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Despite the well-established involvement of the gut microbiome in inflammatory bowel disease (IBD), less is known about how the gut microbiome changes over time and how it varies with clinical disease activity and fecal calprotectin (f-calprotectin). To address this gap, we utilized samples from the population-based inception cohort of the Inflammatory Bowel Disease in South-Eastern Norway III (IBSEN III) study. Data and stool samples from study participants with IBD and symptomatic controls were collected at diagnosis and after 3, 6, and 12 months. Microbiome profiling of stool samples was performed targeting the V3-V4 region of the 16S rRNA gene, and a consensus-based approach of mixed models was employed for the longitudinal microbiome analysis. We included 1251 samples from 744 patients with ulcerative colitis, 618 samples from 356 patients with Crohn' s disease and 266 samples from 164 symptomatic non-IBD controls. In the IBD population, we observed that levels of f-calprotectin decreased over time, as did the patient-reported disease activity (P < .001). Distinct changes in the gut microbiome of IBD patients were observed throughout the first year, such as increased alpha diversity (P < .001) and significant taxonomic changes.Notably, there was no covariation between the changes in alpha diversity and f-calprotectin or symptom score. The gut microbiome during the first year after IBD diagnosis showed changes that paralleled inflammation and clinical disease activity, albeit without covariation, suggesting that there may be a disease-driving impact of gut microbiome independent of inflammation and inflammation-driven symptoms.

The role of calprotectin in psoriasis still remains unclear. To elucidate the associations between the concentrations of serum and faecal calprotectin (CP) and the severity of psoriasis in 20 patients with moderate-to-severe plaque psoriasis and 20 healthy individuals. The CP levels as well as the disease severity including Psoriasis Area and Severity Index (PASI), Body Surface Area (BSA) score and Dermatology Life Quality Index (DLQI) were assessed. The median serum CP level in the psoriasis group was notably higher at 112.24 μg/l (interquartile range, IQR: 81.39-206.82 μg/l) compared to 60.31 μg/l (IQR: 37.41-81.54 μg/l) in the control group ( = 0.001), while the median faecal CP levels were similar between the two groups: 15.00 μg/g (IQR: 6.20-36.13 μg/g) in psoriasis patients and 13.00 μg/g (IQR: 10.26-30.15 μg/g) in controls ( = 0.766). No significant correlations between serum and faecal CP level and the PASI, BSA and DLQI were found. Despite the fact that patients with moderate-to-severe plaque psoriasis seem to present general higher blood calprotectin levels than healthy individuals, they are still within the population cut-off value. The elevated blood calprotectin levels are not conclusively linked to increased severity of psoriasis or to the deterioration in quality of life. Also, in individuals with psoriasis, gastrointestinal inflammation does not differ markedly from healthy controls.

Ulcerative colitis and Crohn’s disease are the principal forms of inflammatory bowel disease. Both represent chronic inflammation of the gastrointestinal tract, which displays heterogeneity in inflammatory and symptomatic burden between patients and within individuals over time. Optimal management relies on understanding and tailoring evidence-based interventions by clinicians in partnership with patients. This guideline for management of inflammatory bowel disease in adults over 16 years of age was developed by Stakeholders representing UK physicians (British Society of Gastroenterology), surgeons (Association of Coloproctology of Great Britain and Ireland), specialist nurses (Royal College of Nursing), paediatricians (British Society of Paediatric Gastroenterology, Hepatology and Nutrition), dietitians (British Dietetic Association), radiologists (British Society of Gastrointestinal and Abdominal Radiology), general practitioners (Primary Care Society for Gastroenterology) and patients (Crohn’s and Colitis UK). A systematic review of 88 247 publications and a Delphi consensus process involving 81 multidisciplinary clinicians and patients was undertaken to develop 168 evidence- and expert opinion-based recommendations for pharmacological, non-pharmacological and surgical interventions, as well as optimal service delivery in the management of both ulcerative colitis and Crohn’s disease. Comprehensive up-to-date guidance is provided regarding indications for, initiation and monitoring of immunosuppressive therapies, nutrition interventions, pre-, peri- and postoperative management, as well as structure and function of the multidisciplinary team and integration between primary and secondary care. Twenty research priorities to inform future clinical management are presented, alongside objective measurement of priority importance, determined by 2379 electronic survey responses from individuals living with ulcerative colitis and Crohn’s disease, including patients, their families and friends.

The management of inflammatory bowel disease (IBD), which is characterized by immunodeficiency, has attracted increasing attention, highlighting the necessity for more precise and streamlined diagnostic approaches in clinics. Calprotectin, an immune cell-derived protein with inherent anti-inflammatory and antimicrobial properties, plays a pivotal role in immune regulation and intestinal homeostasis. Its expression levels are intricately linked to IBD activity, enabling differentiation between inflammatory and non-inflammatory states while predicting recurrence risks. As a non-invasive biomarker, fecal calprotectin (FC) and serum calprotectin (SC) analysis offers high reproducibility and clinical utility, facilitating both IBD diagnosis and real-time disease monitoring. Beyond its diagnostic specificity in distinguishing IBD from other gastrointestinal disorders, calprotectin also emerges as a promising therapeutic target, due to its dual role in modulating inflammatory pathways and interacting with the gut microbiota. With collaborative advancements in standardized detection protocols and innovative research methodologies, it is anticipated that calprotectin-based strategies will be integrated into mainstream clinical practice for IBD.

