistically elevated in "group I" in comparison to "group II". Likewise, there was a statistically significant difference between FC levels in patients infected with assemblage A and assemblage B with a mean of 114 μg/gm and 202 μg/gm, respectively. The study highlighted the possible association between Giardia genotype B and elevated FC levels, further detailed studies are necessary to clarify these finding.

Monogenic inflammatory bowel disease with STXBP2 mutations is not resolved by hematopoietic stem cell transplantation but can be alleviated via immunosuppressive drug therapy

STXBP2, encoding syntaxin-binding protein 2, is involved in intracellular organelle trafficking and is associated with familial hemophagocytic lymphohistiocytosis type 5. Although STXBP2 mutations reportedly cause monogenic inflammatory bowel disease, the clinical course and underlying pathogenic mechanisms remain unclear. We identified a novel mutation in STXBP2 [c.1197delC, p.Ala400fs] in a boy with congenital intractable diarrhea and hemophagocytic lymphohistiocytosis (HLH). HLH was treated with intravenous prednisolone, cyclosporine, and dexamethasone palmitate. Hematopoietic stem cell transplantation (HSCT) along with prophylaxis for graft-versus-host-disease was performed at 5 months of age. Additionally, colonoscopies done before and after HSCT showed mild colitis with cryptitis. The patient showed elevated fecal calprotectin levels and persistent diarrhea even after HSCT and required partial parenteral nutrition. While anti-inflammatory treatment reduced diarrhea, it was not completely normalized even after HSCT, suggesting that the pathogenesis of inflammatory bowel disease associated with STXBP2 mutations involves both hyperinflammation and functional epithelial barrier defects.

Supporting the diagnosis of infantile colic by a point of care measurement of fecal calprotectin.

BackgroundInfantile colic (IC) is a condition characterized by extensive crying which affects about 20% of all infants during their first months of life. Most pediatricians diagnose IC only based on their clinical experience.AimInvestigating if a measurement of fecal calprotectin can support the diagnosis of IC.MethodsThe crying behavior of newborns was assessed using the Wessel's criteria. Fecal calprotectin levels were measured in non-colicky and colicky babies using a standard test that can be used at the time and place of patient care (point of care (PoC) measurement).ResultsColicky babies were found to have significantly elevated fecal calprotectin levels. Calprotectin levels were not influenced by gender, type of feeding, gestation age or birth weight. However, significantly elevated fecal calprotectin levels were found in cesarean section born babies. Fecal calprotectin ≥100 μg/g correlated with a colicky status of an infant while those <100 μg/g indicated a non-colicky status the error margin was 11.2 and 13.2%, respectively. Combining data of fecal calprotectin with information about the type of delivery made it possible to determine the colicky status in vaginally-born infants with fecal calprotectin ≥100 μg/g with an accuracy of 97.8%. As elevated fecal calprotectin levels in cesarean-born infants can be caused by IC, but also by the disturbed gut microbiota commonly found in these babies, the accuracy of diagnosing the colicky status of a cesarean-born infant with calprotectin levels ≥100 μg/g was less accurate (accuracy rate of 76.5%).ConclusionData from the study suggest that measuring fecal calprotectin should be considered by pediatricians to support the diagnosis of IC.The study was registered at ClinicalTrials.gov under NCT04666324.

