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

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hajar Shokri-Afra ◽  
Ahmad Alikhani ◽  
Bahman Moradipoodeh ◽  
Farshid Noorbakhsh ◽  
Hafez Fakheri ◽  
...  
Keyword(s):  
Intestinal Inflammation ◽  
Cell Damage ◽  
Gastrointestinal Symptoms ◽  
Fecal Calprotectin ◽  
Severe Illness ◽  
Intestinal Epithelial ◽  
Inflammation Marker ◽  
Gi Symptoms ◽  
The Relationship ◽  
Patient Subgroups

AbstractIntestinal 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.

scholarly journals Increased Fecal Calprotectin Is Associated with Worse Gastrointestinal Symptoms and Quality of Life Scores in Children with Cystic Fibrosis

2020 ◽  
Vol 9 (12) ◽  
pp. 4080
Author(s):  
Fabien Beaufils ◽  
Emmanuel Mas ◽  
Marie Mittaine ◽  
Martin Addra ◽  
Michael Fayon ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Cystic Fibrosis ◽  
Intestinal Inflammation ◽  
Pancreatic Insufficiency ◽  
Gastrointestinal Symptoms ◽  
Fecal Calprotectin ◽  
Stool Samples ◽  
Digestive Disorders ◽  
Cystic Fibrosis Transmembrane

In cystic fibrosis (CF), cystic fibrosis transmembrane regulator (CFTR) dysfunction leads to digestive disorders that promote intestinal inflammation and dysbiosis enhancing gastrointestinal symptoms. In pancreatic insufficiency CF patients, both intestinal inflammation and dysbiosis, are associated with an increase in the fecal calprotectin (FC) level. However, associations between the FC level, gastrointestinal symptoms, and quality of life (QoL) remain poorly studied. We aimed to assess such associations in pancreatic insufficiency CF children. The FC level was measured in pancreatic insufficiency CF children’s stool samples. Children and their parents completed two questionnaires: The Gastrointestinal Symptoms Scales 3.0-PedsQLTM and the Quality of Life Pediatric Inventory 4.0-PedsQLTM. Lower scores indicated worse symptomatology or QoL. Thirty-seven CF children were included. A FC level above 250 µg/g was associated with worse gastrointestinal symptoms and QoL scores. The FC level was inversely correlated with several gastrointestinal scores assessed by children (i.e., Total, “Heart Burn Reflux”, “Nausea and Vomiting”, and “Gas and Bloating”). Several QoL scores were correlated with gastrointestinal scores. The FC level was weakly associated with clinical parameters. Some gastrointestinal and QoL scores were related to disease severity associated parameters. In CF, the FC level, biomarker previously related to intestinal inflammation and dysbiosis, was associated with worse digestive symptoms and QoL scores.

Utility of Fecal Calprotectin in Evaluation of Chronic Gastrointestinal Symptoms in Primary Care

2017 ◽  
Vol 57 (9) ◽  
pp. 1058-1063 ◽  
Author(s):  
Ramya Ramraj ◽  
Amy Garcia ◽  
David Mosen ◽  
Lisa Waiwaiole ◽  
Ning Smith
Keyword(s):  
Primary Care ◽  
Care Setting ◽  
Primary Care Setting ◽  
Intestinal Inflammation ◽  
Gastrointestinal Symptoms ◽  
Fecal Calprotectin ◽  
Primary Indication ◽  
Inflammatory Bowel ◽  
Excellent Tool