Abstract Background Dogs with chronic enteropathies (CE) displayed elevated IgA seropositivity against specific markers that can be used to develop a novel test. Objective To assess a multivariate test to aid diagnosis of CE in dogs and to monitor treatment-related responses. Animals One hundred fifty-seven dogs with CE/inflammatory bowel disease (IBD), 24 dogs non-IBD gastrointestinal disorders, and 33 normal dogs. Methods Prospective, multicenter, clinical study that enrolled dogs with gastrointestinal disorders. Serum sample collected at enrollment and up to 3 months follow-up measuring OmpC (ACA), canine calprotectin (ACNA), and gliadin-derived peptides (AGA) by ELISA. Results Seropositivity was higher in CE/IBD than normal dogs (66% vs 9% for ACA; 55% vs 15% for ACNA; and 75% vs 6% for AGA; P < .001). When comparing CE/IBD with non-IBD disease, ACA and ACNA displayed discriminating properties (66%, 55% vs 12.5%, 29% respectively) while AGA separated CE from normal cohorts (54% vs 6%). A 3-marker algorithm at cutoff of ACA > 15, ACNA > 6, AGA > 60 differentiates CE/IBD and normal dogs with 90% sensitivity and 96% specificity; and CE/IBD and non-IBD dogs with 80% sensitivity and 86% specificity. Titers decreased after treatment (47%-99% in ACA, 13%-88% in ACNA, and 30%-85% in AGA), changes that were concurrent with clinical improvements. Conclusion and Clinical Importance An assay based on combined measurements of ACA, ACNA, and AGA is useful as a noninvasive diagnostic test to distinguish dogs with CE/IBD. The test also has the potential to monitor response to treatment.

Parkinson’s disease (PD) is characterized by alpha-synuclein misfolding with subsequent intraneuronal amyloid formation and accumulation, low grade neuroinflammatory changes, and selective neurodegeneration. Available evidence suggests that the pathology usually begins in the gut and olfactory mucosa, spreading to the brain via the vagus and olfactory nerves, by a prion-like mechanism. A causal relationship has not been established, but gut dysbiosis is prevalent in PD and may lead to intestinal inflammation and barrier dysfunction. Additionally, epidemiological data indicate a link between inflammatory bowel diseases and PD. Calprotectin and zonulin are markers of intestinal inflammation and barrier permeability, respectively. We evaluated their serum and fecal levels in 22 patients with sporadic PD and 16 unmatched healthy controls. Mean calprotectin was higher in PD, both in serum (14.26 mcg/ml ± 4.50 vs. 5.94 mcg/ml ± 3.80, p = 0.0125) and stool (164.54 mcg/g ± 54.19 vs. 56.19 mcg/g ± 35.88, p = 0.0048). Mean zonulin was also higher in PD serum (26.69 ng/ml ± 3.55 vs. 19.43 ng/ml ± 2.56, p = 0.0046) and stool (100.19 ng/ml ± 28.25 vs. 37.3 ng/ml ± 13.26, p = 0.0012). Calprotectin was above the upper reference limit in 19 PD serums and 6 controls (OR = 10.56, 95% CI = 2.17–51.42, p = 0.0025) and in 20 PD stool samples and 4 controls (OR = 30, 95% CI = 4.75–189.30, p = 0.000045). Increased zonulin was found only in the stool samples of 8 PD patients. Despite the small sample size, our findings are robust, complementing and supporting other recently published results. The relation between serum and fecal calprotectin and zonulin levels and sporadic PD warrants further investigation in larger cohorts.

Fecal calprotectin (FC) is a promising biomarker for diagnosis of inflammatory bowel disease (IBD). However, the utility of FC for assessment of IBD activity has yet to be clearly demonstrated. The aim of our study was to evaluate the diagnostic accuracy of FC for differentiating between patients with active IBD and those in remission.MethodsWe systematically searched the databases Medline, Web of Science, Cochrane Library, and EMBASE for eligible studies from December 2013 or earlier that evaluated activity in ulcerative colitis (UC) and Crohn's disease (CD). A hierarchical summary receiver operating characteristic model was performed to calculate the area under the curve to evaluate the overall diagnostic accuracy. The sensitivities and specificities of each commonly applied cutoff value were pooled using a random effects model.ResultsWe included 13 studies (744 patients with UC and 727 with CD) in the final analysis. The area under the curve values were 0.89 (95% confidence interval, 0.86–0.92), 0.93 (0.89–0.97), and 0.88 (0.83–0.93) in the IBD, UC, and CD groups, respectively. For the IBD group at a cutoff value of 50 μg/g, the pooled sensitivity was 0.92 (0.90–0.94) and specificity 0.60 (0.52–0.67). For a cutoff value at 100 μg/g, the pooled sensitivity was 0.84 (0.80–0.88) and specificity was 0.66 (0.59–0.73). For a cutoff value at 250 μg/g, the pooled sensitivity was 0.80 (0.76–0.84) and specificity was 0.82 (0.77–0.86).ConclusionsThe FC test is a reliable marker for assessing IBD disease activity and may have greater ability to evaluate disease activity in UC than CD.