AB0662 Elevated fecal calprotectin in early systemic sclerosis

BackgroundGastrointestinal (GI) morbidity is prevalent in systemic sclerosis (SSc), causing a reduction in quality of life and increased mortality, but has been difficult to assess objectively [1]. Elevated levels of fecal calprotectin (F-cal), a biomarker of GI inflammation, has previously been observed in patients with SSc [2]. F-cal has not been explored in early SSc and its diagnostic potential in the classification of SSc has not been studied.ObjectivesOur objectives were; 1) study F-cal levels in early SSc; 2) investigate the discriminatory power of F-cal; 3) explore F-cal in relation to GI features of SSc.MethodsConsecutive referred patients with suspected new-onset SSc without concurrent non-SSc GI disease were invited to this study. Patients were classified as SSc if meeting ACR-EULAR criteria, or SSc mimickers if they did not. GI symptoms and use of NSAID or PPI was noted. F-cal was measured and levels &gt;50ug/g were classified as elevated. F-cal was also measured in age- and sex matched controls without rheumatological disease.ResultsOf 137 patients, 92 were classified as SSc and 45 as SSc mimickers. Elevated F-cal was significantly more common in SSc patients compared to the control group (38% vs 7.3%; p &lt; 0.001) but not compared to the SSc mimicker patients (38% vs 31%; p = 0.427). The median F-cal level was higher in SSc patients compared to controls (35 µg/g vs ≤30 µg/g; p ≤ 0.001) but not compared to the SSc mimicker patients (35 µg/g vs ≤30 µg/g; p = 0.248). Elevated F-cal was not associated with any GI symptoms. Elevated F-cal was more common in patients who used PPI (OR 7.14; 95% CI 2.56-29.93; p &lt; 0.001).ConclusionIn this study, we demonstrate that elevated levels of F-cal are prevalent already in the early stages of SSc. These results are in line with previous data suggesting that GI involvement may be present in early SSc.Table 1.Frequency of GI features and association to F-cal elevation (n = 92)GI features (n, %)Normal F-cal, n = 57Elevated F-cal, n = 35Odds Ratio (95% CI)Dysphagia19 (35%)12 (34%)0.99 (0.41-2.41)Reflux symptoms33 (59%)23 (68%)1.46 (0.60-3.56)Fecal incontinence9 (16%)3 (8.6%)0.50 (0.08-2.22)Patient-reported involuntary weightloss11 (20%)8 (23%)1.21 (0.43-3.39)Dilated esophagus on HRCT8 (16%)8 (28%)1.95 (0.64-5.94)NSAID use12 (21%)6 (17%)0.78 (0.26-2.30)PPI use23 (40%)29 (83%)7.14 (2.56-19.93)Figure 1.F-cal measurements by group. Median value represented by horizontal bar.

The Clinical Utility of Faecal Calprotectin in Patients with Differentiated and Undifferentiated Spondyloarthritis: Relevance and Clinical Implications.

There is cumulative evidence in the literature supporting a potential role of faecal calprotectin (FCP) as a biomarker for gut inflammation in spondyloarthritis (SpA). However its relevance in undifferentiated SpA (USpA) is still uncertain. The aim of the current study is to assess the diagnostic significance of FCP levels in patients with differentiated and undifferentiated SpA. A total of 52 differentiated SpA, 33 USpA and 50 controls could be included. For all patients, clinical evaluation, routine laboratory investigations, FCP levels, and occult blood in stool were performed. When indicated imaging and/or endoscopies were performed. The differentiated SpA patients were 12 (23.1%) with ankylosing spondylitis, 21 (40.4%) with psoriatic arthritis, 13 (25%) with ulcerative colitis, 5 (9.6%) with Crohn's disease (CD) and one (1.9%) with reactive arthritis. The mean FCP level in 85 patients correlated with CRP and ESR. Within the SpA group ulcerative colitis and Crohn's disease patients had increased FCP levels compared to other SpA subgroups and USpA patients (p<0.001). The mean FCP levelwas significantly higher in the SpA patients compared to USpA and controls (p<0.001). Elevated FCP levels may identify patients who are most likely to have SpA already in the unclassified phase of the disease. Further studies in different series of patients are needed to evaluate the potential diagnostic and prognostic roles of FCP in both differentiated and undifferentiated phases of the disease.