Fecal calprotectin (FC) is a marker of intestinal inflammation. Data are limited on utility of routine FC testing in pediatric primary care. Participants 0 to 18 years old who had an FC test in the years 2010-2014 were retrospectively identified. Those with less than a year of follow-up or a prior diagnosis of inflammatory bowel disease (IBD) were excluded. In all, 84% (689/822) had normal FC; no participant with normal FC was diagnosed with IBD in the subsequent 12 months. Also, 16% (133/822) had elevated FC, and 31% of those (42/133) were diagnosed with IBD. FC values for IBD and non-IBD groups were 1084 µg/g (interquartile range [IQR] = 514.4-2000) and 27.05 µg/g (IQR = 15.6-62.6; P < .001), respectively. Abdominal pain was the primary indication. In this cohort, sensitivity of FC for IBD is 100%, and specificity is 88%. The FC test can be an excellent tool in the primary care setting to exclude IBD and avoid unnecessary referrals and colonoscopies.

scholarly journals SAT0388 CHROMOENDOSCOPY AND MAGNIFICATION COLONOSCOPY: ANALYSIS OF THE MUCOSA OF THE COLON AND ILEUM IN PATIENTS WITH SPONDYLOARTRHITIS AND GASTROINTESTINAL SYMPTOMS WITHOUT INFLAMMATORY BOWEL DISEASE

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1142.2-1143
Author(s):  
C. Florez ◽  
V. Parra-Izquierdo ◽  
W. Bautista-Molano ◽  
Y. M. Chamorro-Melo ◽  
A. Beltrán-Ostos ◽  
...  
Keyword(s):  
Intestinal Inflammation ◽  
Gastrointestinal Symptoms ◽  
Fecal Calprotectin ◽  
Inflammatory Back Pain ◽  
Vascular Pattern ◽  
Gastrointestinal Involvement ◽  
Histological Techniques ◽  
Asas Criteria ◽  
The Government ◽  
Axial Involvement

Background:Digital chromoendoscopy with magnification is a technique that identify microscopic inflammation, with a better characterize, highlighting specific gastrointestinal findings showing a good correlation with histopathological features. Spondyloarthritis (SpA) patients with the presence of non-specific gastrointestinal symptoms, subclinical intestinal inflammation is defined by endoscopic and histological techniquesObjectives:To detect early structural inflammatory changes by chromoendoscopy and magnification colonoscopy in colonic/ileum digestive mucosa and establish its association with clinical variables in patients with SpA and gastrointestinal symptomsMethods:In total, 180 patients with SpA (ASAS/criteria) were assessed by rheumatologists, of which (n=35) (19.4%) had an indication by a gastroenterologist to perform the chromoendoscopy, magnification colonoscopy and histological analysis. The association between clinical and colonoscopy variables were evaluated using the Chi square or Fisher’s exact test. (Ethical/Code. 2017-023)Results:The average age of the patients included for colonoscopy was 45.4±10.3 years, 57.1% were men and 42.9% presented the HLA-B*27 allele. Axial involvement (91.4%), inflammatory back pain (68.6%) and use of biological therapy (71.4%). High levels of calprotectin (25.7%), CRP>3 (14.3%), positive ESR (22.9%) and positive ANCA (8.6%) was observed. Regarding outcome measures of function and activity, BASDAI >4 (60%) and ASDAS-PCR >2.1 (80.0%) was observedThe loss of vascular pattern in the ileum was associated with high levels of calprotectin levels (p=0.002). At microscopic level, 80% of the patients who presented acute inflammation in the ileum had elevated calprotectin (p=0.013). Cryptitis (77.8%) in the ileum was associated with axial involvement (p=0.017). Ulcers and erosion in the ileum were associated with positive ESR (p=0.003). All patients who presented ulcerations and inflammation (64.3%) in ileum were HLA-B27 positive (p=0.029) and (p=0.052) respectively. The 50% of patients with atrophy of villi in ileum were receiving biological treatment (p=0.035)Conclusion:Digital chromoendoscopy and augmentation colonoscopy provided an improved and detailed contrast of the surface of the gastrointestinal mucosa. The tissue sampling showed the loss of vascular pattern as main finding in ileum with interesting associations with fecal calprotectin levels in patients with SpA. The interest of proposing the active search for symptoms, signs and biomarkers of gastrointestinal involvement in patients with SpA without IBD is to define subclinical gastrointestinal involvement and early remission through an endoscopic evaluation and objective histological and propose a specific clinical and therapeutic treatment.Acknowledgments:The Government Institute of Science, Technology, and Innovation, Francisco Jose de Caldas—COLCIENCIAS(Grant No. 130877757442). Universidad El Bosque (PCI-2018-10091), Hospital Militar Central (Grant 2017-023), Clínicos IPS, Gastroadvanced, Fundación Instituto de Reumatología Fernando Chalem-Bogota, Colombia and Biomedicina de Chihuahua, MéxicoDisclosure of Interests:None declared