Background Calprotectin (S100A8/S100A9 protein) is known as a damage-associated molecular pattern (DAMP) protein and reflects mainly neutrophil activation. Serum calprotectin levels might be a good alternative to acute-phase protein as a biomarker in inflammatory rheumatic diseases. The aim of this study is to investigate the association of serum calprotectin with disease activity and severity in rheumatoid arthritis (RA), axial spondyloarthritis (axSpA), and psoriatic arthritis (PsA). Methods Serum calprotectin was measured in patients with RA, axSpA, and PsA from the prospective Swiss Clinical Quality Management (SCQM) registry. Asymptomatic first-degree relatives of RA patients were used as healthy controls (HC). Outcomes included swollen joint count (SJC), Disease Activity Score (DAS), Health Assessment questionnaire (HAQ), joint radiographs, and ultrasound power Doppler (USPD) score for RA; Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Ankylosing Spondylitis Disease Activity Score (ASDAS) and coxitis for axSpA; and SJC and Disease Activity Index for PSoriatic Arthritis (DAPSA) for PsA. Comparison of outcomes by calprotectin quartile levels was performed using Kruskal-Wallis tests for continuous outcomes or trend tests for categorical outcomes. Results A total of 1729 subjects [RA = 969, axSpA = 451, PsA = 237, and HC = 72] were included. Median levels of serum calprotectin were higher in each disease group compared to HC ( p  < 0.01). In RA patients, all clinical outcomes were statistically different between quartiles of serum calprotectin, indicating an association between calprotectin levels and higher disease activity (SJC, DAS, and USPD scores) and severity (joint radiographs and HAQ). In axSpA, an association between calprotectin levels and ASDAS score ( p  < 0.01) and prevalence of coxitis ( p  = 0.02) was observed. For PsA patients, SJC and DAPSA did not differ across calprotectin quartiles. Conclusions This large study supports the association of serum calprotectin levels with disease activity in both RA and axSpA, but not in PsA.

Studies of patients with COVID-19 have demonstrated markedly dysregulated coagulation and a high risk of morbid arterial and venous thrombotic events. Elevated levels of blood neutrophils and neutrophil extracellular traps (NETs) have recently been described in patients with COVID-19. However, their potential role in COVID-19-associated thrombosis remains incompletely understood. In order to elucidate the potential role of hyperactive neutrophils and NET release in COVID-19-associated thrombosis, we conducted a case–control study of patients hospitalized with COVID-19 who developed thrombosis, as compared with gender- and age-matched COVID-19 patients without clinical thrombosis. We found that remnants of NETs (cell-free DNA, myeloperoxidase-DNA complexes, and citrullinated histone H3) and neutrophil-derived S100A8/A9 (calprotectin) in patient sera were associated with higher risk of morbid thrombotic events in spite of prophylactic anticoagulation. These observations underscore the need for urgent investigation into the potential relationship between NETs and unrelenting thrombosis in COVID-19, as well as novel approaches for thrombosis prevention.

INTRODUCTION:The purpose of this study was to investigate the relationship between ultra-processed food (UPF) consumption and (i) symptomatic disease and (ii) intestinal inflammation among adults with inflammatory bowel disease (IBD).METHODS:We identified participants (Crohn's disease [CD] and ulcerative colitis [UC]) from the Manitoba Living with IBD study. Active disease was defined using the IBD Symptom Inventory (score >14 for CD; >13 for UC); fecal calprotectin was measured for intestinal inflammation (>250 μg/g). Diet data were collected using the Harvard Food Frequency Questionnaire. UPF consumption was determined by the NOVA classification system. Percentage of energy consumption from UPFs was calculated and divided into 3 tertiles (T1 = low; T3 = high). Multiple linear regression analysis was used for active disease and inflammation predicted by UPF consumption.RESULTS:Among 135 participants (65% with CD), mean number of episodes of active disease (14.2 vs 6.21) and active inflammation (1.6 vs 0.6) was significantly higher among participants with UC in T3 compared with T1 of UPF consumption (P < 0.05). When adjusting for age, sex, disease type, and duration, number of episodes of active disease was lower in T1 compared with T3 (β = −7.11, P = 0.02); similarly, number of episodes of intestinal inflammation was lower in T1 (β = −0.95, P = 0.03). No significant differences were observed among participants with CD.DISCUSSION:UPF consumption may be a predictor of active symptomatic disease and inflammation among participants with UC. Reducing UPF consumption is a dietary strategy that can be suggested for minimizing symptoms and inflammation among people living with IBD.