P539 COVID-19 is Associated with Long-term Elevated Fecal Calprotectin Levels in Patients with Crohn’s Disease but not in Ulcerative Colitis

BackgroundData regarding the long-term effects of COVID-19 on patients with Inflammatory bowel disease is scarce. Fecal calprotectin (FC) correlates with IBD clinical and endoscopic activity. We compared fecal calprotectin levels between patients with COVID-19 to a control group tested negative to SARS-CoV-2.MethodsWe gathered data from a large health medical organization in Israel of insured individuals who underwent a SARS-COV-2 PCR test from March 1, 2020, to December 31, 2020. Among patients with IBD, data regarding fecal calprotectin taken 30–365 days before SARS-CoV-2 testing was gathered. We compared fecal calprotectin levels taken at least 30 days following COVID-19 infection to those who tested negative.Results1924 Crohn’s disease (CD) patients and 949 Ulcerative Colitis (UC) patients were tested for SARS-CoV-2. 322 (16.7%) were tested positive in the CD group and 114 (13.7%) in the UC group.Pre-COVID-19 calprotectin levels did not show statistically significant differences between patients who ended up testing positive for SARS-CoV-2 and those who tested negative in CD (377 ±759.08 vs. 451.84±869, p-value = 0.4) and in UC (466.93±766.69 vs. 617.91 ±1243.99 p-value=0.37). Post-COVID-19 fecal calprotectin was higher among patients with CD who were tested positive than those who tested negative for SARS-CoV-2 (617.42±832.68 vs. 355.94±1207.46, p value=0.04). In a multivariate linear regression controlling for age, gender, BMI, smoking status, and pre-COVID-19 fecal calprotectin, SARS-CoV-2 positivity was associated with higher fecal calprotectin levels (p value=0.03). In contrast, there was no statistically significant change in fecal calprotectin levels among patients with UC and SARS-CoV-2 positivity (547.2±1089 vs.458.32± 689 p value=0.9). In a 2:1 propensity score-matched cohort (n=264), calprotectin levels were higher among patients with CD who suffered from COVID-19 compared to controls (657.64 vs. 384.94 p-value = 0.03)ConclusionPatients with CD who had COVID-19 have higher FC levels compared to similar CD patients who did not have COVID-19. This finding was not found in patients with UC.

A Randomized, Double-Blind, Placebo-Controlled Trial to Assess the Efficacy and Safety of Lactiplantibacillus plantarum CJLP243 in Patients with Functional Diarrhea and High Fecal Calprotectin Levels.

Micro-inflammation in the gut, assessed by fecal calprotectin (FC), is considered a component of the pathogenesis of functional diarrhea (FD). Since probiotics may suppress micro-inflammation in the intestine by competing with harmful bacteria, we hypothesized that they would reduce the ratio of loose stool symptoms and gut inflammation in patients with FD. We conducted a double-blind, placebo-controlled trial to assess the clinical and laboratory effects of Lactobacillus plantarum CJLP243 in FD patients with elevated FC levels for two months. Twenty-four patients diagnosed with FD with elevated FC levels were randomly assigned to either a probiotic group or a placebo group. After 2 months, 10 patients in the probiotic group and 12 patients in the placebo group completed the study, and FD symptoms, FC values, and intestinal flora were re-evaluated in these subjects. The percentage of subjects who had adequate FD relief (decrease in loose stool frequency) in the probiotic group was significantly increased after two months compared with the baseline. In addition, the probiotic group showed a statistically significant decrease in log-transformed FC values compared with the pre-treatment group, whereas the placebo group showed no difference before and after the intervention. Furthermore, the levels of Leuconostoc genus organisms in the gut microbiota composition in the probiotic group increased significantly after the end of the study compared with the baseline values. In this preliminary exploratory research, we found that two months of Lactiplantibacillus plantarum CJLP243 treatment resulted in FD symptom improvement, reduced FC values, and increased Leuconostoc levels, suggesting that the intake of Lactiplantibacillus plantarum was helpful in those patients. These findings need to be validated via further clinical studies.

Juvenile Polyps in Bangladeshi Children and Their Association with Fecal Calprotectin as a Biomarker.