scholarly journals Calprotectin as a marker of bowel inflammation

2013 ◽  
Author(s):  
Gianluca Terrin ◽  
Andrea Pietravalle
Keyword(s):  
Inflammatory Process ◽  
Intestinal Inflammation ◽  
Inflammatory Diseases ◽  
Functional Gastrointestinal Disorders ◽  
Gastrointestinal Symptoms ◽  
Fecal Calprotectin ◽  
Bacterial Degradation ◽  
Human Neutrophils ◽  
Gastrointestinal Disorders ◽  
Non Invasive

In the last years the need for a non-invasive diagnostic tool that would help to discriminate between organic and functional gastrointestinal disorders directed research towards potential immunological markers. A great number of non-invasive bio-markers has been proposed, including eosinophilic cationic protein, elastase, esterase, myeloperoxidase, lysozyme, lactoferrin, and calprotectin. Compared to other biomarkers, calprotectin (also called MRP8/14, calgranulin A/B , S100 A8/A9) may offer advantages based on its biological characteristics. Calprotectin is a 36.5-kDa, calcium and zinc binding polypeptide which constitutes about 60% of soluble cytosol proteins in human neutrophils. It is also found in monocytes, keratinocytes, muscle tissue and infiltrating tissue macrophages. When bound to calcium it becomes resistant to proteolysis and colonic bacterial degradation. This make is stable for up to 1 week at room temperature and facilitate its determination in feces. Calprotectin is involved in the regulation of the inflammatory process, participate to the early innate immune response and exert antimicrobial, anti-proliferative and apoptotic properties. Fecal calprotectin is a direct measure of mucosal inflammation activity and becomes detectable when intestinal inflammation is still at an insufficient level to cause an increase in serum inflammation markers. In the last decade fecal calprotectin has been proposed as a marker to rule out acute and chronic intestinal inflammatory diseases in children with typical gastrointestinal symptoms. Many studies demonstrated its diagnostic utility in identifying children and adults with inflammatory bowel disease and correlate with the degree of disease activity. The detection of elevated levels of fecal calprotectin in healthy infants during the first few weeks of age, limits their use as screening test for intestinal inflammatory diseases in early life. Despite this evidence, the measurement of calprotectin in the serum has been proposed to identify neonates with necrotizing enterocolitis. Recent studies have shown higher fecal calprotectin levels in infants with irritable bowel syndrome and colics, compared with healthy controls. Additionally, a correlation was found between fecal calprotectin concentration and IBS clinical presentation severity. However, these studies do not provide data on diagnostic accuracy in distinguish between organic and functional gastrointestinal disorders. Despite significant limitations, these evidences suggest the presence of a subtle inflammatory process underlying functional gastrointestinal disorders and open new perspectives on their pathogenesis. Fecal calprotectin may play a role that could be revealed in further, specifically designed, studies. Changes in microflora, permeability, calprotectin excretion and other inflammatory biomarkers, should be investigated to clarify if a continuum exists between inflammatory conditions and intestinal functional diseases.

scholarly journals Calprotectin as a marker of bowel inflammation

2013 ◽  
Author(s):  
Gianluca Terrin ◽  
Andrea Pietravalle
Keyword(s):  
Inflammatory Process ◽  
Intestinal Inflammation ◽  
Inflammatory Diseases ◽  
Functional Gastrointestinal Disorders ◽  
Gastrointestinal Symptoms ◽  
Fecal Calprotectin ◽  
Bacterial Degradation ◽  
Human Neutrophils ◽  
Gastrointestinal Disorders ◽  
Non Invasive