PurposeColonoscopy is considered the most reliable method for the diagnosis of juvenile polyps. However, colonoscopic screening is an invasive and expensive procedure. Fecal calprotectin (FCP), a marker of intestinal inflammation, has been shown to be elevated in patients with polyps. Therefore, this study aimed to evaluate FCP as a screening biomarker for the diagnosis of juvenile polyps.MethodsThis cross-sectional, observational study was conducted at the Pediatric Gastroenterology and Nutrition Department, Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh. For children with polyps, colonoscopic polypectomy and histopathology were performed. FCP levels were analyzed before and 4 weeks after polypectomy in all patients. Information was recorded in a datasheet and analyzed using the computer-based program SPSS.ResultsThe age of the children was between 2.5 and 12 years. Approximately 93% of the polyps were found in the rectosigmoid region. Children with juvenile polyps had elevated levels of FCP before polypectomy that subsequently normalized after polypectomy. The mean FCP levels before and after polypectomy were 277±247 µg/g (range, 80–1,000 µg/g) and 48.57±38.23 µg/g (range, 29–140 µg/g) (p<0.001), respectively. The FCP levels were significantly higher in patients with multiple polyps than in those with single polyps. Moreover, mean FCP levels in patients with single and multiple polyps were 207.6±172.4 µg/ g and 515.4±320.5 µg/g (p<0.001), respectively.ConclusionColonic juvenile polyps were found to be associated with elevated levels of FCP that normalized after polypectomy. Therefore, FCP may be recommended as a noninvasive screening biomarker for diagnosis of colonic juvenile polyps.

Gut dysbiosis and gut-derived inflammation contribute to endothelial dysfunction in Alzheimer's disease: An in-vivo cross-sectional study.

Although recent data support an association between certain bacterial strains and Alzheimer's Disease (AD), it is not clear how these alterations contribute to different aspects of the disease. Increasing evidences also from our group (Cattaneo, AAIC 2020), suggest that endothelial dysfunction, reflected by the upregulation of cell adhesion molecules (CAMs), might have a role in AD pathology development and might be affected by inflammatory mediators. This study aimed at evaluating the gut microbiota (GMB) profile and its association with CAMs and local and systemic inflammation in AD patients. Sixty-six older persons without cognitive performance (HC) and 68 AD patients were recruited and stool and blood samples were collected. Bacterial composition of fecal samples was inferred using 16S sequencing, analyzed with QIIME 2 (Quantitative Insights into Microbial Ecology, https://qiime2.org/). Inflammatory mediators were quantified in the blood using the mesoscale platform (for cytokines) and in the stools using ELISA (for calprotectin), CAMs by FACS. Compared to HC, AD patients showed i) lower abundance of genera known to have anti-inflammatory, neuroprotective or other beneficial effects on the epithelial barrier (as Akkermansia, Roseburia and Fusicatenibacter) as well as higher abundance in pro-inflammatory genera (as Desulfovibrio) (Lefse, p< 0.039); ii) higher levels of the proinflammatory cytokine IL8 (p= 0.044) in the blood and calprotectin in the stools (p= 0.012); iii) higher level of several adhesion molecules (NCAM, PECAM-1, P-, L-, E-Selectin; p< 0.024) in the blood. Low abundance of the beneficial genera as well as high abundance of the proinflammatory genera were associated with elevated levels of fecal calprotectin and blood CAMs (0.19<|rho|<0.30, p<.048). Finally, high calprotectin levels were associated with elevated CAMs expression (0.22<|rho|<0.32, p<.017). These findings confirm our previous results showing that gut dysbiosis was associated with endothelial dysfunction. In addition, we showed that gut derived inflammation, linked to both altered bacteria abundance and CAMs upregulation, might contribute to AD.

Fecal calprotectin levels used as a noninvasive method for screening for chronic gastritis in pediatric patients. A descriptive study.

Gastritis consists of inflammation of the gastric mucosa and is one of the main causes of dyspeptic symptoms in children. To investigate the presence of inflammation by evaluating fecal calprotectin (FC) in children diagnosed with chronic gastritis. Descriptive study in Pediatric Gastroenterology Department of Ondokuz Mayis University Hospital in Turkey. Between January 2016 and July 2018, FC levels were compared retrospectively in children with chronic gastritis (histopathology-based diagnosis), patients with inflammatory bowel disease (IBD) and healthy children. A total of 67 chronic gastritis patients (61.2% girls) with a mean age of 13.09 ± 3.5 years were evaluated. The mean FC levels were 153.4 μg/g in the chronic gastritis group, 589.7 μg/g in the IBD group and 43.8 μg/g in the healthy group. These levels were higher in chronic gastritis patients than in healthy individuals (P = 0.001) and higher in IBD patients than in the other two groups (P < 0.001). The FC level in the patients with chronic active gastritis (156.3 μg/g) was higher than in those with chronic inactive gastritis (150.95 μg/g) (P = 0.011). Among the patients with chronic active gastritis, the FC level was significantly higher in Helicobacter pylori-positive individuals than in negative individuals (P = 0.031). We confirmed the association between increased FC and chronic gastritis. Elevated FC levels may be seen in patients with chronic active gastritis. In order to be able to use FC as a screening tool for chronic gastritis, further studies in a larger study group are needed.

Elevated fecal and serum calprotectin in COVID-19 are not consistent with gastrointestinal symptoms

Intestinal epithelial cell damage caused by SARS-CoV-2 infection was thought to be associated with gastrointestinal symptoms and decreased fecal consistency. The association of the gastrointestinal symptoms with the COVID-19-mediated inflammatory response triggered by the gastrointestinal immune system was investigated in this paper. Intestinal inflammation marker fecal calprotectin along with serum calprotectin and other inflammatory markers were measured in COVID-19 cases with and without GI manifestations as well as healthy individuals. Analyses were performed to compare COVID-19 patient subgroups and healthy controls and examine the relationship between fecal and serum calprotectin levels with gastrointestinal symptoms and disease severity. COVID-19 patients (n = 70) were found to have markedly elevated median levels of fecal (124.3 vs. 25.0 µg/g; P < 0/0001) and serum calprotectin (3500 vs. 1060 ng/mL; P < 0/0001) compared with uninfected controls. Fecal and serum calprotectin levels were not significantly different between COVID-19 patients who displayed GI symptoms and those who did not. Compared with other acute phase markers, both fecal and serum calprotectin were superior in identifying COVID-19 patients who progressed to severe illness. Although the progression of COVID-19 disease is marked by an elevation of fecal and serum calprotectin, gastrointestinal symptoms or diarrhea were not correlated with calprotectin increase level.

S2947 A Case of Small Bowel Neuroendocrine Tumor Presenting With Elevated Fecal Calprotectin

Introduction: Fecal calprotectin (FC) is a marker of intestinal inflammation most useful in the management of inflammatory bowel diseases (IBD). It is mostly found in the cytoplasm of granulocytes, and to a lesser extent, monocytes. Conditions such as diverticular disease, Microscopic colitis, and Graft versus Host Disease have been associated with elevated FC levels. Historically, this calcium and zinc binding protein has been used to distinguish between IBD and functional bowel disease. We find that any mechanism causing gut mucosal injury can lead to increased migration of neutrophils into the gut lumen, with eventual release of calprotectin by these leukocytes. Gastrointestinal malignancy, particularly colorectal cancer, is one such entity that has been studied to show elevated FC. On the other hand, no cases of neuroendocrine tumors (NET) of the gastrointestinal tract with elevated FC have been reported. Case Description/Methods: Our patient is a healthy 48-year old male who presented to gastroenterology clinic for evaluation of abdominal cramping and loose stools. Initial EGD and colonoscopy with biopsies were normal. His symptoms persisted and stool studies resulted an elevated FC of 595 μg/g (normal 0-120 μg/g). CT enterography showed a small bowel stricture near the ileocecal valve (Figure 1). Suspecting Crohn’s disease, we performed a push enteroscopy and repeat colonoscopy with biopsy-once again which were negative. Subsequent laparoscopic resection of small bowel, 12.5 x 5.0cm in diameter, was performed. A 1.0 x 1.0 x 0.4cm well-circumscribed tan mass was identified within the aforementioned small bowel stricture. Pathology sent was consistent with well-differentiated neuroendocrine tumor. Patient had resolution of symptoms and follows with oncology for surveillance. Discussion: FC is a biomarker of gastrointestinal inflammation that can be elevated in multiple conditions. The most studied medical pathologies linked with elevated FC include IBD, infectious gastroenteritis/colitis, microscopic colitis, and diverticular disease. Perhaps due to the wide use of other neuroendocrine biomarkers such as Chromogranin A and 5-hydroxyindoleacetic acid, coupled with the infrequency of small bowel NETs, FC level correlation has not been investigated. Neuroendocrine tumors of the small bowel are uncommon and often present with vague symptoms and metastatic disease. The differential diagnosis for unexplained elevated FC remains broad and it should include small bowel malignancies such as neuroendocrine tumors.Figure 1.: Coronal view of CT enterography showing small bowel stricture and dilated proximal small bowel.