In the last years the need for a non-invasive diagnostic tool that would help to discriminate between organic and functional gastrointestinal disorders directed research towards potential immunological markers. A great number of non-invasive bio-markers has been proposed, including eosinophilic cationic protein, elastase, esterase, myeloperoxidase, lysozyme, lactoferrin, and calprotectin. Compared to other biomarkers, calprotectin (also called MRP8/14, calgranulin A/B , S100 A8/A9) may offer advantages based on its biological characteristics. Calprotectin is a 36.5-kDa, calcium and zinc binding polypeptide which constitutes about 60% of soluble cytosol proteins in human neutrophils. It is also found in monocytes, keratinocytes, muscle tissue and infiltrating tissue macrophages. When bound to calcium it becomes resistant to proteolysis and colonic bacterial degradation. This make is stable for up to 1 week at room temperature and facilitate its determination in feces. Calprotectin is involved in the regulation of the inflammatory process, participate to the early innate immune response and exert antimicrobial, anti-proliferative and apoptotic properties. Fecal calprotectin is a direct measure of mucosal inflammation activity and becomes detectable when intestinal inflammation is still at an insufficient level to cause an increase in serum inflammation markers. In the last decade fecal calprotectin has been proposed as a marker to rule out acute and chronic intestinal inflammatory diseases in children with typical gastrointestinal symptoms. Many studies demonstrated its diagnostic utility in identifying children and adults with inflammatory bowel disease and correlate with the degree of disease activity. The detection of elevated levels of fecal calprotectin in healthy infants during the first few weeks of age, limits their use as screening test for intestinal inflammatory diseases in early life. Despite this evidence, the measurement of calprotectin in the serum has been proposed to identify neonates with necrotizing enterocolitis. Recent studies have shown higher fecal calprotectin levels in infants with irritable bowel syndrome and colics, compared with healthy controls. Additionally, a correlation was found between fecal calprotectin concentration and IBS clinical presentation severity. However, these studies do not provide data on diagnostic accuracy in distinguish between organic and functional gastrointestinal disorders. Despite significant limitations, these evidences suggest the presence of a subtle inflammatory process underlying functional gastrointestinal disorders and open new perspectives on their pathogenesis. Fecal calprotectin may play a role that could be revealed in further, specifically designed, studies. Changes in microflora, permeability, calprotectin excretion and other inflammatory biomarkers, should be investigated to clarify if a continuum exists between inflammatory conditions and intestinal functional diseases.

scholarly journals Meta-analysis of the Parkinson’s disease gut microbiome suggests alterations linked to intestinal inflammation

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Stefano Romano ◽  
George M. Savva ◽  
Janis R. Bedarf ◽  
Ian G. Charles ◽  
Falk Hildebrand ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Fatty Acids ◽  
Parkinson's Disease ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
Intestinal Inflammation ◽  
Meta Analysis ◽  
Gastrointestinal Symptoms ◽  
Short Chain Fatty Acids ◽  
Inflammatory Status

AbstractThe gut microbiota is emerging as an important modulator of neurodegenerative diseases, and accumulating evidence has linked gut microbes to Parkinson’s disease (PD) symptomatology and pathophysiology. PD is often preceded by gastrointestinal symptoms and alterations of the enteric nervous system accompany the disease. Several studies have analyzed the gut microbiome in PD, but a consensus on the features of the PD-specific microbiota is missing. Here, we conduct a meta-analysis re-analyzing the ten currently available 16S microbiome datasets to investigate whether common alterations in the gut microbiota of PD patients exist across cohorts. We found significant alterations in the PD-associated microbiome, which are robust to study-specific technical heterogeneities, although differences in microbiome structure between PD and controls are small. Enrichment of the genera Lactobacillus, Akkermansia, and Bifidobacterium and depletion of bacteria belonging to the Lachnospiraceae family and the Faecalibacterium genus, both important short-chain fatty acids producers, emerged as the most consistent PD gut microbiome alterations. This dysbiosis might result in a pro-inflammatory status which could be linked to the recurrent gastrointestinal symptoms affecting PD patients.