Investigation of asymptomatic intestinal inflammation in ankylosing spondylitis by fecal calprotectin

Background and Study AimsThis study aimed to investigate the prevalence of intestinal inflammation in patients with ankylosing spondylitis (AS) by assessing fecal calprotectin (FC) levels and comparing them with those in patients with rheumatoid arthritis (RA) and non-inflammatory rheumatic diseases. Our secondary aim was to correlate FC levels with antirheumatic treatment, nonsteroidal anti-inflammatory drug (NSAID) usage, and disease activity measures. Patients and MethodsThis cross-sectional study included 97 patients with AS fulfilling the modified New York criteria, 48 patients with RA fulfilling the American College of Rheumatology criteria, and 49 patients with non-inflammatory rheumatic diseases. All patients were questioned about intestinal complaints, and symptomatic patients were excluded. Disease activity was measured in the AS and RA patient groups. ResultsThe AS group had a significantly higher FC test positivity rate than the RA group (p = 0.016). Furthermore, the AS group had FC levels that were negatively correlated with disease duration (p = 0.04). FC levels were not correlated with any disease activity index, erythrocyte sedimentation rate, C-reactive protein, uveitis, or peripheral arthritis. Patients with AS who used NSAIDs had significantly higher FC levels than nonusers (p = 0.001). ConclusionsThis study revealed that 11% of patients with AS without intestinal complaints had elevated FC levels. FC levels were not correlated with disease activity in AS. Subclinical intestinal inflammation was higher in the early stages of AS. The AS group had a significantly higher FC test positivity than the RA group. In the AS group, NSAID users had significantly higher FC levels than nonusers; thus, no statistically significant difference was observed between biological agent users and nonusers.

Experimental infectious challenge in pigs leads to elevated fecal calprotectin levels following colitis, but not enteritis

BackgroundFecal calprotectin is largely applied as a non-invasive intestinal inflammation biomarker in human medicine. Previous studies in pigs investigated the levels of fecal calprotectin in healthy animals only. Thus, there is a knowledge gap regarding its application during infectious diarrhea. This study investigated the usefulness of fecal calprotectin as a biomarker of intestinal inflammation in Brachyspira hyodysenteriae and Salmonella Typhimurium infected pigs.ResultsFecal samples from pigs with colitis (n = 18) were collected from animals experimentally inoculated with B. hyodysenteriae (n = 8) or from sham-inoculated controls (n = 3). Fecal samples from pigs with enteritis (n = 14) were collected from animals inoculated with Salmonella enterica serovar Typhimurium (n = 8) or from sham-inoculated controls (n = 4). For both groups, fecal samples were scored as: 0 = normal; 1 = soft, wet cement; 2 = watery feces; 3 = mucoid diarrhea; and 4 = bloody diarrhea. Fecal calprotectin levels were assayed using a sandwich ELISA, a turbidimetric immunoassay and a point-of-care dipstick test. Fecal calprotectin levels were greater in colitis samples scoring 4 versus ≤ 4 using ELISA, and in feces scoring 3 and 4 versus ≤ 1 using immunoturbidimetry (P < 0.05). No differences were found in calprotectin concentration among fecal scores for enteritis samples, regardless of the assay used. All samples were found below detection limits using the dipstick method.ConclusionsFecal calprotectin levels are increased following the development of colitis, but do not significantly change due to enteritis. While practical, the use of commercially available human kits present sensitivity limitations. Further studies are needed to validate the field application of calprotectin as a marker of intestinal inflammation.