Colorectal Inflammation is Well Predicted by Fecal Calprotectin in Children with Gastrointestinal Symptoms

2005 ◽  
Vol 40 (4) ◽  
pp. 450-455 ◽  
Author(s):  
Ulrika Lorentzon Fagerberg ◽  
Lars L????f ◽  
Urban Myrdal ◽  
Lars-Olof Hansson ◽  
Yigael Finkel
Keyword(s):  
Gastrointestinal Symptoms ◽  
Fecal Calprotectin

scholarly journals Neuropeptide Y (NPY) promotes inflammation-induced tumorigenesis by enhancing epithelial cell proliferation

2017 ◽  
Vol 312 (2) ◽  
pp. G103-G111 ◽  
Author(s):  
Sabrina Jeppsson ◽  
Shanthi Srinivasan ◽  
Bindu Chandrasekharan
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Neuropeptide Y ◽  
Intestinal Inflammation ◽  
Enteric Neurons ◽  
Intestinal Epithelial ◽  
Epithelial Proliferation ◽  
Proliferation And Apoptosis

We have demonstrated that neuropeptide Y (NPY), abundantly produced by enteric neurons, is an important regulator of intestinal inflammation. However, the role of NPY in the progression of chronic inflammation to tumorigenesis is unknown. We investigated whether NPY could modulate epithelial cell proliferation and apoptosis, and thus regulate tumorigenesis. Repeated cycles of dextran sodium sulfate (DSS) were used to model inflammation-induced tumorigenesis in wild-type (WT) and NPY knockout ( NPY−/−) mice. Intestinal epithelial cell lines (T84) were used to assess the effects of NPY (0.1 µM) on epithelial proliferation and apoptosis in vitro. DSS-WT mice exhibited enhanced intestinal inflammation, polyp size, and polyp number (7.5 ± 0.8) compared with DSS- NPY−/− mice (4 ± 0.5, P < 0.01). Accordingly, DSS-WT mice also showed increased colonic epithelial proliferation (PCNA, Ki67) and reduced apoptosis (TUNEL) compared with DSS- NPY−/− mice. The apoptosis regulating microRNA, miR-375, was significantly downregulated in the colon of DSS-WT (2-fold, P < 0.01) compared with DSS- NPY−/−-mice. In vitro studies indicated that NPY promotes cell proliferation (increase in PCNA and β-catenin, P < 0.05) via phosphatidyl-inositol-3-kinase (PI3-K)-β-catenin signaling, suppressed miR-375 expression, and reduced apoptosis (increase in phospho-Bad). NPY-treated cells also displayed increased c-Myc and cyclin D1, and reduction in p21 ( P < 0.05). Addition of miR-375 inhibitor to cells already treated with NPY did not further enhance the effects induced by NPY alone. Our findings demonstrate a novel regulation of inflammation-induced tumorigenesis by NPY-epithelial cross talk as mediated by activation of PI3-K signaling and downregulation of miR-375. NEW & NOTEWORTHY Our work exemplifies a novel role of neuropeptide Y (NPY) in regulating inflammation-induced tumorigenesis via two modalities: first by enhanced proliferation (PI3-K/pAkt), and second by downregulation of microRNA-375 (miR-375)-dependent apoptosis in intestinal epithelial cells. Our data establish the existence of a microRNA-mediated cross talk between enteric neurons producing NPY and intestinal epithelial cells, and the potential of neuropeptide-regulated miRNAs as potential therapeutic molecules for the management of inflammation-associated tumors in the gut.

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