P204 Elevated Fecal Calprotectin Levels Predict Flare-up in Patients with Inflammatory Bowel Disease During International Air Travel

Abstract Background Inflammatory bowel disease (IBD) patients often experience disease flare-ups during international air travel. We aimed to evaluate the proportion of patients that experiences IBD flares during international air travel and identify risk factors associated with enhanced disease activity. Methods Patients with scheduled international air travel were enrolled in the study from the Seoul National University Bundang Hospital IBD clinic. Flight information and clinical data were collected via questionnaires and personal interviews, and risk factors associated with IBD flares were determined. Results Between May 2018 and February 2020, 94 patients were enrolled in the study (mean age, 33.0 years; males, 53.2%; mean disease duration, 56.7 months), including 56 (59.6%) with ulcerative colitis and 38 (40.4%) with Crohn’s disease. Of the 94 patients enrolled, 15 (16.0%) experienced an IBD flare-up and 79 (84.0%) remained in remission throughout travel. Logistic regression analysis revealed that high fecal calprotectin levels before travel (odds ratio [OR]: 1.001, 95% confidence interval [CI]: 1.000–1.001, p = 0.016), the presence of a comorbidity (OR: 6.334, 95% CI: 1.129–35.526, p = 0.036), and a prior emergency room visit (OR: 5.283, 95% CI: 1.085–25.724, p = 0.039) were positively associated with disease flare-up. The previous and current use of immunomodulators and biologics, time of flight, altitude, number countries visited, travel duration, objective of visit, and previous medical consultations were not associated with disease flare-up. Conclusion Factors including fecal calprotectin levels, prior visit(s) to the ER, and the presence of a comorbidity predicted IBD flare-up during international travel.

Pathophysiological mechanisms underlying gastrointestinal symptoms in patients with COVID-19.

Gastrointestinal (GI) symptoms, such as diarrhea, abdominal pain, vomiting, and anorexia, are frequently observed in patients with coronavirus disease 2019 (COVID-19). However, the pathophysiological mechanisms connecting these GI symptoms to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections remain elusive. Previous studies indicate that the entry of SARS-CoV-2 into intestinal cells leads to downregulation of angiotensin converting enzyme 2 (ACE2) receptors resulting in impaired barrier function. While intestinal ACE2 functions as a chaperone for the amino acid transporter B0AT1, the B0AT1/ACE2 complex within the intestinal epithelium acts as a regulator of gut microbiota composition and function. Alternations to the B0AT1/ACE2 complex lead to microbial dysbiosis through increased local and systemic immune responses. Previous studies have also suggested that altered serotonin metabolism may be the underlying cause of GI disorders involving diarrhea. The findings of elevated plasma serotonin levels and high fecal calprotectin in COVID-19 patients with diarrhea indicate that the viral infection evokes a systemic inflammatory response that specifically involves the GI. Interestingly, the elevated proinflammatory cytokines correlate with elevated serotonin and fecal calprotectin levels further supporting the evidence of GI inflammation, a hallmark of functional GI disorders. Moreover, the finding that rectal swabs of COVID-19 patients remain positive for SARS-CoV-2 even after the nasopharynx clears the virus, suggests that viral replication and shedding from the GI tract may be more robust than that of the respiratory tract, further indicating fecal-oral transmission as another important route of viral spread. This review summarized the evidence for pathophysiological mechanisms (impaired barrier function, gut inflammation, altered serotonin metabolism and gut microbiota dysbiosis) underlying the GI symptoms in patients with COVID-19.